81 results about "Multisystem atrophy" patented technology

This invention provides specifically substituted 1,2,4-thiadiazole derivatives for use in the treatment of an α-synucleopathy such as Parkinson's disease, diffuse Lewy body disease, traumatic brain injury, amyotrophic lateral sclerosis, Niemann-Pick disease, Hallervorden-Spatz syndrome, Down syndrome, neuroaxonal dystrophy, multiple system atrophy and Alzheimer's disease. This invention also provides various methods for producing such substituted 1,2,4-thiadiazole derivatives.

The invention relates to novel monoclonal anti-alpha-synuclein antibodies. The antibodies can be used for treating a synucleinopathy such as Parkinson's disease (including idiopathic and inherited forms of Parkinson's disease), Diffuse Lewy Body Disease (DLBD), Lewy body variant of Alzheimer's disease (LBV), Combined Alzheimer's and Parkinson disease, pure autonomic failure and multiple system atrophy.

Novel peptides, whose individual components are L-amino acids or D-amino acids are used as active ingredients in medicaments for treating diseases in which the increased occurrence of free radicals plays a pathophysiological role, or for treating diseases involving acute hypoxia or ischaemia in an organ system of the body, in particular in the central nervous system, or for treating iron-storage diseases such as Hallervorden-Spatz syndrome, or for treating neurodegenerative diseases, in particular Alzheimer's disease, the Lewy body variant of Alzheimer's disease, Parkinson's disease, multi-system atrophy, Lewy body dementia or Huntington's chorea and all syndromes that are similar to the neurodegenerative diseases.

This invention relates to bis- and tris-dihydroxyaryl compounds and their methylenedioxy analogs and pharmaceutically acceptable salts and their use in the modulation of Sirtuin 1 (Sirt1) and there use in neuroprotection for subject suffering from neurodegenerative diseases such as Alzheimer's disease, Huntington's disease, Amyotrophic lateral sclerosis, frontotemporal dementia, Parkinson's disease, including Parkinson's plus diseases such as multiple system atrophy, progressive supranuclear palsy, corticobasal degeneration and dementia with Lewy bodies, and in the manufacture of medicaments for such Sirt1 modulation and neuroprotection.

This invention provides compounds, compositions, and methods for treating a disorder selected from cancer, hyperinsulinemia, hypoglycemia, hyperinsulinemia with hypoglycemia, atypical Parkinson's disease, Huntington's disease, multiple systems atrophy, GM3 synthase deficiency, GM2 synthase deficiency or tauopathy.

This invention provides thiazolylpiperazine derivatives, and N-sulfonyl heterocyclic derivatives including phenyl- and benzyl-thiazolylpiperidine derivatives, and pharmaceutically acceptable salts thereof, which are useful active ingredients for administration in a method for the treatment of an α-synucleopathy such as Parkinson's disease, diffuse Lewy body disease, traumatic brain injury, amyotrophic lateral sclerosis, Niemann-Pick disease, Hallervorden-Spatz syndrome, Down syndrome, neuroaxonal dystrophy, multiple system atrophy and Alzheimer's disease. This invention also provides methods for making such derivatives, and pharmaceutical compositions including such derivatives together with pharmaceutically acceptable excipients.

The present invention relates to certain di- and tri-heteroaryl derivatives, pharmaceutical compositions containing them, and methods of using them, including methods for preventing, reversing, slowing, or inhibiting protein aggregation, and methods of treating diseases that are associated with protein aggregation, including neurodegenerative diseases such as Parkinson's disease, Alzheimer's disease, Lewy body disease, and multiple system atrophy.

The invention provides monoclonal antibody 5C1 and related antibodies. The 5C1 antibody binds to an epitope within residues 118-126 of α-synuclein. The antibodies of the invention are useful, for example, for treating and/or diagnosing disorders associated with α-synuclein, particularly accumulation of α-synuclein deposits. Such disorders include Lewy body diseases, such as Parkinson's disease, Diffuse Lewy Body Disease (DLBD), Lewy body variant of Alzheimer's disease (LBV), Combined Alzheimer's and Parkinson disease, pure autonomic failure and multiple system atrophy (MSA).

The present invention relates to bis-heteroaryl compounds of formula (I), pharmaceutical compositions containing them, and methods of using them, including methods for preventing, reversing, slowing, or inhibiting protein aggregation, and methods of treating diseases that are associated with protein aggregation, including neurodegenerative diseases such as Parkinson's disease, Alzheimer's disease, Lewy body disease, Parkinson's disease with dementia, fronto-temporal dementia, Huntington's Disease, amyotrophic lateral sclerosis, and multiple system atrophy, and cancer including melanoma.

