 Patent Application Title |
Patent App Num. |
Date |
| Pirenzepine as an agent in cancer treatment | 20110294791 | 20111201 |
| The present invention generally relates to the neuroprotective activity of condensed diazepinones, e.g. condensed benzodiazepinones such as pirenzepine or compounds which are metabolized to condensed benzodiazepinones such as olanzapine. These compounds are suitable as co-medicaments for the prevention and/or treatment of drug-induced neurotoxic effects in general and neurotoxic side effects during cancer treatments with cytostatic drugs such as platinum-derivatives, e.g. cis-, carbo- and oxaliplatin, taxanes, bleomycin, cyclophosphamide and vincristine etc. Further, these compounds have an intrinsic anti-cancer activity on their own due to PARP-1 inhibition, which prevents NADH depletion in oxidative metabolism of healthy cells thus preventing the shift to anoxygenic, glycolytic metabolism present in many types of tumour cells thus eliminating this crucial metabolic advantage favoring tumour growth. These results exploit the fact of differential... |
| Neurotoxic sterol glycosides | 20110280805 | 20111117 |
| The invention relates to compositions for use in animal models of neurodegenerative disease and methods therefor. More particularly, the invention relates to the use of neurotoxic sterol glycosides or neurotoxic glycolipids, or combinations thereof, in animal models of neurodegenerative disease. Neurotoxicity-modulating chromenols can also be used in these animal models in combination with the neurotoxic sterol glycosides or neurotoxic glycolipids, or combinations thereof.
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| Immunoassay for detection of neurotoxic amino acid associated with neurological disorders | 20110223624 | 20110915 |
| An immunoassay for screening a sample to detect the presence of β-N-methylamino-L-alanine (BMAA) is disclosed. Antibodies specific for BMAA are disclosed. Antibodies that bind to BMAA on immunoblots are disclosed. Immunoassays and kits to detect the presence of BMAA in a sample by contacting the sample with an antibody that binds to BMAA, and detecting the antibody bound to the sample, are disclosed. Immunoassays and kits for screening for the presence of BMAA in a subject by analyzing a tissue sample obtained from the subject to detect the present of BMAA in the tissue sample, where the presence of BMAA in the tissue sample indicates exposure of the subject to an environmental source of BMAA, are disclosed. Immunoassays and kits for detecting an environmental source of... |
| Clostridial neurotoxins with altered persistency | 20110189158 | 20110804 |
| (c) at least one further LC domain or fragment thereof of the neurotoxic component of a clostridial toxin wherein the first and the at least one further LC domain may be the same or different from each other, and wherein each of said fragments of said first and of said at least one further LC domain still exhibits proteolytic activity.
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| Screening for neurotoxic amino acid associated with neurological disorders | 20110183424 | 20110728 |
| Methods for screening for neurological disorders are disclosed. Specifically, methods are disclosed for screening for neurological disorders in a subject by analyzing a tissue sample obtained from the subject for the presence of elevated levels of neurotoxic amino acids or neurotoxic derivatives thereof associated with neurological disorders. In particular, methods are disclosed for diagnosing a neurological disorder in a subject, or predicting the likelihood of developing a neurological disorder in a subject, by determining the levels of β-N-methylamino-L-alanine (BMAA) in a tissue sample obtained from the subject. Methods for screening for environmental factors associated with neurological disorders are disclosed. Methods for inhibiting, treating or preventing neurological disorders are disclosed.
... |
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| Protein biomarkers for in vitro testing of developmental toxicity and enbryotoxicity of chemical substances | 20110143366 | 20110616 |
| Presently, the toxicological assessment of chemicals is mainly performed in vivo using a variety of animal species and in addition taking into account human clinical, biochemical, pathological and morphological data. Over the past years it became increasingly clear that some substances are particularly harmful for children and thus there is a focus on the special vulnerability of the developing human brain. Meanwhile there is a recommendation to test substances with a known neurotoxic or teratogenic (in particular a neuroteratogenic) risk additionally for embryotoxicity. Moreover the US Environmental Protection Agency (EPA) requires embryotoxicity tests for pesticides. Further tests are required if substances shall be used as medicaments (S7A Safety Pharmacology Studies for Human Pharmaceuticals, Guidelines of the International Conference on Harmonization, ICH, 2001).
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| Treatment of renal hypertension or carotid sinus syndrome with adventitial pharmaceutical sympathetic denervation or neuromodulation | 20110104061 | 20110505 |
| Sympathetic nerves run through the adventitia surrounding renal arteries and are critical in the modulation of systemic hypertension. Hyperactivity of these nerves can cause renal hypertension, a disease prevalent in 30-40% of the adult population. Hypertension can be treated with neuromodulating agents (such as angiotensin converting enzyme inhibitors, angiotensin II inhibitors, or aldosterone receptor blockers), but requires adherence to strict medication regimens and often does not reach target blood pressure threshold to reduce risk of major cardiovascular events. A minimally invasive solution is presented here to reduce the activity of the sympathetic nerves surrounding the renal artery by locally delivering neurotoxic or nerve-blocking agents into the adventitia. Extended elution of these agents may also be accomplished in order to tailor the therapy to the patient.
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| Treatment of hypertension by renal vascular delivery of guanethidine | 20110104060 | 20110505 |
| Sympathetic nerves run through the adventitia surrounding renal arteries and are critical in the modulation of systemic hypertension. Hyperactivity of these nerves can cause renal hypertension, a disease prevalent in 30-40% of the adult population. Hypertension can be treated with neuromodulating agents (such as angiotensin converting enzyme inhibitors, angiotensin II inhibitors, or aldosterone receptor blockers), but requires adherence to strict regimens and often does not reach target blood pressure threshold to reduce risk of major cardiovascular events. A minimally invasive solution is presented here to reduce the activity of the sympathetic nerves surrounding the renal artery by locally delivering neurotoxic or sympathetic nerve-blocking agents into the adventitia. Extended elution of these agents may also be accomplished in order to tailor the therapy to the patient.
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| Methods of inhibiting the formation of amyloid-beta diffusable ligands using acylhydrazide compounds | 20110098309 | 20110428 |
| Disclosed are methods of inhibiting, regulating, and/or modulating the formation of soluble, globular, non-fibrillar, neurotoxic amyloid β1-42 oligomers from amyloid β1-42 monomers using acylhydrazide compounds. Also disclosed are methods of treating a patient suffering from diseases associated with the formation of soluble, globular, non-fibrillar, neurotoxic amyloid β1-42 oligomers using acylhydrazide compounds.
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| Quninoline methanol compounds for the treatment and prevention of parasitic infections | 20110092488 | 20110421 |
| Malaria is responsible for 1-2 million deaths and 300-500 million clinical cases annually and is an ever present problem for the military, tourists and business travelers. Mefloquine is known and used for malaria prophylaxis. However it is associated with neurological effects. The present invention is directed to providing new and novel quinoline analogs that are less neurotoxic than mefloquine without compromising efficacy. The present invention is also directed to the prevention and treatment of other microbial, parasitic, protozoan, bacterial and fungal diseases.
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| Vaccine for the treatment of alzheimer's disease | 20110002949 | 20110106 |
| The invention provides a method for the treatment of a patient having a more severe form of Alzheimer's disease (AD), where the severe form of AD is characterized by pathogenic deposits of amyloid beta peptide (Aβ), comprising the administration of an immunogenic fragment of Aβ capable of inducing an immune response in the form of antibodies to specific to the pathogenic deposits of Aβ and, in particular, to neurotoxic forms of Aβ including N-terminally truncated forms of Aβ. The invention further provides a method for selecting a suitable immunogenic fragment of Aβ for the treatment of a more severe form of AD.
... |
| Use of transplatin to prevent hearing loss | 20110014302 | 20110120 |
| Methods and compositions for treating and preventing toxic side effects of platinum-based chemotherapy agents are disclosed, in which transplatin is administered to a subject. Transplatin is shown to have protective effects against cisplatin-induced ototoxicity, nephotoxicity and neurotoxicity. Anti-inflammatory activity of transplatin is demonstrated and methods and compositions for treating and preventing inflammatory pain are described.
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| Modulators of amyloid aggregation | 20110009343 | 20110113 |
| Compounds that modulate the aggregation of amyloidogenic proteins or peptides are disclosed. The modulators of the invention can promote amyloid aggregation or, more preferably, can inhibit natural amyloid aggregation. In a preferred embodiment, the compounds modulate the aggregation of natural β amyloid peptides (β-AP). In a preferred embodiment, the β amyloid modulator compounds of the invention are comprised of an Aβ aggregation core domain and a modifying group coupled thereto such that the compound alters the aggregation or inhibits the neurotoxicity of natural β amyloid peptides when contacted with the peptides. Furthermore, the modulators are capable of altering natural β-AP aggregation when the natural β-APs are in a molar excess amount relative to the modulators. Pharmaceutical compositions comprising the compounds of the invention, and diagnostic and... |
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| Vaccine for the treatment of alzheimer's disease | 20110002949 | 20110106 |
| The invention provides a method for the treatment of a patient having a more severe form of Alzheimer's disease (AD), where the severe form of AD is characterized by pathogenic deposits of amyloid beta peptide (Aβ), comprising the administration of an immunogenic fragment of Aβ capable of inducing an immune response in the form of antibodies to specific to the pathogenic deposits of Aβ and, in particular, to neurotoxic forms of Aβ including N-terminally truncated forms of Aβ. The invention further provides a method for selecting a suitable immunogenic fragment of Aβ for the treatment of a more severe form of AD.
