Abstract: An assay for using signaling kinases alone or in combination with oligomeric forms of neurodegenerative proteins can include: a) providing a biological sample, e.g., a blood sample, from a subject; b) enriching for neuronally (e.g., central nervous system (“CNS”)) derived microparticles, e.g., exosomes, from the blood sample; c) removing proteins from the surface of the isolated exosomes to produce scrubbed exosomes; d) determining, in the isolated internal contents, set of biomarkers including: (1) at least one signaling kinase and, optionally, at least one oligomeric form of a neurodegenerative protein; or (2) a plurality of different signaling kinases.

Abstract: The present invention describes the use of a NK1-antagonist, in constant combination with pyridostigmine, to facilitate the treatment of a patient suffering from myasthenia gravis by providing a therapeutically effective pyridostigmine bromide daily dose without the dose-limiting gastro-intestinal adverse effects.

Abstract: The present invention describes the administration of an NK1 antagonist, in combination with neostigmine methylsulfate, intravenously, via subcutaneous infusion, or both intravenously and via subcutaneous infusion to facilitate the treatment of a patient suffering from myasthenia gravis by providing a therapeutically effective neostigmine methylsulfate daily dose without the dose-limiting gastrointestinal adverse effects associated with neostigmine methylsulfate.

Abstract: The present invention describes the use of a NK1-antagonist, in constant combination with neostigmine, to facilitate the treatment of a patient suffering from myasthenia gravis by providing a therapeutically effective neostigmine bromide or methylsulfate daily dose without the dose-limiting gastrointestinal adverse effects.

Abstract: An assay for alpha synuclein and its various forms includes: a) providing a blood sample from a subject; b) isolating central nervous system (“CNS”) derived exosomes from the blood sample; c) removing proteins from the surface of the isolated exosomes to produce scrubbed exosomes; d) isolating the internal contents of the scrubbed exosomes; e) determining, in the isolated internal contents, a quantitative measure of oligomeric ?-synuclein protein and, optionally, one or a plurality of protein forms selected from: monomeric ?-synuclein, phosphorylated ?-synuclein, monomeric tau, oligomeric tau, phosphorylated tau, amyloid beta (“a-beta”) 1-40, amyloid beta 1-42, and oligomeric amyloid beta; f) separating species of oligomeric ?-synuclein into a plurality of fractions; g) determining a quantitative measure of each of one or a plurality of the separated oligomeric ?-synuclein species and, optionally, one or a plurality of species selected from: monomeric ?-synuclein, tau-synuclein co-polymers, amyloid beta-synuc

Abstract: Provided are new methods for treating myasthenia gravis or other myasthenic syndromes comprising use of a therapeutically effective amount of a 5HT3-antagonist in combination with a therapeutically effective amount of a neostigmine compound, that attenuates or even abrogates the dose-limiting gastrointestinal adverse effects of neostigmine. The unique properties of the combination allow for the administration of neostigmine at markedly higher doses, e.g., about 4 times higher than recommended oral doses, and about 100 times higher than recommended parenteral doses, as compared with currently marketed products, without affecting its efficacy in treating symptoms of muscle weakness associated with myasthenia gravis or other myasthenic syndromes.

Abstract: Provided herein are methods of developing pharmaceuticals for treatment of neurodegenerative conditions, such as synucleopathic conditions, amyloidopathic conditions, tauopathic conditions, and Huntington's disease. The methods involve using a biomarker to determine the effect of a candidate pharmaceutical on the condition. The biomarker profile includes quantitative measures of each of one or a plurality of neurodegenerative protein forms, wherein the neurodegenerative proteins are, e.g., alpha-synuclein and, amyloid beta, tau or huntingtin. Biomarker profiles include one or more oligomeric forms and, optionally, one or more monomeric forms of the neurodegenerative protein. Neurodegenerative proteins can be quantified from, e.g., CNS-derived exosomes from the blood of a subject.

Abstract: The present invention describes the use of a NK1-antagonist, in constant combination with neostigmine, to facilitate the treatment of a patient suffering from myasthenia gravis by providing a therapeutically effective neostigmine bromide or methylsulfate daily dose without the dose-limiting gastrointestinal adverse effects.

Abstract: The present invention describes the use of a NK1-antagonist, in constant combination with pyridostigmine, to facilitate the treatment of a patient suffering from myasthenia gravis by providing a therapeutically effective pyridostigmine bromide daily dose without the dose-limiting gastro-intestinal adverse effects.

Abstract: The present invention describes the use of a 5HT3-antagonist, in combination with neostigmine, to facilitate the treatment of a patient suffering from myasthenia gravis or other myasthenic syndromes by providing a therapeutically effective neostigmine bromide or methylsulfate daily dose that attenuates or even abrogates the dose-limiting gastrointestinal adverse effects of neostigmine.

Abstract: The use of R(+)-2-amino-3-hydroxypropanoic acid derivatives, nitrogen substituted by a (C1-C6)alkyl, (C3-C6)alkenyl, 3-oxo(C5-C6)alkyl, 3-oxo(C4-C6)alken-2-yl, phenyl(C1-C6)alkyl, phenyl(C2-C6)alkenyl, gem-diphenyl(C1-C6)alkyl, gem-diphenyl(C2-C6)alkenyl, (C1-C6)alcanoyl, optionally N-substituted alanyl, optionally N,N?-disubstituted lysinoyl, phenyl(C1-C6)alkylydene or gem-diphenyl(C1-C6)alkylidene group, and of the pharmaceutically acceptable salts thereof, for preparation of medicaments intended for the treatment of CNS diseases due to reduced glycinergic transmission, particularly for the treatment of autism, schizophrenia and Alzheimer's disease, is described.

Abstract: The use of R(+)-2-amino-3-hydroxypropanoic acid derivatives, nitrogen substituted by a (C1-C6)alkyl, (C3-C6)alkenyl, 3-oxo(C5-C6)alkyl, 3-oxo(C4-C6)alken-2-yl, phenyl(C1-C6)alkyl, phenyl(C2-C6)alkenyl, gem-diphenyl(C1-C6)alkyl, gem-diphenyl(C2-C6)alkenyl, (C1-C6)alcanoyl, optionally N-substituted alanyl, optionally N,N?-disubstituted lysinoyl, phenyl(C1-C6)alkylydene or gem-diphenyl(C1-C6)alkylidene group, and of the pharmaceutically acceptable salts thereof, for preparation of medicaments intended for the treatment of CNS diseases due to reduced glycinergic transmission, particularly for the treatment of autism, schizophrenia and Alzheimer's disease, is described.