The invention provides new methods for treating certain disorders resulting from neurodegeneration and for treating depression which comprise administration of NR2B subunit selective NMDA antagonists. The disorders that can be treating by the invention include hearing loss, vision loss, neurodegeneration caused by epileptic seizures, neurotoxin poisoning, Restless Leg Syndrome, multi-system atrophy, non-vascular headache, and depression.

The present invention relates to certain bicyclic bis-heteroaryl compounds of Formula (I), pharmaceutical compositions containing them, and methods of using them, including methods for preventing, reversing, slowing, or inhibiting protein aggregation, and methods of treating diseases that are associated with protein aggregation, including neurodegenerative diseases such as Parkinson's disease, Alzheimer's disease, Lewy body disease, Parkinson's disease with dementia, fronto-temporal dementia, Huntington's Disease, amyotrophic lateral sclerosis, and multiple system atrophy, and cancer including melanoma.

The invention discloses a method for enriching or detecting astrocyte-derived exosomes from biological fluids. The method for enriching the astrocyte-derived exosomes comprises the steps of (a) contacting a biological fluid containing an astrocyte-derived exosome with an anti-GLT1 antibody to form an immune complex, wherein the biological fluid is one or more selected from blood, serum, plasma, saliva and urine; and (b) enriching the astrocyte-derived exosome through the immune complex by adoption of a solid-phase or liquid-phase method. A biomarker capable of detecting the astrocyte-derived exosomes is used for assisted diagnosis, differential diagnosis and monitoring of central nervous system diseases such as Alzheimer's disease, Parkinson's disease, multiple system atrophy, prion disease and nervous system tumors such as gliomas and the like, so that markers are prevented from being obtained through traumatic operations.

Present inventions demonstrates that alpha synuclein toxicity such as α-synuclein mediated cell death, alpha synuclein induced reactive oxygen species (ROS) in a cell requires the proapoptotic endonuclease G and that the deletion of the endonuclease G or suppressing of the endonuclease G apoptotic pathway attenuates or counteracts such alpha synuclein toxicity. The present invention compositions and methods for inhibition of α-synuclein toxicity. The inhibiting α-synuclein toxicity can be used in methods of treatment of synucleinopathies, such as Parkinson's disease (PD), dementia with Lewy bodies (DLB), pure autonomic failure (PAF), and multiple system atrophy (MSA) and the manufacture of medicaments for such treatment. In particular The subject matter provided in herein relates to a pharmaceutical compositions containing inhibitors of endonuclease G, and their use in the treatment of synucleinopathies, such as Parkinson's disease, dementia with Lewy bodies, pure autonomic failure, and multiple system atrophy and the manufacture of medicaments for such treatment. Furthermore the present invention relates to a method for the identification of compounds attenuating the synuclein toxicity, said method comprising evaluating the inhibitory action of said compound on the endonuclease G dependent apoptosis.

Novel quinolinone farnesyl transferase inhibitors are provided. These new compounds are useful in the treatment or prevention of synucleinopathies, such as Parkinson's Disease, Diffuse Lewy Body Disease, multiple system atrophy, and disorders of brain iron concentration including pantothenate kinase-associated neurodegeneration (e.g., PANK1), or other neurodegenerative/neurological diseases. Provided compounds are also useful in the treatment of proliferative diseases such as cancer, and in the treatment of neurological diseases, such as cognitive impairment, depression, and anxiety.

The treatment including administering to a subject a therapeutically effective amount of an inventive farnesyl transferase inhibitor compound.

The invention relates to an improved method for predicting the onset of, diagnosing, prognosticating and/or treating dementing diseases. The method comprises determining the level of heme oxygenase-1 suppressor (HOS) activity and/or factor in tissue or body fluid obtained from a patient, and comparing said level with the corresponding level of HOS activity and/or factor in corresponding tissue or body fluid obtained from at least one control person. The tissue or body fluid is suitably blood, plasma, lymphocytes, cerebrospinal fluid, urine, saliva, epithelia or fibroblasts. The method is useful where the dementing disease is any of Alzheimer Disease, Age-Associated Cognitive Decline, Mild Cognitive Impairment, Parkinson disease with dementia, Progressive Supranuclear Palsy, Vascular (i.e. multi-infarct) Dementia, Lewy Body Dementia, Huntington's Disease, Down's syndrome, normal pressure hydrocephalus, corticobasal ganglionic degeneration, multisystem atrophy, head trauma, neurosyphilis, Creutzfeld-Jacob disease and other prion diseases, HIV and other encephalitides, and metabolic disorders such as hypothyroidism and vitamin B12 deficiency. The method may also prove useful in differentiating the“pseudodementia” of depression from Alzheimer disease.