... |
| Compounds, compositions and methods for preventing neurodegeneration in acute and chronic injuries in the central nervous system | 20100331284 | 20101230 |
| The present invention provides compositions and methods for prevention and prophylaxis of neurological diseases accompanied by neuronal death. The invention includes synthesis of 5-benzylamino salicylic acid (BAS) and its derivatives. BAS and its derivatives protect cortical neurons from toxic insults by N-methyl-D-aspartate, Zn2+, and reactive oxygen species. Thus, the present invention provides compositions and methods for treating stroke, traumatic brain and spinal cord injury, epilepsy, and neurodegenerative diseases that are accompanied by severe neuronal loss via excitotoxicity, Zn2+ neurotoxicity, and free radical neurotoxicity.
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| Use of a neurotoxic component of a clostridium botulinum toxin complex to reduce or prevent side effects. | 20100331259 | 20101230 |
| Use of a neurotoxic component of a Clostridium botulinum toxin complex for the facial cosmetic treatment of a human or animal susceptible to suffering from doll's face or frozen face, or the neurotoxic component of a Clostridium botulinum toxin complex for the treatment of a disease or disorder caused by or associated with hyperactive cholinergic innervation of muscles or exocrine glands in a human or animal susceptible to side effects associated with the treatment of said disease or disorder with a Clostridium botulinum toxin complex:
... |
| Compounds, compositions and methods for preventing neurodegeneration in acute and chronic injuries in the central nervous system | 20100323995 | 20101223 |
| The present invention provides compositions and methods for prevention and prophylaxis of neurological diseases accompanied by neuronal death. The invention includes synthesis of 5-benzylamino salicylic acid (BAS) and its derivatives. BAS and its derivatives protect cortical neurons from toxic insults by N-methyl-D-aspartate, Zn2+, and reactive oxygen species. Thus, the present invention provides compositions and methods for treating stroke, traumatic brain and spinal cord injury, epilepsy, and neurodegenerative diseases that are accompanied by severe neuronal loss via excitotoxicity, Zn2+ neurotoxicity, and free radical neurotoxicity.
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| Electrophysiology methods for identification of protein structures in membranes associated to neurodegenerative diseases | 20100311102 | 20101209 |
| This invention corresponds to an in vitro method that employs an electrophysiology technique; in particular, an embodiment of the patch-clamp technique in its perforated type, which will allow us evaluating the neurotoxic capacity of protein structures associated to the generation of neurodegenerative diseases. It addition, it allows evaluating potential pharmacologic capacities of candidate molecules (drugs) in order to prevent, treat, or cure the said diseases. The invention involves the use of peptides that cause neurodegenerative diseases in order to form a spontaneous perforated recording that only occurs with peptides in the patch clamp glass pipette.
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| High-potency botulinum toxin formulations | 20100279945 | 20101104 |
| The present invention provides improved formulations of botulinum toxin that increase delivery of the botulinum toxin to neural and associated tissues and exhibit a higher specific neurotoxicity and higher potency (in LD50 Units) than available formulations of botulinum toxins. These improved formulations enable physicians to treat a wide variety of pathological conditions with a lower toxin load that reduces the risk of inducing an immune response against the toxin and its associated proteins that may ultimately lead to the development of toxin resistance. These benefits are particularly important in the treatment of conditions that require high-dose or chronic administration of botulinum toxin. Additionally, the decreased in LD50 Unit doses of inventive formulations allows for controlled administration limits diffusion. The present invention also provides methods of treating... |
| Amethod of treating neurodegenerative diseases | 20100272787 | 20101028 |
| This invention provides compositions and methods for treating a subject suffering from a disease or disorder of the nervous system, associated with an inflammatory response. This invention further provides a pharmaceutical composition comprising, inter alia, an agent which increases brain levels of interferon-γ; and an agent which reduces the number of brain T regulatory (Treg) cells, and optionally further comprising an agent which suppresses neurotoxic inflammatory brain responses.
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| Cruciferous 3h-1,2-dithiole-3-thione (d3t) and methods of protecting against cell injury | 20100261783 | 20101014 |
| Astrocytes possess important roles in maintaining normal brain function and providing trophic support to the neurons. They also suffer a range of toxic insults, being a chief target of prooxidants such as 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), 1-methyl-4-phenylpyridinium (MPP+), 6-hydroxydopamine (6-OHDA), 4-hydroxy-2-nonenal (HNE), and acrolein. Recently, we have observed that the cellular antioxidants and phase 2 enzymes can be upregulated by 3H-1,2-dithiole-3-thione (D3T), a nutraceutical found in cruciferous vegetables, against many prooxidants in human neuroblastoma cell lines (SH-SY5Y). However, the regulation of the above cellular factors by D3T in astrocytes and their role in ameliorating the neurotoxic effects of the above neurotoxins have not been investigated. In this study, we show that incubation of human primary astrocytes with micromolar concentrations (5-100 IM) of D3T for 24 h resulted in... |
| Compounds for inhibiting beta-amyloid production and methods of identifying the compounds | 20100216784 | 20100826 |
| Provided are compounds useful for treating diseases associated with a cerebral accumulation of Alzheimer's amyloid, such as Alzheimer's disease. Also provided are methods for screening for such compounds, by measuring capacitative calcium entry in cells which optionally overexpress APP or a fragment thereof. Also provided are methods of treating or reducing the risk of developing β-amyloid production, β-amyloid deposition, β-amyloid neurotoxicity (including abnormal hyperphosphorylation of tau) and microgliosis associated with cerebral accumulation of Alzheimer's amyloid by administering therapeutically effective amounts of compounds which decrease β-amyloid production and capacitative calcium entry in cells. Further provided are methods for diagnosing diseases associated with cerebral accumulation of Alzheimer's amyloid in animals or humans by administering diagnostically effective amounts of compounds which inhibit capacitative calcium entry in cells.
... |
| Compounds for inhibiting beta-amyloid production and methods of identifying the compounds | 20100215735 | 20100826 |
| Provided are compounds useful for treating diseases associated with a cerebral accumulation of Alzheimer's amyloid, such as Alzheimer's disease. Also provided are methods for screening for such compounds, by measuring capacitative calcium entry in cells which optionally overexpress APP or a fragment thereof. Also provided are methods of treating or reducing the risk of developing β-amyloid production, β-amyloid deposition, β-amyloid neurotoxicity (including abnormal hyperphosphorylation of tau) and microgliosis associated with cerebral accumulation of Alzheimer's amyloid by administering therapeutically effective amounts of compounds which decrease β-amyloid production and capacitative calcium entry in cells. Further provided are methods for diagnosing diseases associated with cerebral accumulation of Alzheimer's amyloid in animals or humans by administering diagnostically effective amounts of compounds which inhibit capacitative calcium entry in cells.
... |
| Molecular target of neurotoxicity | 20100204251 | 20100812 |
| The present invention relates to the fields of biology, genetics and medicine. In particular it concerns new methods for the detection, characterisation and/or treatment (or management) of neurodegenerative diseases, particularly amyotrophic lateral sclerosis. The invention equally concerns methods for identifying or screening compounds active in these diseases. The invention further concerns the compounds, genes, cells, plasmids or compositions useful for implementing the hereinabove methods. In particular, the invention describes the role of PDE4B in these diseases and its use as a therapeutic, diagnostic or experimental target.
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| Systems and methods for treating post- operative, acute, and chronic pain using an intra-muscular catheter administrated combination of a local anesthetic and a neurotoxin protein | 20100184685 | 20100722 |
| Systems, and methods for the use of such systems, are described that allow for the administration of a combination of a sustained release local anesthetic compound (such as bupivicaine) through a catheter based administration device and direct visualization or percutaneous injection of a neurotoxic protein compound (such as botulinum toxin) for post-operative and refractory treated muscle pain and discomfort in patients having undergone spinal surgery and other muscle splitting or treatments aimed at improving muscle pain. The systems utilize specific catheter-based administration protocols and methods for placement of the catheter in association with muscles surrounding the spine and other anatomical sites within the patient. The utilization of an initial bolus of a specific combination of medications (local anesthetic compound and\or neurotoxic protein compound) followed by a... |
| Pharmaceutical compositions for reducing amyloid deposition, amyloid neurotoxicity, and microgliosis | 20100183711 | 20100722 |
| The present invention provides methods for reducing Aβ deposition, Aβ neurotoxicity and microgliosis in an animal or human afflicted with a cerebral amyloidogenic disease, such as Alzheimer's disease (AD), by administering therapeutically effective amounts of the (R)-enantiomer of the dihydropyridine compound nilvadipine, also known as (−)-nilvadipine, to the animal or human. Further provided are methods for reducing the risk of Aβ deposition, Aβ neurotoxicity and microgliosis in animals or humans suffering from traumatic brain injury by administering (−)-nilvadipine after the traumatic brain injury and continuing treatment for a prescribed period of time thereafter.
