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: The present invention provides a method of treating a tau-mediated cognitive or neurodegenerative disease, comprising administering to a patient in need of such treatment an effective amount of an anti-Tau antibody and an effective amount of an OGA inhibitor.

Abstract: A method for diagnosing a disease can include detecting, in a sample from a patient, an autoantibody binding to Septin-7. A polypeptide comprising Septin-7 or a variant thereof can be used for the diagnosis of a disease. Preferably, the polypeptide is used to detect an autoantibody binding to Septin-7 in a sample. A kit is useful for the diagnosis of a disease. The kit may include a polypeptide that includes Septin-7 or a variant thereof or a medical device that includes a polypeptide that includes Septin-7 or a variant thereof and an autoantibody to Septin-7.

Abstract: A method of generating a cellular model of Alzheimer's disease (AD) comprises integrating AD related gene to hiPSC to induce increased beta secretase and/or Abeta 42 peptides, and the cellular model of Alzheimer's disease (AD) is prepared by the method.

Abstract: The invention provides methods for treating Systemic Sclerosis by administering a dual-V region bispecific antibody that specifically binds IL-4 and IL-13.

Abstract: Disclosed herein are anti-?-synuclein antibodies which preferentially bind to oligomeric ?-synuclein over monomeric ?-synuclein, therapeutic compositions comprising the antibodies, and methods of using the antibodies to treat synucleinopathies.

Abstract: Dosing regimens and methods are disclosed for upregulating protein kinase C (PKC) while reducing subsequent downregulation, comprising administering a PKC activator once a week for three consecutive weeks followed by cessation of administration or dosing for three consecutive weeks. Also described are methods for improving or enhancing cognitive ability, preventing or treating cognitive impairment, preventing or treating a neurodegenerative disease or condition, and/or preventing or treating a disease or condition associated with neuronal or synaptic loss according to the disclosed regimens.

Abstract: Disclosed herein are multifunctional polypeptides comprising a first domain comprising an anti-tau antigen binding domain and a second domain comprising a proteasome-targeting PEST motif, and methods for using these polypeptides in treatment of tauopathies.

Abstract: The present invention describes a method of treating, preventing, reducing the likelihood of or alleviating a symptom of Alzheimer's disease and associated conditions by increasing OPN expression. The invention further provides for a method of improving cognitive function in a subject in need thereof.

Abstract: The present invention provides a vaccine composition for use in neurodegenerative diseases and an infectious virus vaccine composition for inducing an antibody recognizing the conformation of antigens. The vaccine composition of the present invention induces the production of an antibody recognizing the conformation of antigens. The antibody recognizing the conformation of antigens has high specificity for an antigen, and thus can be useful for ameliorating, preventing or treating diseases.

Abstract: Enhanced methods for the generation of medial ganglionic eminence (MGE) cells from pluripotent stem cells are provided that involve an additional step of contacting the cells with an activator of FGF8 signaling while differentiating Pax6+ cells progenitor cells into MGE cells with an activator of sonic hedgehog, and optionally a Wnt inhibitor. The activator of FGF8 signaling shifts the differentiation of the population of cells to NKX2.1+ MGE cells, rather than to CopuTFII+ caudal ganglionic eminence (CGE) cells. Methods for treatment of neurological disorders, such as epilepsy, by transplant of MGE cells, or GABAergic interneurons derived from human pluripotent stem cells, into a subject in need of treatment are also provided. Human pluripotent stem cell derived MGE cells when transplanted successfully suppress spontaneous seizures, e.g. in epilepsy.

Abstract: The present disclosure provides methods of using a calcium oscillation assay and/or a sequence score calculation to identify a molecule that is safe for administration. The disclosure also includes a method of selecting or identifying a molecule having tolerable in vivo neurotoxicity using a calcium oscillation assay, a sequence score method, an in vivo tolerability assay, or any combination thereof.

