Abstract: Disclosed is a method for detecting aSyn-specific antibodies in a biological sample, comprising the following steps: —contacting the sample with aSyn-comprising-aggregates and allowing the aSyn-specific antibodies to bind to the aSyn-comprising-aggregates, and —detecting the aSyn-specific antibodies bound to the aSyn-comprising-aggregates by a single particle detection technique, preferably by fluorescence activated cell sorting (FACS).

Abstract: Provided are compositions, articles and methods that relate to promoting neurogenesis or neuroregeneration in mammalian nervous system. Embodiments relate to use of groups of compounds that contain Crizotinib (Cri), Flurbiprofen, Lithium Chloride (Li), Vitamin C (VC), Ceritinib (Cer) or Pirfenidone (PFD). In certain implementations glial cells are converted into functional neurons.

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 invention relates to a novel thyrotropin releasing hormone (TRH) receptor subtype in human central nervous system (CNS) that is pharmacologically distinct from the TRH receptor subtype in human pituitary. The invention provides a means to understand how the central actions of TRH are mediated and to isolate and characterize the novel receptor, as well as methods applicable to research and development of diagnostic and therapeutic applications in human CNS disorders.

Abstract: The present invention relates to the fields of life sciences and medicine. Specifically, the invention relates to therapies of neurodegenerative diseases. More specifically, the present invention relates to interleukin-33 (IL-33), a fragment thereof, a polynucleotide encoding IL-33 or a fragment thereof for use in treatment or prevention of a neurodegenerative disease involving inflammation in a subject and to a method of treating or preventing a neurodegenerative disease involving neuroinflammation in a subject. Still, the present invention relates to IL-33, a fragment thereof, a polynucleotide encoding IL-33 or a fragment thereof for use in improving or restoring neuronal function or endogenous neuronal repair mechanisms, or enhancing endogenous neurogenesis, oligodendrogenesis or neuronal differentiation in a subject.

Abstract: The present invention concerns the use of a population of cells comprising: (a) neural precursor cells committed to an oligodendroglial fate; (b) uncommitted neural precursor cells (c) differentiated oligodendrocytes; or (d) a combination of any one of (a) to (c) for the treatment of CNS autoimmune diseases, or for the preparation of a pharmaceutical composition for treating CNS autoimmune diseases, the population of cells being derived from human pluripotent stem cells. The invention also provides methods for obtaining such populations of cells, namely, neural precursor cells committed to an oligodendroglial fate as well as differentiated oligodendrocytes which then can be used in the treatment of CNS autoimmune diseases. A preferred autoimmune disease in the context of the present invention is multiple sclerosis where the population of cells is administered to the CNS for local treatment of the disease.

Abstract: The present application relates to the field of single-domain antibodies (also called nanobodies), more particularly single-domain antibodies against SOD1 protein isoforms. It also relates to the use of these nanobodies in medicine. Accordingly, methods to treat a disease using these nanobodies are provided herein. The single-domain antibodies are particularly envisaged for treatment of ALS.

Abstract: Antibody for human amyloid beta. Antibody selectively binds human amyloid beta 42 peptide over human amyloid beta 40 peptide. Antibodies specific for amyloid beta 42 as therapeutic agents for binding amyloid beta 42 peptide and treating conditions associated with amyloidosis, such as Alzheimer's disease.

Abstract: Methods of treating a central nervous system (CNS) disorder or mood disorder in a subject in need of such treatment are described. A therapeutically effective amount of a composition comprising a melanocortin 5 receptor (MC5R) peptide ligand in a pharmaceutically acceptable carrier is administered to the subject. The MC5R peptide ligand is a selective MC5R antagonist, in which administration thereof to the subject can treat the CNS disorder or mood disorder with clinical improvement observed in a relatively short time.

Abstract: Methods of treating a depressive disorder or an anxiety disorder in a subject in need of such treatment are described. A therapeutically effective amount of a composition comprising Ac-Nle4-c[Asp5-His6-(NMe)D-Nal(2?)7-Arg8-Trp9-(NMe)Lys10]-NH2 (PEPTIDE 9), in a pharmaceutically acceptable carrier is administered to the subject. PEPTIDE 9 is a selective MC5R antagonist, in which administration thereof to the subject can treat the depressive or generalized anxiety disorder with clinical improvement observed in a relatively short time.