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| Use of agents that down-regulate expression of tanis and/or p21 waf1/cip1/sd1 genes, and use of agents that inhibit, degrade, sequester or prevent the neurotoxicity of gene product proteins of tanis and p21 waf1/cip1/sd1 genes | 20100173852 | 20100708 |
| The present invention provides compositions and methods for treating glaucoma, ocular hypertension, and age-related macular degeneration. More specifically, the present invention describes the use of agents that down-regulate expression of tanis and/or p21Waf1/Cip1/Sd1 genes to treat such disorders of the eye.
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| Pediculicidal process and composition | 20100172947 | 20100708 |
| Pediculicidal process which make it possible to combat the growth of the louse Pediculus humanus, according to which the louse is brought into contact with a composition devoid of neurotoxic compounds comprising at least 60% by weight of alkali metal bicarbonate.
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| Methods of inhibiting metastatic cancer by administration of streptolysin o | 20100144602 | 20100610 |
| The invention provides a method for administering streptolysin O for treatment of various conditions including connective tissue disorders, reproductive fibroses and conditions mediated by the CD44 receptor. The invention also provides methods for protecting nerve cells from the effects of neurotoxic agents by the administration of streptolysin O.
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| Cytidine derivative-containing antitumor agent for continuous intravenous administration | 20100120709 | 20100513 |
| The invention provides an antitumor agent containing ECyd or a salt thereof, which is administered to a cancer patient through continuous intravenous administration at a dose of 1.30 to 8.56 mg/m2 as reduced to ECyd, for each administration period of 2 to 336 hours.
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| Polyhydroquinoline compounds and dihydropyridine compounds for inhibiting beta-amyloid production | 20100119599 | 20100513 |
| Provided are methods of treating or reducing the risk of developing beta-amyloid production, beta-amyloid deposition, beta-amyloid neurotoxicity (including abnormal hyperphosphorylation of tau) and microgliosis associated with cerebral accumulation of Alzheimer's amyloid by administering therapeutically effective amounts of polyhydroquinoline and dihydropyridine compounds which decrease Abeta production in cells. Further provided are methods for diagnosing diseases associated with cerebral accumulation of Alzheimer's amyloid in animals or humans by administering diagnostically effective amounts of polyhydroquinoline and dihydropyridine compounds which decrease Abeta production in cells.
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| Pharmaceutical compositions for reducing amyloid deposition, amyloid neurotoxicity, and microgliosis | 20100093810 | 20100415 |
| The present invention provides methods for reducing Aβ deposition, Aβ neurotoxicity and microgliosis in an animal or human afflicted with a cerebral amyloidogenic disease, such as Alzheimer's disease (AD), by administering therapeutically effective amounts of the (R)-enantiomer of the dihydropyridine compound nilvadipine, also known as (−)-nilvadipine, to the animal or human, or by administering a non-racemic enantiomeric mixture of the dihydropyridine compound nilvadipine, to the animal or human. Further provided are methods for reducing the risk of Aβ deposition, Aβ neurotoxicity and microgliosis in animals or humans suffering from traumatic brain injury by administering (−)-nilvadipine, or non-racemic mixture of nilvadipine enantiomers, after the traumatic brain injury and continuing treatment for a prescribed period of time thereafter.
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| Neurodegenerative disease treatment using jak/stat inhibition | 20100069479 | 20100318 |
| The invention relates to treatment of neurodegenerative diseases with JAK/STAT pathway inhibitors to eliminate extracellular cell signaling events leading to cell cycle abrogation and/or apoptosis. Primary neurons were administered neurotoxic proteins, such as gp120, Tat, or gp120 and Tat, with or without IFN-γ added, resulting in neuronal death, and simulated neurodegenerative diseases. The neurodegenerative disease is treated using a JAK/STAT pathway inhibitor, including (—)-epigallocatechin-3-gallate (EGCG), to modulate JAK1 or STAT1 phosphorylation, resulting in resistance to gp120 or Tat neurotoxicity. The invention may be used to treat neurons afflicted with HIV-associated Dementia, multiple sclerosis, Alzheimer's Disease, Parkinson's Disease, amyotrophic lateral sclerosis, or Pick's Disease, and may act in conjunction with antiviral treatment, like HAART.
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| Pyrrolo[1,2-a]imidazoledione effective in the treatment of peripheral neurotoxicity induced by chemotherapeutic agents | 20100062077 | 20100311 |
| The use of a compound of formula (I), is disclosed in treating and/or preventing 5 chemotherapy-induced peripheral neurotoxicity (CIPN). The invention includes pharmaceutical compositions wherein the compound of formula (I) is present in a mixture with anticancer agents. An improved anticancer treatment with reduced CIPN-related side effects is also provided.
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| Targets for human micro rnas in avian influenza virus (h5n1) genome | 20100016414 | 20100121 |
| The present invention relates to targets for Human microRNAs in Avian Influenza Virus (H5N1) Genome and provides specific miRNA targets against H5N1 virus. Existing therapies for Avian flu are of limited use primarily due to genetic re-assortment of the viral genome, generating novel proteins, and thus escaping immune response. In animal models, baculovirus-derived recombinant H5 vaccines were immunogenic and protective, but results in humans were disappointing even when using high doses. Currently, two classes of drugs are available with antiviral activity against influenza viruses: inhibitors of the M2 ion channel, amantadine and rimantadine, and inhibitors of neuraminidase, oseltamivir, and zanamivir. There is paucity of information regarding effectiveness of these drugs in H5N1 infection. These drugs are also well known to have side effects like neurotoxicity. Thus... |
| Reduction of zinc-induced neurotoxic injury by blockade of nitric oxide synthesis | 20090325858 | 20091231 |
| The present invention provides methods of inhibiting release of zinc from neurons and of preventing zinc-mediated brain injury. Also provided are methods of improving cerebral blood flow while preventing zinc-mediated brain injury. Inhibitors of or activators of nitric oxide synthases modulate nitric oxide synthesis to reduce nitric oxide-induced release of neurotoxic amounts of zinc, thereby reducing zinc-mediated neuronal injury after brain trauma.
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| Use of the neurotoxic component of a botulinum toxin for treating arthritis | 20090318360 | 20091224 |
| A method and composition for treating a patient suffering from a disease, disorder or condition and associated pain include the administration to the patient of a therapeutically effective amount of a neurotoxin selected from a group consisting of Botulinum toxin types A, B, C, D, E, F and G.
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| Carrier for targeting nerve cells | 20090311275 | 20091217 |
| The present invention relates to a transport protein which can be obtained by modifying the heavy chain of the neurotoxin formed by Clostridium botulinum wherein (i) the protein binds specifically to nerve cells with a higher or lower affinity as the native neurotoxin; (ii) the protein has an increased or reduced neurotoxicity compared to the native neurotoxin, the neurotoxicity being preferably determined in the hemidiaphragma assay; and/or (iii) the protein comprises a lower affinity against neutralizing antibodies compared to the native neurotoxin. The invention also relates to methods for producing the same and the use thereof in cosmetic and pharmaceutical compositions.
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| Therapeutic indications of colony stimulating factors | 20090305974 | 20091210 |
| The present invention relates to the use of at least one colony stimulating factor (CSF) for the production of medicinal products in the treatment or prophylaxis of coma or neurotoxicity.
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| Neurotoxic oligomers | 20090297538 | 20091203 |
| This invention relates to methods and compositions for the treatment or alleviation of Alzheimer's disease and of other conditions related to abnormal protein aggregation. In particular, the invention relates to methods and compositions for the immunotherapy of Alzheimer's disease, Parkinson's disease, and cataract. In one aspect the invention provides a method of prophylaxis, treatment or alleviation of a condition characterized by pathological aggregation and accumulation of a specific protein associated with an immunizing-effective dose of one or more tyrosine cross-linked compounds, and optionally also comprising copper ions complexed to the compound. Alternatively passive immunization against a tyrosine cross-linked compound may be used. Prophylactic or therapeutic compositions and diagnostic methods are also disclosed and claimed.
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| Non-neurotoxic plasminogen activating factors for treating of stroke | 20090263373 | 20091022 |
| The invention concerns the use and the production of non-neurotoxic plasminogen activating factors, derived, for example, from the common vampire Desmodus rotundus (DSPA), for therapeutic treatment of stroke in humans. The invention provides a novel therapeutic base for treating stroke in humans.
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| Compositions and methods for the treatment of disorders of the central and peripheral nervous systems | 20090258844 | 20091015 |
| The present invention relates to methods and compositions for treating selected conditions of the central and peripheral nervous systems employing non-synaptic mechanisms. More specifically, one aspect of the present invention relates to methods and materials for treating seizure and seizure disorders, epilepsy, status epilepticus, migraine, spreading depression, intracranial hypertension; for treating the pathophysiological effects of head trauma, stroke, ischemia and hypoxia; for treating or protecting from the pathophysiological effects of neurotoxic agents such as ethanol; and for treating neuropsychiatric disorders and central nervous system edema by administering agents that modulate ionic concentrations and/or ionic gradients in the brain, particularly ion-dependent or cation-chloride cotransporter antagonists. Electrolyte cotransport antagonists and combinations of such compositions with other agents for treating various conditions are disclosed.
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| Use of agents that prevent the generation of amyloid-like proteins and/or drusen, and/or use of agents that promote sequestration and/or degradation of, and/or prevent the neurotoxic effects of such proteins in the treatment of macular degeneration | 20090203614 | 20090813 |
| The present invention provides compositions and methods for treating age-related macular degeneration (AMD). More specifically, the methods of the invention target amyloid proteins and drusen that tend to accumulate in the eyes of those patients suffering from AMD. AMD is treated in the methods of the invention by providing agents that sequester and/or degrade such amyloid deposits and/or drusen such that a patient's vision is improved or restored.
