Abstract: The present invention is based in part methods for treating neurodegenerative diseases and disorders. Specifically, the present invention disclose methods for treating neurodegenerative disorders suing neural stem cells (NSCs) and/or pluripotent stem cell (PSC) derived neurons or neuron precursor cells. The present invention also discloses methods to induce endogenous dopaminergic neurons to release dopamine and increase the levels of dopamine in a subject.

Abstract: Methods and compositions relating to motor neurons derived from induced pluripotent stem cells of subjects having a neurodegenerative disease, where the motor neurons exhibit phenotypes characteristic of the neurodegenerative disease, are provided herein. In particular, the present invention provides methods for screening putative therapeutic agents and methods for diagnosing living subjects as having a neurodegenerative disease. In addition, the present invention provides therapeutic gene transfer methods for treating or preventing a neurodegenerative disease in a subject in need thereof.

Abstract: The present invention relates to Protoxin-II variants, polynucleotides encoding them, and methods of making and using the foregoing.

Abstract: A method is used for diagnosing a disease by detecting in a sample with antibodies from a patient an autoantibody binding to DAGLA.

Abstract: The invention relates to antibodies, and in particular, to antibodies used in the diagnosis and treatment of neurodegenerative disorders, such as Alzheimer's disease and Parkinson's disease. The invention extends to methods of diagnosis and therapy of neurodegenerative disorders, and to assays and screens for isolating novel therapeutic compounds for treating such diseases.

Abstract: Methods of treating an adult mammal for an aging-associated impairment are provided. Aspects of the methods include reducing cell surface VCAM-1 activity in the mammal in a manner sufficient to treat the mammal for the aging-associated impairment. A variety of aging-associated impairments may be treated by practice of the methods, which impairments include cognitive impairments.

Abstract: The present invention relates to a binding molecule having a binding site within the ectodomain of the triggering receptor expressed on myeloid cells 2 (TREM2), wherein the binding molecule inhibits TREM2 cleavage. Said binding molecule is particularly useful for treating and/or preventing a neurological disorder, such as a neurodegenerative disorder. Also encompassed by the present invention is a pharmaceutical composition for use in treating and/or preventing a neurological disorder, wherein the pharmaceutical composition comprises the binding molecule of the present invention. Neurodegenerative disorders that may be treated and/or prevented by using the binding molecule of the present invention include Alzheimer's disease (AD), Frontotemporal lobar degeneration (FTLD), FTLD-like syndrome, Parkinson's disease, Nasu-Hakola disease, Multiple sclerosis (MS), Huntington disease, immune-mediated neuropathies, or Amyotrophic lateral sclerosis (ALS).

Abstract: The present invention relates, in general, to polypeptides capable of transmigrating the blood-brain barrier, and uses thereof. More specifically, the present invention relates to polypeptides derived by site-directed mutagenesis of an existing antibody fragment and uses thereof, and methods of making such molecules. The polypeptides of the present invention show enhanced blood-brain barrier crossing and brain exposure levels in vitro and in vivo.

Abstract: Methods for treating and preventing neurodegenerative disease, neurological injury, including stroke, via administration of Transient receptor potential M2 (TRPM2)-inhibitors. The inhibitors may be administered in conjunction with another therapeutic agent or therapeutic regimen. The peptides may be administered to a human male. The peptides may be administered within eight hours of a neurological injury, such as a stroke.

Abstract: The present disclosure provides methods of screening, diagnosing, monitoring and/or treating acid sphingomyelinase (ASM) disorders such as Niemann-Pick disease. In particular, the methods encompass techniques for improved diagnosis and/or treatment of an ASM disorder, for example using enzyme replacement therapy.

Abstract: The invention relates to methods and compositions for developing basal forebrain cholinergic neurons (BFCNs) from stem cells, and in particular, BFCNs having repaired electrophysiological defects relating to one or more mutations in PSEN2, and to the use of such BFCNs in cell-based therapies to treat Alzheimer's disease.

Abstract: The invention provides antagonistic antibodies to BACE1 and methods of using the same for the treatment of neurological disease and disorders.

Abstract: The present invention provides a method for inducing differentiation of neural stem cells. The present invention provides optimized differentiation conditions of neural stem cells into neurons using a patterned hydrogel.

Abstract: The invention is directed to compositions and methods for treating or reducing the likelihood of the development of epilepsy in an individual. The method comprises administering to the central nervous system of an individual in need of such treatment a therapeutically effective amount of an agent capable of increasing the expression and/or activity of miR-128.

Abstract: The present invention mainly addresses the problem of providing an antibody against semaphorin 3A protein, said antibody enabling effective prevention and/or treatment of a disease, in which Sema 3A protein participates, such as a neurodegenerative disease, autoimmune disease, inflammatory disease, cancer, infectious disease, etc. or disseminated intravascular coagulation syndrome. An anti-Sema 3A antibody comprising CDRs having specific amino acid sequences (SEQ ID NOS: 1-6, 60-62, 64-66, 68-70, 72-74, 76-78, 80-82, 84-86 and 88-90) enables effective prevention and/or treatment of a disease, in which Sema 3A protein participates, such as a neurodegenerative disease, autoimmune disease, inflammatory disease, cancer, infectious disease, etc. or disseminated intravascular coagulation syndrome and, therefore, remarkably ameliorates symptoms associated with such a disease.

Abstract: The present invention relates to a pharmaceutical composition for preventing and treating hearing loss. More particularly, the present invention relates to a composition including a telomerase-derived peptide, the composition being effective in the treatment and prevention of hearing loss due to an ototoxic drug. A peptide having a sequence of SEQ ID NO: 1, a peptide having 80% or more sequence homology to the sequence, or a fragment thereof, according to the present invention, has an excellent effect in the treatment and prevention of hearing loss due to an ototoxic drug.

Abstract: The present invention relates to the field of disorders of the central nervous system, in particular neurological and psychiatric disorders, and the prevention and/or treatment thereof. In particular, the present invention relates to the finding that soluble amyloid precursor protein a (sAPP?) presents a particular binding site, which allows for binding to the GABABR1a receptor, thereby causing an agonistic effect through specific binding to Sushi domain 1 of GABABR1a. As a result, the frequencies of excitatory and inhibitory postsynaptic currents are reduced. Accordingly, the invention provides compounds able to interfere with the association of sAPP? with Sushi domain 1 of GABABR1a and as such with selective impairment of GABABR1sa beneficial in neurological and psychiatric disorders. The invention as well provides methods and (high content) screening assays for the production of said compounds.

Abstract: Cardiac neural crest cells and methods for making and using the same to effect cardiac injury is described herein.

Abstract: Compositions and methods useful for the treatment of neuromyelitis optica (NMO) or neuromyelitis optica spectrum disorder (NMOSD) are disclosed.

Abstract: The present invention pertains to a method for the generation of neurotoxin-sensitive, neuronal differentiated cells comprising the steps of: a) cultivating tumor cells which are able to differentiate into neuronal cells in a culture medium under conditions and for a time which primes said tumor cells for neuronal differentiation; and b) cultivating the tumor cells primed for neuronal differentiation of a) in a differentiation medium having an osmolality of 100 to 270 mOsm/kg, and comprising (i) B27 supplement and/or (ii) N2 supplement, for at least 3 days, thereby obtaining neurotoxin-sensitive, neuronal differentiated cells. The invention further relates to neurotoxin-sensitive, neuronal differentiated cells obtainable by the method of the invention.