Abstract: A antibody has as a target molecule a ubiquitin protein comprising a phosphorylated serine residue at position 65. In addition, a method is provided for specifically detecting Parkinson's disease at an early stage, in which a target molecule is a ubiquitin protein comprising a phosphorylated serine residue at position 65, a pharmaceutical composition for definitively treating or preventing Parkinson's disease, and a method for screening for the pharmaceutical composition.

Abstract: The present invention provides a method for producing astrocytes from neural progenitor cells, the method comprising: (1) culturing neural progenitor cells in a culture medium comprising a neurotrophic factor; (2) dissociating the cells obtained in the step (1); and (3) subjecting the cells obtained in the step (2) to adherent culture in a culture medium comprising a neurotrophic factor using an uncoated culture vessel.

Abstract: The present invention relates to methods of diagnosing Alzheimer's Disease as well as to methods of confirming the presence or absence of Alzheimer's Disease in a subject. The present invention is also directed to methods of identifying a lead compound useful for the treatment of Alzheimer's Disease by contacting non-Alzheimers cells with an amyloid beta peptide, stimulating the cells with a protein kinase C activator, contacting the cells with a test compound, and determining the value of an Alzheimer's Disease-specific molecular biomarker. The present invention is also directed to methods of diagnosing Alzheimer's Disease in a subject by detecting alterations in the ratio of specific phosphorylated MAP kinase proteins in cells after stimulation with a protein kinase C activator.

Abstract: Provided are methods of isolating a novel cell population of midbrain dopaminergic neuronal progenitor cells derived from stem cells using a novel combination markers. The cell population may be used for cell therapies for the treatment of Parkinson's disease and as substrates in pharmacological assays.

Abstract: Provided are methods and compositions from reprogramming human glial cells into human neurons. The reprogramming is achieved using combinations of compounds that can modify signaling via Transforming growth factor beta (TGF-?), Bone morphogenetic protein (BMP), glycogen synthase kinase 3 (GSK-3), and ?-secretase/Notch pathways. The reprogramming is demonstrated using groups of three or four compounds that are chosen from the group thiazovivin, LDN193189, SB431542, TTNPB, CHIR99021, DAPT, VPA, SAG, purmorphamine. Reprogramming is demonstrated using the group of LDN193189/CHIR99021/DAPT, the group of B431542/CHIR99021/DAPT, the group of LDN193189/DAPT/SB431542, the group of LDN193189/CHIR99021/SB431542, a three drug combination of SB431542/CHIR99021/DAPT. Reprogramming using functional analogs of the compounds is also provided, as are pharmaceutical formulations that contain the drug combinations.

Abstract: A method and system that is directed to the local delivery of growth factors to the mammalian CNS to treat CNS disorders associated with neuronal death and/or dysfunction is described.

Abstract: This invention relates to a method of inhibiting neuronal cell death, including protecting neuronal cells from cell death and the effects of stress, such as high or low pH, comprising administering to the cells an effective amount of Teneurin C-terminal Associated Peptide (TCAP). The invention provides the use of TCAP to prevent and/or treat a number of brain conditions, such as hypoxia-ischemia and brain alkalosis or various brain or spinal cord injuries due to physical or physiological stresses. In one aspect the invention provides a use of TCAP to increase ?-tubulin, ?-actin levels in neuronal cells and/or to increase fasciculation among neuronal cells, in culture or in tissue. In another aspect, the invention provides a method of treating various pH induced neuronal conditions.

Abstract: The present invention relates to methods of treatment of Hypoxia Inducible Factor (HIF)-related conditions, and in particular to methods of treatment of HIF-related conditions comprising the administration of a composition comprising transferrins.

Abstract: The present invention features anti-SOD1 antibodies and methods of using the antibodies for the treatment of amyotrophic lateral sclerosis (ALS) or the amelioration of symptoms associated with ALS.

Abstract: Methods for inducing non-embryonic lesioned central nervous system neurons to survive, integrate, extend axons over long distances, induce intra-lesion ingrowth of neurons into the lesion from host tissue and form synapses in vivo. Pluripotent neural stem cells are grafted into the lesioned CNS tissue within a tissue adhesive suspension, optionally in the presence of growth factors. No modification of the neuronal regenerative inhibitory environment of the CNS is necessary.