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| Use of agents that prevent generation of amyloid and amyloid-like lipoproteins, and/or use of agents that promote sequestration and/or degradation of, and/or prevent neurotoxicity of such proteins in the treatment of hearing loss and improving body balanc | 20090181893 | 20090716 |
| The present invention provides compositions and methods for treating otic disorders. More specifically, the present invention describes the use of agents that down-regulate expression of Tanis and/or p21Waf1/Cip1/Sd1 genes to treat such disorders of the ear.
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| Antidotes to exogenous neurotoxic agents | 20090176802 | 20090709 |
| A novel method for treating a mammal exposed to an exogenous neurotoxic agent is disclosed.
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| Tnp-470 polymer conjugates and use thereof | 20090176874 | 20090709 |
| The present invention relates to conjugates of water-soluble polymers and o-(chloracetyl-carbamoyl) fumagillol (TNP-470) and use of those conjugates as specific intracellular carriers of the TNP-470 into tumor vessels. The present invention further relates to use of those conjugates to lower the neurotoxicity of TNP-470. Preferably, the polymer has a molecular weight in the range of 100 Da to 800 kDa. More preferably, the polymer has a molecular weight no greater than 60 kDa. Most preferably, the polymer has a molecular weight in the range of 15 kDa to 40 kDa.
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| Use of adnf polypeptides for treating peripheral neurotoxicity | 20090137469 | 20090528 |
| This invention relates to the use of ADNF polypeptides in the treatment of neurotoxicity induced by chemical agents or by disease processes. The ADNF polypeptides include ADNF I and ADNF III (also referred to as ADNP) polypeptides, analogs, subsequences such as NAP and SAL, and D-amino acid versions (either wholly D-amino acid peptides or mixed D- and L-amino acid peptides), and combinations thereof which contain their respective active core sites.
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| Compositions and method for the diagnosis, prevention and treatment of alzheimer's disease | 20090123459 | 20090514 |
| Disclosed herein are methods of diagnosing, preventing and treating Alzheimer's disease based on the use of an inhibitor for the binding of amyloid-β (Aβ) to FcγRIIb, and a method of screening the inhibitor. The inhibitor is selected from the group consisting of an FcγRIIb protein or a variant thereof, an FcγRIIb extracellular domain, an anti-FcγRIIb antibody, an FcγRIIb-specific peptide and an FcγRIIb-specific siRNA. The inhibitor reduces the toxic signaling and intracellular translocation of Aβ and the neurotoxicity, neuronal cell death and memory impairment mediated by Aβ by inhibiting the binding between Aβ and FcγRIIb. Thus, the inhibitor is useful in the diagnosis, prevention and treatment of Alzheimer's disease.
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| Method for reducing amyloid deposition, amyloid neurotoxicity, and microgliosis with (-)-nilvadipine enantiomer | 20090092667 | 20090409 |
| The present invention provides methods for reducing Aβ deposition, Aβ neurotoxicity and microgliosis in an animal or human afflicted with a cerebral amyloidogenic disease, such as Alzheimer's disease (AD), by administering therapeutically effective amounts of the (R)-enantiomer of the dihydropyridine compound nilvadipine, also known as (−)-nilvadipine, to the animal or human. Further provided are methods for reducing the risk of Aβ deposition, Aβ neurotoxicity and microgliosis in animals or humans suffering from traumatic brain injury by administering (−)-nilvadipine after the traumatic brain injury and continuing treatment for a prescribed period of time thereafter.
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| Methods of identifying lead compounds that modulate toxicity of neurotoxic polypeptides | 20090068111 | 20090312 |
| Methods of screening candidate agents to identify lead compounds for the development of therapeutic agents for the treatment of a neurodegenerative disease, such as Huntington's Disease and Parkinson's Disease and methods for identifying a mutation in, or changes in expression of, a gene associated with neurodegenerative disease, such as Huntington's Disease and Parkinson's Disease, are provided.
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| Cells and methods for estimation of effects on neurological dysfunction | 20090061474 | 20090305 |
| The invention provides neuron-derived cells obtained by transfecting a receptor-expressing nucleic acid having an aryl hydrocarbon receptor gene, wherein outgrowth of neurites is not observed without adding a substance for the aryl hydrocarbon receptor, and outgrowth of neurites is observed by adding the substance for the aryl hydrocarbon receptor. The invention also provides a method for determining the presence of neurotoxicity of a test substance, a method for acquiring a marker for determining the presence of neurotoxicity of the test substance, a method for acquiring a marker for neurological dysfunction, and a method for determining the effect of the test substance on neurological dysfunction using such cells.
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| Process for providing a temperature-stable muscle relaxant on the basis of the neurotoxic component of botulinum toxin in a solid form | 20090028906 | 20090129 |
| The present invention relates to a method for providing a muscle relaxant at temperatures above 20° C., wherein said muscle relaxant is a solid dry composition comprising the neurotoxic component of botulinum toxin free of complexing proteins.
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| Str50 and uses thereof | 20090029456 | 20090129 |
| The present invention relates to use of a novel gene, STR50 and to STR50 modulators in diagnostic, therapeutic and screening aspects related to neurotoxic events. More particularly, the present invention concerns diagnosing and treating neurodegenerative diseases, and screening for species which can be useful in treating the same.
... |
| Multi-intelligent system for toxicogenomic applications (mista) | 20090024547 | 20090122 |
| A system (100) and method (800) to predict toxicological effects of molecules is provided. The method can include obtaining (802) a three-dimensional (3-D) structure of a molecule from a database, transforming (804) the 3-D structure to a one-dimensional (1-D) geometrical representation using a combination of a molecular transform (114) and wavelet transform (115), computing a topology and electronic structure of the molecule via topological indices, and generating a feature vector (500) comprising the 1-D geometrical representation (510), and the topology and the electronic structure (520). The system can predict at least one among metabolic processes, modes of action, hepatotoxicity, and neurotoxicity.
... |
| Compounds for inhibiting beta-amyloid production | 20090017112 | 20090115 |
| Provided are compounds useful for treating diseases associated with a cerebral accumulation of Alzheimer's amyloid, such as Alzheimer's disease. Also provided are methods of treating or reducing the risk of developing β-amyloid production, β-amyloid deposition, β-amyloid neurotoxicity (including abnormal hyperphosphorylation of tau) and microgliosis associated with cerebral accumulation of Alzheimer's amyloid by administering therapeutically effective amounts of the compounds. Further provided are methods for diagnosing diseases associated with cerebral accumulation of Alzheimer's amyloid in animals or humans by administering diagnostically effective amounts of the compounds.
... |
| Methods of restoring cognitive ability using non-peptidic compounds | 20090018084 | 20090115 |
| Disclosed are methods of enhancing cognitive impairment in a patient wherein the cognitive impairment is due to ADDL neurotoxicity. The methods employ non-peptidic compounds having a molecular weight of less than 1000 and which can antagonize against formation of neurotoxic ADDLs from Aβ1-42 monomers.
... |
| Methods of modifying amyloid beta oligomers using non-peptidic compounds | 20090018218 | 20090115 |
| Disclosed are methods of inhibiting, regulating, and/or modulating the formation of soluble, globular, non-fibrillar, neurotoxic amyloid β1-42 oligomers from amyloid β1-42 monomers. Also disclosed are methods of treating a patient suffering from diseases associated with the formation of soluble, globular, non-fibrillar, neurotoxic amyloid β1-42 oligomers.
... |
| Process for providing a temperature-stable muscle relaxant on the basis of the neurotoxic component of botulinum toxin | 20090010965 | 20090108 |
| d. Stable if stored in containers of different material.
... |
| Non-neurotoxic plasminogen activating factors for treating of stroke | 20090004176 | 20090101 |
| The invention pertains to the use and production of non-neurotoxic plasminogen activating factors e.g. of Desmodus rotundus (DSPA) for the therapeutic treatment of stroke in humans in order to provide a new therapeutic concept for treating stroke in humans.
... |
| Imaging of neural and organ injury or damage | 20080311036 | 20081218 |
| In vivo determination of regional damage with neural and organ injury specific imaging agents. Rapid, and non-invasive imaging compositions and methods for assessment of the extent of neurotoxic cell loss or nervous system damage resulting from nervous system injury due to ischemia, stroke, trauma, chemical or electrical insult, acute drug overdose or exposure to substance abuse (such as “recreational drugs”) infection or other insults. The same or similar rapid, and non-invasive imaging compositions and methods for assessment of the extent of the organ injury comprises any damage, injury or infection, functional failure to specific organs such as liver, kidney, prostate, lung, skeletal muscle, heart, pancreas, stomach, small and large intestine, bladder and the reproductive system as well as damage, injury or infection, functional failure to multi-organs,... |
| Phosphoinositide modulation for the treatment of alzheimer's disease | 20080312187 | 20081218 |
| The present invention relates to methods of treating Alzheimer's Disease which utilize agents that increase neuronal phosphotidylinositol 4,5-biphosphate (PIP2), and to differentiated stem cell-based assay systems that may be used to identify agents that modulate phosphoinositide levels and thereby treat a variety of diseases. It is based, at least in part, on the discovery that edelfosine, an agent that increases PIP2 levels by inhibiting an enzyme that catalyzes PIP2 breakdown, decreases levels of neurotoxic A&bgr;42 peptide, particularly in cells expressing a mutant presenilin gene associated with Familial Alzheimer's Disease.