Abstract: Provided herein are methods, assays and devices for the differential diagnosis and detection of disease progression of autoimmune diseases. The methods, assays and devices provided herein produce and analyze binding patterns of peripheral-blood antibodies on mimetic peptide arrays that differentiate autoimmune diseases, and identify patients progressing to internal organ complications such as interstitial lung disease (ILD), and gastric antral vascular ectasia (GAVE), or renal involvement.

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 relates to the pharmaceutical use of FAM19A5 involved in regulating gliogenesis, and more specifically, to the use of FAM19A5 in the prevention, diagnosis, or treatment of central nervous system injuries, degenerative brain diseases, or central nervous system diseases, FAM19A5 being spread in the neural stem cells in vertebrates and regulating gliogenesis.

Abstract: The present disclosure is directed to methods (e.g., in vitro methods) for use of nicotinamide phosphoribosyltransferase (NAMPT) as a biomarker in radiation-induced lung injury (RILI). Provided herein is an in vitro method for the diagnosis, prognosis, and/or monitoring of RILI in a human subject by providing a tissue or plasma sample from the subject and detecting the level of NAMPT therein, wherein a higher level of NAMPT in the tissue or plasma sample from the subject compared to a healthy control or a reference value is indicative for the presence of RILI in the subject. Further provided herein is a method of detecting NAMPT in a human subject by obtaining a biological sample from the subject, detecting the presence of NAMPT in the sample by contacting the sample with a capture agent that specifically binds NAMPT, and detecting binding between NAMPT and the capture agent.

Abstract: The invention describes fully native human neutralizing monoclonal antibodies against tetanus toxin. The invention developed fully native human neutralizing monoclonal antibodies against tetanus toxin through a systematic high through-put platform that is specialized for identifying and developing human native antibody. The neutralizing monoclonal antibodies described in the invention can be used in the prevention, treatment and detection of Clostridium tetani infection. The fully human neutralizing monoclonal antibodies developed in the invention have a high affinity toward tetanus toxin, as well as possessing high neutralizing activities against the toxin, safe of use with high disease prevention effectiveness, free of exogenous virus contamination, and are widely applicable to various human groups with strong industrial applications.

Abstract: The present invention relates to an immunoassay method for the detection of Chromogranin A (or fragment(s) thereof) comprising the steps of contacting a sample suspected of comprising Chromogranin A with a first antibody or an antigen-binding fragment or derivative thereof specific for Chromogranin A and a second antibody or an antigen-binding fragment or derivative thereof specific for Chromogranin A under conditions allowing for the formation of a ternary complex between Chromogranin A and the two antibodies or antigen-binding fragments or derivates thereof, and detecting the binding of the two antibodies or antigen-binding fragments or derivates thereof to Chromogranin A. Also provided are antibodies directed against amino acid residues 124 to 144 and 280 to 301 of Chromogranin A and their use in the immunoassay method.

Abstract: Methods, compositions and kits useful in the detection, assessment, diagnosis, prognosis and/or treatment of brain injuries, especially mild traumatic brain injury (mTBI) or concussion, are based upon detection of changes in levels of certain protein biomarkers in a subject undergoing testing, or upon detection of changes in levels of certain protein biomarkers in conjunction with neuroimaging analyses to detect changes in vascular or blood brain barrier (BBB) permeability in the brain, or to detect damage to fiber tracts in the brain, in which changes in biomarker levels correlate with detection of changes in BBB permeability or in brain fiber tract or white matter damage in a subject with brain injury such as mTBI or concussion.

Abstract: The present disclosure is directed to a method of treating a neuropsychiatric disorder. This method involves selecting a subject having the neuropsychiatric disorder and administering to the selected subject a preparation of glial progenitor cells at a dosage effective to treat the neuropsychiatric disorder in the subject. Another aspect of the disclosure is directed to a method of treating a neuropsychiatric disorder that includes selecting a subject having the neuropsychiatric disorder and administering, to the selected subject, a potassium (K+) channel activator at a dosage effective to restore normal brain interstitial glial K+ levels in the selected subject and treat the neuropsychiatric disorder is also disclosed.