... |
| Pulsatilla spp. extracts effective in brain function | 20080248143 | 20081009 |
| This invention relates to Pulsatillae Radix extract for improving brain functions. More specifically, this invention relates to Pulsatillae Radix extract, its active fractions and a pharmaceutical product and a health food containing the same respectively having a protective activity against neurotoxicity and a growth inhibitory effect induced by beta-amyloid, an anti-oxidizing effect, a neuron proliferating effect and improving memory thereby effective in improving brain functions such as Mild Cognitive Impairment and dementia.
... |
| In vitro model for neuronal death | 20080227201 | 20080918 |
| This invention demonstrates the formation of a novel polarized membrane lipid raft signaling module in neurons, in response to several diverse neurotoxic stimuli. This polarization occurs well before neurons commit to die, and is an early mechanism in death signaling. The formation of this signaling module is dependent on cholesterol for its formation and provides a mechanistic explanation for the protective effects of cholesterol depleting drugs in several non-neural models of cell death. As such, the formation of the signaling module lends itself as a novel screen for the identification of new drugs and therapeutics which would retard its formation and protect against neuronal injury and death.
... |
| Astrocyte elevated gene-1 and its promoter in treatments for neurotoxicity and malignancy | 20080200412 | 20080821 |
| The present invention is based, at least in part, on the discovery that Astrocyte Elevated Gene-1 (‘AEG-1’) expression (i) suppresses the Excitatory Amino Acid Transporter-2 (‘EAAT-2’) promoter, thereby inhibiting glutamate transport; (ii) supports anchorage independent colony formation of cells, in which it is synergistic with the RAS oncogene; and (iii) is increased in a number of different malignancies. The invention, in various embodiments, provides for methods of treatment of malignancies and neurodegenerative disorders using inhibitors of AEG-1 activity, and provides for screening assays for identifying other compounds that have therapeutic benefit.
... |
| Neurodegenerative protein aggregation inhibition methods and compounds | 20080182792 | 20080731 |
| Methods and compositions are provided for reducing aggregation of neurodegenerative proteins associated with neurotoxicity or other proteins. The compounds comprise a first domain or targeting element for binding to the target proteins linked to a second domain or recruiting element that binds to an aggregation inhibiting protein, e.g. a prolyl isomerase. By associating the aggregating forming proteins or neuronal cells under conditions where aggregating proteins are produced with the compound and the aggregation inhibiting protein, aggregation is reduced. The subject agents can be used in assays, investigating the etiology of the neuronal diseases and for prophylaxis and therapy.
... |
| Treatment of parkinson's disease and related disorders | 20080167216 | 20080710 |
| Described herein are compositions and methods for the treatment of Parkinson's disease (PD) and/or to protect dopaminergic nigrostriatal neuronal cell bodies from 6-OHDA-induced neurotoxicity in a mammal. In various embodiments of the invention, the dopaminergic neuron differentiation factor sonic hedgehog (Shh) and/or its downstream transcription factor target Gli-1 are used in connection with gene therapeutic techniques or direct peptide injection for the aforementioned indications. Kits useful in practicing the inventive method are also disclosed, as are animal models useful for studying various neurodegenerative conditions.
... |
| Use of lactulose in the treatment of autism | 20080161265 | 20080703 |
| A treatment for autism in which an effective amount of lactulose is administered in order to bind excess ammonia in the gastrointestinal tract, the bloodstream, and the nervous system in order to prevent or reverse ammonia poisoning caused by the administration of certain antibiotics. Lactulose molecules in the colon are fermented by certain bacteria. The fermentation process lowers the colonic pH, and ammonia, in the form of ammonium ions, is used by the bacteria for amino acid and protein synthesis. This lowers the serum ammonia levels and reduces neurotoxicity.
... |
| High throughput functional genomics | 20080124789 | 20080529 |
| This invention focuses on the marriage of solid-state electronics and neuronal function to create a new high-throughput electrophysiological assay to determine a compound's acute and chronic effect on cellular function. Electronics, surface chemistry, biotechnology, and fundamental neuroscience are integrated to provide an assay where the reporter element is an array of electrically active cells. This innovative technology can be applied to neurotoxicity, and to screening compounds from combinatorial chemistry, gene function analysis, and basic neuroscience applications. The system of the invention analyzes how the action potential is interrupted by drugs or toxins. Differences in the action potentials are due to individual toxins acting on different biochemical pathways, which in turn affects different ion channels, thereby changing the peak shape of the action potential differently for each... |
| Treatment of neurodegenerative diseases and conditions using par1 antagonists | 20080125498 | 20080529 |
| The present invention features methods for treating and/or preventing neurodegenerative and/or neurotoxic diseases, conditions, and injuries, by inhibiting the activity of protease-activated receptor-1 (PAR1) on neurons and glial cells using PAR1 antagonists.
... |
| Tnp-470 polymer conjugates and use thereof | 20080112919 | 20080515 |
| The present invention relates to conjugates of water-soluble polymers and o-(chloracetyl-carbamoyl) fumagillol (TNP-470) and use of those conjugates as specific intracellular carriers of the TNP-470 into tumor vessels. The present invention further relates to use of those conjugates to lower the neurotoxicity of TNP-470. Preferably, the polymer has a molecular weight in the range of 100 Da to 800 kDa. More preferably, the polymer has a molecular weight no greater than 60 kDa. Most preferably, the polymer has a molecular weight in the range of 15 kDa to 40 kDa.
... |
| Neuroprotectant methods, compositions, and screening methods thereof | 20080107603 | 20080508 |
| The present invention relates in general to methods of protecting a mammalian central nervous system cell from damage, and to methods of treating or ameliorating neurodegenerative diseases. The invention further relates to screening for neuro-protective agents that may alone, or in combination with other neuroprotective agents, aid in protecting cells of the central nervous system from damage attributed to neurotoxic compounds, free radicals, or neurodegenerative diseases. The invention further relates to pharmaceutical compositions comprising L-ergothioneine or other newly identified compounds and pharmaceutically acceptable carriers for administration to a mammal in need of neuroprotection.
... |
| Use of the neurotoxic component of a botulinum toxin for treating a spastic muscle | 20080107763 | 20080508 |
| A method and composition for treating a patient suffering from a disease, disorder or condition and associated pain include the administration to the patient of a therapeutically effective amount of a neurotoxin selected from a group consisting of Botulinum toxin types A, B, C, D, E, F and G.
... |
| Use of the neurotoxic component of a botulinum toxin | 20080096822 | 20080424 |
| A method and composition for treating a patient suffering from a disease, disorder or condition and associated pain include the administration to the patient of a therapeutically effective amount of a neurotoxin selected from a group consisting of Botulinum toxin types A, B, C, D, E, F and G.
... |
| Stop-and-go oxaliplatin treatment regimens | 20080085881 | 20080410 |
| Methods of treating an oxaliplatin-sensitive cancer are disclosed in which a therapy comprising oxaliplatin is initiated, continued until a predetermined endpoint, stopped, then reintroduced after specific criteria are met. This stop-and-go approach reduces or eliminates the neurotoxicity associated with oxaliplatin administration while at the same increasing one or more of the beneficial effects of oxaliplatin therapy.
... |
| Intravenous injection of plasminogen non-neurotoxic activators for treating cerebral stroke | 20080057050 | 20080306 |
| The invention refers to the use of non-neurotoxic plasminogen activating factors, e.g., from Desmodus rotundus (DSPA) or genetically modified plasminogen activating factors, for example of human origin, for the therapeutic treatment of stroke in mammals.
... |
| Use of lactulose in the treatment of autism | 20080058282 | 20080306 |
| A treatment for autism in which an effective amount of lactulose is administered in order to bind excess ammonia in the gastrointestinal tract, the bloodstream, and the nervous system in order to prevent or reverse ammonia poisoning caused by the administration of certain antibiotics. Lactulose molecules in the colon are fermented by certain bacteria. The fermentation process lowers the colonic pH, and ammonia, in the form of ammonium ions, is used by the bacteria for amino acid and protein synthesis. This lowers the serum ammonia levels and reduces neurotoxicity.
... |
| Compounds and combinations thereof for inhibiting beta-amyloid production and methods of use thereof | 20080058330 | 20080306 |
| Provided are compounds which can be used in combination for treating diseases associated with a condition associated with cerebral accumulation of Alzheimer's amyloid, such as Alzheimer's disease. Also provided are methods of treating or reducing the risk of developing β-amyloid production, β-amyloid deposition, β-amyloid neurotoxicity (including abnormal hyperphosphorylation of tau) and microgliosis associated with cerebral accumulation of Alzheimer's amyloid by administering therapeutically effective amounts of compounds which in combination can decrease β-amyloid production and capacitative calcium entry in cells. Further provided are methods for diagnosing diseases associated with cerebral accumulation of Alzheimer's amyloid in animals or humans by administering diagnostically effective amounts of the compounds.
... |
| Method for screening for anti-amyloidogenic properties and method for treatment of neurodegenerative disease | 20080051337 | 20080228 |
| The methodologies of the present invention demonstrate that a critical balance between pro- and anti-amyloidogenic molecules exists that regulates amyloid formation and cell death in Alzheimer's disease and Parkinson's disease. β-Synuclein, the non-amyloidogenic homologue of α-synuclein, is a negative modulator of α-synuclein and Aβ aggregation, having neuroprotective properties against α-synuclein and Aβ neurotoxicity and that β-synuclein and therapeutic agents derived therefrom block amyloidogenesis and neurodegeneration in vivo. The method of the present invention establishes that β-synuclein blocks Aβ aggregation either by direct inhibition of Aβ amyloidogenesis or indirectly via either α-synuclein or its 35 a.a. NAC region, inferring neuroprotective characteristics within the effected cells. The generation of a transgenic mouse line and a cell system overexpressing α-synuclein characterizes the mechanisms by which β-synuclein blocks α-synuclein and... |
| Nmda receptor antagonist formulation with reduced neurotoxicity | 20080041367 | 20080221 |
| The present invention is directed to pharmaceutical compositions of effective amounts of NMDA receptor antagonists and preservative for the administration to a patient in need of effective analgesia and anesthesia. The compositions of the invention advantageously do not cause any significant neurotoxicity. The preferred NMDA receptor antagonist is ketamine. The preferred preservative is benzalkonium chloride.
... |
| Targets for human micro rnas in avian influenza virus (h5n1) genome | 20080045472 | 20080221 |
| The present invention relates to targets for Human microRNAs in Avian Influenza Virus (H5N1) Genome and provides specific miRNA targets against H5N1 virus. Existing therapies for Avian flu are of limited use primarily due to genetic re-assortment of the viral genome, generating novel proteins, and thus escaping immune response. In animal models, baculovirus-derived recombinant H5 vaccines were immunogenic and protective, but results in humans were disappointing even when using high doses. Currently, two classes of drugs are available with antiviral activity against influenza viruses: inhibitors of the M2 ion channel, amantadine and rimantadine, and inhibitors of neuraminidase, oseltamivir, and zanamivir. There is paucity of information regarding effectiveness of these drugs in H5N1 infection. These drugs are also well known to have side effects like neurotoxicity. Thus... |
| Composition and method to inhibit tissue plasminogen activator (tpa) - potentiated neurotoxicity | 20080039471 | 20080214 |
| The present invention relates to methods of treating, preventing or ameliorating ischemia-related, neural cell degeneration in a subject being treated with a thrombolytic agent, by administering to the subject one or more neuroprotective thiosemicarbazone compounds. More particularly, the present invention relates to methods of preventing, treating or ameliorating the adverse neurological side effects of tissue plasminogen activator, which is used in the treatment of ischemic stroke, by co-administering one or more compounds of the present invention. One such neuroprotective compound is PAN-811. The invention also relates to compositions comprising PAN-811 or analogs thereof in admixture with a thrombolytic agent, such as tPA.
... |
| Neurotoxicity methods process | 20080020369 | 20080124 |
| A method for testing the cytotoxicity of an implant comprising: providing neuronal cells in-vitro; providing one or more compounds of the implantable medical device; adding the one or more compounds from the implantable medical device to the in-vitro neuronal cells; and determining a measure of the cytotoxicity of the one or more compounds based on an assessment of the neuronal cells.
... |
| High frequency application of botulinum toxin therapy | 20080003241 | 20080103 |
| The present invention relates to methods for treating diseases and disorders by administering a composition containing the neurotoxic component of a Clostridium botulinum toxin complex, wherein the composition is devoid of any other protein of the Clostridium botulinum toxin complex and wherein the composition is administered at short intervals and/or in high doses.
... |
| Neurotoxic component of a botulinum toxin | 20080003318 | 20080103 |
| A method and composition for treating a patient suffering from a disease, disorder or condition and associated pain include the administration to the patient of a therapeutically effective amount of a neurotoxin selected from a group consisting of Botulinum toxin types A, B, C, D, E, F and G.
... |
| Method for treating smooth muscle disorders with a neurotoxic component of a botulinum toxin | 20080004219 | 20080103 |
| A method and composition for treating a patient suffering from a disease, disorder or condition and associated pain include the administration to the patient of a therapeutically effective amount of a neurotoxin selected from a group consisting of Botulinum toxin types A, B, C, D, E, F and G.
... |
| Screening for neurotoxic amino acid associated with neurological disorders | 20070292893 | 20071220 |
| Methods for screening for neurological disorders are disclosed. Specifically, methods are disclosed for screening for neurological disorders in a subject by analyzing a tissue sample obtained from the subject for the presence of elevated levels of neurotoxic amino acids or neurotoxic derivatives thereof associated with neurological disorders. In particular, methods are disclosed for diagnosing a neurological disorder in a subject, or predicting the likelihood of developing a neurological disorder in a subject, by determining the levels of β-N-methylamino-L-alanine (BMAA) in a tissue sample obtained from the subject. Methods for screening for environmental factors associated with neurological disorders are disclosed. Methods for inhibiting, treating or preventing neurological disorders are disclosed.
... |
| Novel methods for ester detoxication | 20070286846 | 20071213 |
| This invention relates to a method for detoxication of inorganic or organic esters including OP nerve agents, cocaine, and respective analogs. More specifically, this invention pertains to the treatment of potentially neurotoxic esters or other ester groups by elaborating a more effective hydrolytic enzyme for therapeutic application. The structures of the synthesized OP analogs are provided. This invention also provides a diagnostic method and an Array Biosensor for detecting OP agents in biological and environmental samples.
... |
| Ginkgo biloba extract as a treatment for therapeutic-induced neurotoxicity | 20070269539 | 20071122 |
| The invention features methods for treating neurotoxicity associated with therapeutic agents, e.g., chemotherapeutic agents, and compositions and kits for use therein. The methods employ an extract of Ginkgo biloba to mitigate the neurotoxic effects of the therapeutic agents.
... |
| Screening for neurotoxic amino acid associated with neurological disorders | 20070254315 | 20071101 |
| Methods for screening for neurological disorders are disclosed. Specifically, methods are disclosed for screening for neurological disorders in a subject by analyzing a tissue sample obtained from the subject for the presence of elevated levels of neurotoxic amino acids or neurotoxic derivatives thereof associated with neurological disorders. In particular, methods are disclosed for diagnosing a neurological disorder in a subject, or predicting the likelihood of developing a neurological disorder in a subject, by determining the levels of β-N-methylamino-L-alanine (BMAA) in a tissue sample obtained from the subject. Methods for screening for environmental factors associated with neurological disorders are disclosed. Methods for inhibiting, treating or preventing neurological disorders are disclosed.
... |
| Composition and methods for alleviating symptoms of neurotoxicity | 20070248690 | 20071025 |
| A composition for alleviating symptoms associated with neurotoxicity. The composition may comprise compounds for preventing glutamate mediated neurotoxicity. The composition may include one or more of the following elements: at least one glutamate antagonist, at least one cAMP stimulating agent, at least one antioxidant, vitamin B12, at least one transporter and at least one surfactant. The composition may be used in methods for alleviating tinnitus, Ménière's Disease and/or hearing loss.
... |
| Botulinum toxin neurotoxic component for treating juvenile cerebral palsy | 20070224221 | 20070927 |
| The invention provides for the use of a presynaptic neurotoxin (for example a bacterial neurotoxin such as botulinum toxin A) for the manufacture of a medicament for the treatment of cerebral palsy in juvenile patients. The juvenile patients are preferably juveniles of up to 6 years in age.
... |
| Method of treatment of tendonitis by administration of streptolysin o | 20070219119 | 20070920 |
| The invention provides a method for administering streptolysin O for treatment of various conditions including connective tissue disorders, reproductive fibroses and conditions mediated by the CD44 receptor. The invention also provides methods for protecting nerve cells from the effects of neurotoxic agents by the administration of streptolysin O.
... |
| Novel non-psychotropic cannabinoids | 20070213369 | 20070913 |
| Novel non-psychotropic cannabinoids are disclosed and pharmaceutical compositions comprising these novel compounds are described for preventing neurotoxicity, neuroinflammation, immune or inflammatory disorders comprising as active ingredient the stereospecific (+) enantiomer, having (3S,4S) configuration of Δ6 tetrahydrocannabinol type compounds. The compositions are particularly effective in alleviating and even preventing neurotoxicity due to acute injuries to the central nervous system, including mechanical trauma, compromised or reduced blood supply as may occur in cardiac arrest or stroke, or poisonings. They are also effective in the treatment of certain inflammatory disorders and chronic degenerative diseases characterized by neuronal loss and chronic pain including neuropathic pain.
... |
| Use of the neurotoxic component of a botulinum toxin for the treatment of pain associated with muscle activity or contracture | 20070202129 | 20070830 |
| A method and composition for treating a patient suffering from a disease, disorder or condition and associated pain include the administration to the patient of a therapeutically effective amount of a neurotoxin selected from a group consisting of Botulinum toxin types A, B, C, D, E, F and G.
... |
| Compounds for inhibiting beta-amyloid production and methods of identifying the compounds | 20070191409 | 20070816 |
| Provided are compounds useful for treating diseases associated with a cerebral accumulation of Alzheimer's amyloid, such as Alzheimer's disease. Also provided are methods for screening for such compounds, by measuring capacitative calcium entry in cells which optionally overexpress APP or a fragment thereof. Also provided are methods of treating or reducing the risk of developing β-amyloid production, β-amyloid deposition, β-amyloid neurotoxicity (including abnormal hyperphosphorylation of tau) and microgliosis associated with cerebral accumulation of Alzheimer's amyloid by administering therapeutically effective amounts of compounds which decrease β-amyloid production and capacitative calcium entry in cells. Further provided are methods for diagnosing diseases associated with cerebral accumulation of Alzheimer's amyloid in animals or humans by administering diagnostically effective amounts of compounds which inhibit capacitative calcium entry in cells.
... |
| Compounds for inhibiting beta-amyloid production and methods of identifying the compounds | 20070185130 | 20070809 |
| Provided are compounds useful for treating diseases associated with a cerebral accumulation of Alzheimer's amyloid, such as Alzheimer's disease. Also provided are methods for screening for such compounds, by measuring capacitative calcium entry in cells which optionally overexpress APP or a fragment thereof. Also provided are methods of treating or reducing the risk of developing β-amyloid production, β-amyloid deposition, β-amyloid neurotoxicity (including abnormal hyperphosphorylation of tau) and microgliosis associated with cerebral accumulation of Alzheimer's amyloid by administering therapeutically effective amounts of compounds which decrease β-amyloid production and capacitative calcium entry in cells. Further provided are methods for diagnosing diseases associated with cerebral accumulation of Alzheimer's amyloid in animals or humans by administering diagnostically effective amounts of compounds which inhibit capacitative calcium entry in cells.
... |
| Pharmaceutical composition containing obovatol as an active ingredient for the prevention and treatment of neurodegenerative diseases | 20070185215 | 20070809 |
| Disclosed herein a pharmaceutical composition, comprising obovatol as an active ingredient, for the prevention and treatment of neurodegenerative diseases. Having superior inhibitory activity against the production of neurotoxic nitric oxides, the obovatol isolated and purified from Magnoliaceae can be used as active ingredient for a pharmaceutical composition or a neuroprotective agent for the prevention and treatment of neurodegenerative diseases, such as Alzheimer's disease, Parkinson's disease, and multiple sclerosis.
... |
| Secreted neural apoptosis inhibiting proteins | 20070128667 | 20070607 |
| A novel neuroprotectant was identified by microarray analysis that is differentially expressed between the ventricular zone and the cortex of human adult and fetal brain. The secreted protein antagonizes Wnt action in Xenopus embryos. Methods are described for modulating free radical neurotoxicity by contacting cells with the protein, treating neuronal diseases associated with free radical-mediated cell death by administering the protein, determining neuroprotective genomic targets associated with select free radical toxicity pathways by screening with the protein and using the protein to identify other compounds that modulate the biological activity of the secreted protein and the cell machinery that reacts to the secreted protein.
... |
| Use of r-enantiomer of n-propargyl-1-aminoindan, salts, compositions and uses thereof | 20070100001 | 20070503 |
| The subject invention provides methods of treating a subject afflicted with Parkinson's disease, memory disorder, depression, hyperactive syndrome, Attention Deficit Disorder, dementia, brain ischemia, stroke, head trauma injury, spinal trauma injury, neurotrauma, neurodegenerative disease, neurotoxic injury, multiple sclerosis, nerve damage, affective illness, schizophrenia or symptoms of withdrawal from an addictive substance, using the mesylate salt of R(+)-N-propargyl-1-aminoindan.
... |
| Detoxification depot for alzheimer's disease | 20070092508 | 20070426 |
| The invention is directed to a device that is placed inside an Alzheimer's disease (AD) patient for the purpose of extracting and accumulating neurotoxic beta-amyloid peptides (nt-bAP) from body fluids. AD is the consequence of a process in which nt-bAP aggregates to form fibrils and plaques which can cause nerve damage. Since nt-bAP can cross the blood-brain barrier (BBB), the concentration in the central nervous system and in the periphery are in equilibrium. By sequestering nt-bAP, our device will act as a “sink.” It should draw nt-bAP across the BBB, reducing the concentration of soluble nt-bAP in the brain, thereby halting or slowing plaque deposition in the brain. Since plaques and possibly soluble, aggregated nt-bAP are the cause of nerve damage in AD, this process should... |
| Melanocytes in therapy of neurodegenerative diseases | 20070071727 | 20070329 |
| In vitro cultivation method for producing human melanocytes which are capable of melanin and/or L-dopa synthesis, and to various uses of said melanocyte(s). In one preferred aspect, said melanocyte(s) are used in an autologous implantation method in a patient suffering from a neurodegenerative disease, e.g. Parkinson's disease. In another aspect, a screening method is provided utilizing melanocyte(s) from said cultures, wherein substances are screened for which may in any way effect said melanocyte(s). Said substances may e.g., be neurotoxic, neuroprotective, or particularly lethal to melanocytes obtained from a patient suffering from Parkinson's disease. The invention also relates to other uses of said melanocytes, all of which are disclosed herein.
... |
| Transgenic rat as animal model for human huntingdon's disease | 20070044162 | 20070222 |
| Huntington's Disease (HD) is an autosomal-dominant inherited progressive neurodegenerative disease from the group of CAG repeat/polyglutamine diseases and is characterized by a triad of psychiatric alterations, dementia and motor dysfunction. On a sub-cellular level, a mutation with extended CAG tri-nucleotide repeats has been identified as the cause of HD. The therapeutic effects of certain substances can be tested on neurotoxically-induced or transgenic animal models with expanded CAG-repeats. In the present invention, transgenic rats were generated and characterized for human HD. Said rat model for human HD and other diseases of the CNS carries 51 CAG repeats under the control of a rat promoter and has a slow progressive neurological phenotype, closely reflecting human HD syndrome. The comparability of the rat model in relation to human HD... |
| Compounds for inhibiting beta-amyloid production and methods of identifying the compounds | 20070037855 | 20070215 |
| Provided are compounds useful for treating diseases associated with a cerebral accumulation of Alzheimer's amyloid, such as Alzheimer's disease. Also provided are methods for screening for such compounds, by measuring capacitative calcium entry in cells which optionally overexpress APP or a fragment thereof. Also provided are methods of treating or reducing the risk of developing β-amyloid production, β-amyloid deposition, β-amyloid neurotoxicity (including abnormal hyperphosphorylation of tau) and microgliosis associated with cerebral accumulation of Alzheimer's amyloid by administering therapeutically effective amounts of compounds which decrease β-amyloid production and capacitative calcium entry in cells. Further provided are methods for diagnosing diseases associated with cerebral accumulation of Alzheimer's amyloid in animals or humans by administering diagnostically effective amounts of compounds which inhibit capacitative calcium entry in cells.
... |
| Identification, diagnosis, and treatment of neuropathologies, neurotoxicities, tumors, and brain and spinal cord injuries using electrodes with microvoltammetry | 20070026440 | 20070201 |
| The present invention relates to devices and methods of use thereof for detection of biomolecules, in vitro, in vivo, or in situ. The invention relates to methods of diagnosing and/or treating a subject as having or being at risk of developing a disease or condition that is associated with abnormal levels of one or more biomolecules including, but not limited to, inter alia, epilepsy, diseases of the basal ganglia, athetoid, dystonic diseases, neoplasms, Parkinson's disease, brain injuries, spinal cord injuries, and cancer. The invention also provides methods of differentiating white matter from gray matter. In some embodiments, regions of the brain to be resected or targeted for pharmaceutical therapy are identified using sensors. The invention further provides methods of measuring the neurotoxicity of a material by... |
| Method and apparatus for the treatment of fluid waste streams | 20060286006 | 20061221 |
| This invention relates generally to methods and apparatus for the detoxification of fluid streams, for example, wastewater contaminated with neurotoxins, particularly organophosphorous compounds, and comprises contacting the fluid stream with a bioactive coating. More particularly, the invention relates to chemical reactors for detoxifying fluid streams and also, bioactive coated support components comprising rigid, semi-rigid, or flexible support materials coated with a bioactive coating compriseing dessicated whole cells, whole cell fragments, enzymes, and combinations thereof that are capable of hydrolizing neurotoxic organophosphorous chemical compounds. Organophosphorus hydrolases that are capable of detoxifying organophosphorus compounds that are: chemical weapons agents, in particular, tabun (“GA”), sarin (“GB”), soman (“GD”), cyclosarin, VX, and its isometric analog Russian VX (“VR” or “R-VX”); chemical weapons agent analogs, chemical weapons surrogates; and pesticides are... |
| Process for the manufacture of 1,2-benzisoxazole-3-methanesulphonamide | 20060287535 | 20061221 |
| The present invention provides an improved process for the preparation of 1,2-Benzisoxazole-3-methanesulphonamide (Zonisamide), an anti-epileptic agent having anti-convulsant and anti-neurotoxic effects. In another aspect, the invention provides a key intermediate, 1,2-benzisoxazole-3-methane sodium sulfonate (BOS-Na:NaCl), isolated as a crystalline sodium chloride associated compound. The BOS-Na:NaCl isolated is directly converted to Zonisamide using a controlled molar ratio of chlorosulfonic acid to avoid conversion to the disulfonated side products.
... |
| Neurotoxic agents and devices to treat atrial fibrillation | 20060282120 | 20061214 |
| Devices and methods to treat atrial fibrillation via inhibition of nerves which innervate the pulmonary vein are provided.
... |
| Cells and methods for estimation of effects on neurological dysfunction | 20060275275 | 20061207 |
| The invention provides neuron-derived cells obtained by transfecting a receptor-expressing nucleic acid having an aryl hydrocarbon receptor gene, wherein outgrowth of neurites is not observed without adding a substance for the aryl hydrocarbon receptor, and outgrowth of neurites is observed by adding the substance for the aryl hydrocarbon receptor. The invention also provides a method for determining the presence of neurotoxicity of a test substance, a method for acquiring a marker for determining the presence of neurotoxicity of the test substance, a method for acquiring a marker for neurological dysfunction, and a method for determining the effect of the test substance on neurological dysfunction using such cells.
... |
| Methods for treatment of neuro- and nephro- disorders and therapeutic toxicities using aminothiol compounds | 20060270636 | 20061130 |
| The present invention relates to new uses of S-2-(3-aminopropylamino)ethyl dihydrogen phosphorothioate, (amifostine) and other aminothiol compounds to treat and reverse toxicities caused by therapeutic agents, radiation treatment or diabetes. In particular, the invention provides a method for treating neurotoxicity and nephrotoxicity associated with the administration of chemotherapeutic agents.
... |
| Dosing regimen | 20060258736 | 20061116 |
| This invention relates to a twice weekly administration of 3′-tert-Butyl-3′-N-tert-butyloxycarbonyl-4-deacetyl-3′-dephenyl-3′-N-debenzoyl-4-O-methoxycarbonyl-paclitaxel that has been found to reduce the neurotoxicity of the drug and allow for better patient compliance in the use of this oral cancer drug.
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| Use of adnf polypeptides for treating peripheral neurotoxicity | 20060247168 | 20061102 |
| This invention relates to the use of ADNF polypeptides in the treatment of neurotoxicity induced by chemical agents or by disease processes. The ADNF polypeptides include ADNF I and ADNF III (also referred to as ADNP) polypeptides, analogs, subsequences such as NAP and SAL, and D-amino acid versions (either wholly D-amino acid peptides or mixed D- and L-amino acid peptides), and combinations thereof which contain their respective active core sites.
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| Sigma-1 receptor ligand with acetylcholinesterase | 20060247248 | 20061102 |
| A novel compound and method for preventing or treating neurodegenerative diseases by inhibiting acetylcholinesterase and binding the sigma-1 receptor are disclosed. Dimethylcarbamic acid 2,3-bis-dimethylcarbamoyloxy-6-[4-(4-ethyl-piperazin-yl)-butyryl]-phenyl ester and its derivatives represent a novel therapeutic strategy against β-amyloid peptide induced neurotoxicity, in inhibiting acetylcholinesterase, in improving cholinergic transmission, in binding the sigma-1 receptor, and in releasing a metabolite that is active both as a sigma-1 receptor ligand and an antioxidant.
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| Extract of petasites japonicus having neuroprotective effect and antioxidant activity | 20060210652 | 20060921 |
| The present invention relates to an extract of Petasites japonicus having antioxidant activity, and more particularly, to an extract of Petasites japonicus having antioxidant activity which is extracted using an alcohol and an antioxidant for the prevention and treatment of a brain disease comprising the extract as an effective ingredient. The Petasites japonicus extract according to the present relief of neurotoxicity and neuroprotective prevention and treatment of brain diseases such as Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, hypoxic-ischemic injury and chronic spinal cord injury.
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| Compounds for inhibiting beta-amyloid production and methods of identifying the compounds | 20060188938 | 20060824 |
| Provided are compounds useful for treating diseases associated with a cerebral accumulation of Alzheimer's amyloid, such as Alzheimer's disease. Also provided are methods for screening for such compounds, by measuring capacitative calcium entry in cells which optionally overexpress APP or a fragment thereof. Also provided are methods of treating or reducing the risk of developing β-amyloid production, β-amyloid deposition, β-amyloid neurotoxicity (including abnormal hyperphosphorylation of tau) and microgliosis associated with cerebral accumulation of Alzheimer's amyloid by administering therapeutically effective amounts of compounds which decrease β-amyloid production and capacitative calcium entry in cells. Further provided are methods for diagnosing diseases associated with cerebral accumulation of Alzheimer's amyloid in animals or humans by administering diagnostically effective amounts of compounds which inhibit capacitative calcium entry in cells.
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| High-potency botulinum toxin formulations | 20060182767 | 20060817 |
| The present invention provides improved formulations of botulinum toxin that increase delivery of the botulinum toxin to neural and associated tissues and exhibit a higher specific neurotoxicity and higher potency (in LD50 Units) than available formulations of botulinum toxins. These improved formulations enable physicians to treat a wide variety of pathological conditions with a lower toxin load that reduces the risk of inducing an immune response against the toxin and its associated proteins that may ultimately lead to the development of toxin resistance. These benefits are particularly important in the treatment of conditions that require high-dose or chronic administration of botulinum toxin. Additionally, the decreased in LD50 Unit doses of inventive formulations allows for controlled administration limits diffusion. The present invention also provides methods of treating... |
| Hsp20 inhibits amyloidogenesis and neurotoxicity | 20060147463 | 20060706 |
| The present invention compositions and methods of using at least a portions of an isolated and purified α-crystallin polypeptide that includes one or more β-pleated sheets and that prevents neurotoxicity and amyloidogenesis.
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| Non-neurotoxic plasminogen activating factors for treating of stroke | 20060142195 | 20060629 |
| The invention pertains to the use and production of non-neurotoxic plasminogen activating factors e.g. of Desmodus rotundus (DSPA) for the therapeutic treatment of stroke in humans in order to provide a new therapeutic concept for treating stroke in humans.
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| Intravenous injection of plasminogen non-neurotoxic activators for treating cerebral stroke | 20060135425 | 20060622 |
| The invention refers to the use of non-neurotoxic plasminogen activating factors, e.g., from Desmodus rotundus (DSPA) or genetically modified plasminogen activating factors, for example of human origin, for the therapeutic treatment of stroke in mammals.
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| Compounds, compositions and methods for preventing neurodegeneration in acute and chronic injuries in the central nervous system | 20060128677 | 20060615 |
| The present invention provides compositions and methods for prevention and prophylaxis of neurological diseases accompanied by neuronal death. The invention includes synthesis of 5-benzylamino salicylic acid (BAS) and its derivatives. BAS and its derivatives protect cortical neurons from toxic insults by N-methyl-D-aspartate, Zn2+, and reactive oxygen species. Thus, the present invention provides compositions and methods for treating stroke, traumatic brain and spinal cord injury, epilepsy, and neurodegenerative diseases that are accompanied by severe neuronal loss via excitotoxicity, Zn2+ neurotoxicity, and free radical neurotoxicity.
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| Use of agents that prevent the generation of amyloid-like proteins and/or drusen, and/or use of agents that promote sequestration and/or degradation of, and/or prevent the neurotoxic effects of such proteins in the treatment of macular degeneration | 20060121039 | 20060608 |
| The present invention provides compositions and methods for treating age-related macular degeneration (AMD). More specifically, the methods of the invention target amyloid proteins and drusen that tend to accumulate in the eyes of those patients suffering from AMD. AMD is treated in the methods of the invention by providing agents that sequester and/or degrade such amyloid deposits and/or drusen such that a patient's vision is improved or restored.
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| Methods and compositions for treatment and prevention of major depressive disorder | 20060105394 | 20060518 |
| The present invention relates to methods of diagnosing, prognosing or treating diseases or disorders in which elevated levels of Abeta protein, including abeta1-42 are prevalent. In particular, the present invention relates to methods of diagnosing, prognosing or treating a major or minor depressive episode/disorder attributed to elevated levels of Abeta protein, including abeta1-42, found particularly in body fluids including whole blood, blood cells, serum, plasma, urine and CSF. The invention also relates to the treatment of these disorders by administering an agent that either prevents production of Abeta, prevents aggregation of Abeta fibrils, or that increases the degradation or clearance of Abeta. In addition, the invention provides a method of treating or preventing a major or minor depressive disorder comprising administering an agent that prevents or... |
| Use of r-enantiomer of n-propargyl-1-aminoindan, salts, compositions and uses thereof | 20060094783 | 20060504 |
| The subject invention provides methods of treating a subject afflicted with Parkinson's disease, memory disorder, depression, hyperactive syndrome, Attention Deficit Disorder, dementia, brain ischemia, stroke, head trauma injury, spinal trauma injury, neurotrauma, neurodegenerative disease, neurotoxic injury, multiple sclerosis, nerve damage, affective illness, schizophrenia or symptoms of withdrawal from an addictive substance, using the mesylate salt of R(+)-N-propargyl-1-aminoindan.
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| Methods and compositions for reducing toxicity of a pharmaceutical compound | 20060089331 | 20060427 |
| The present disclosure is related to clear aqueous solutions of one or more bile acids and either an aqueous soluble starch conversion product or a non-starch polysaccharide. Solutions of the disclosure may be administered to a subject in conjunction with a pharmaceutical compound having one or more toxic effects. In some embodiments, solutions of the disclosure are administered to a mammal in conjunction with a pharmaceutical compound associated with a peripherial neurotoxicity (e.g., cisplatin and/or suramin) to reduce or eliminate the neuropathic effect(s).
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