Abstract: Methods for producing heterologous multi-subunit proteins in transformed cells are disclosed. In particular, the present disclosure provides improved methods of producing multi-subunit proteins, including antibodies and other multi-subunit proteins, which may or may not be secreted, with a higher yield and decreased production of undesired side-products. In exemplary embodiments, the transformed cells are a yeast, e.g., methylotrophic yeast such as Pichia pastoris.

Abstract: Provided is a method for inducing differentiation of neural crest cells into neurons of the autonomic nervous system, the method including the step of culturing neural crest cells in the presence of at least one of a BMP signaling pathway activator, an SHH signaling pathway inhibitor, and a Wnt signaling pathway inhibitor.

Abstract: The present disclosure provides compositions, kits, and methods of promoting neural growth and/or neural survival using IL-17c. The compositions, kits, and methods can be used to promote neural growth and/or neural survival in a variety of conditions where such growth and survival is beneficial.

Abstract: The present invention relates to isolated Nato3 mutant polypeptides. Methods for stimulating a brain cell to differentiate into a dopaminergic progenitor neuronal cell or a dopaminergic neuron comprises increasing phosphorylation of Nato3 in the brain cells and culturing the brain cells until a progenitor dopaminergic neuronal cell marker or a dopaminergic neuronal cell marker is expressed in the cultured brain cells. Methods for treating Parkinson's disease (PD) in a subject comprises administering to the subject in need thereof, a composition comprising progenitor dopaminergic neuronal cells and/or dopaminergic neuronal cells expressing a Nato3 mutant polypeptide to the brain of the subject.

Abstract: The present invention discloses nerve growth factor composition and an injection powder comprising the following components: 10 ?g/mL-100 ?g/mL of a nerve growth factor; 10 mg/mL-80 mg/mL of disaccharide stabilizer; 0 mg/mL-30 mg/mL of an amino acid stabilizer; 0.01 mg/mL-1 mg/mL of surfactant, 10 mg/mL-50 mg/mL of a supporting agent; a pH buffer for maintaining the nerve growth factor composition at 6.0-7.4, and solvent being water. The nerve growth factor composition and the injection powder can avoid the potential risk resulting from the virus of other unknown components carried in albumin by using a disaccharide or a combination of a disaccharide and an amino acid instead of albumin as a stabilizer; not only have protective effect on mNGF, but also can ensure the stability of hNGF and rhNGF in the preparation, transportation and storage processes, and have better medication safety and quality control.

Abstract: Compositions and methods of use are provided for intrabodies that bind and alter the effects of poly-glutamate protein aggregation in poly-glutamate associated diseases, such as in Huntington's disease. Intrabodies are provided that prevent poly-glutamate aggregation, gene dysregulation, and negative effects of Huntington's disease.

Abstract: The present invention has a function of enabling the penetration of the blood-brain barrier and the blood-spinal cord barrier of the central nervous system, which have not been significantly penetrated, with excellent efficiency, thereby enabling a rapid, quick, and more efficient therapeutic effect to be obtained through low dose administration. In addition, the present invention enables local administration unlike conventional therapeutic agents, thereby decreasing side effects, and enables local administration of a therapeutic agent at a high concentration, thereby enabling potentially new treatments and prescriptions.

Abstract: The invention relates to antibodies, antibody fragments and binding agents that specifically recognize TDP-43 associated with frontotemporal dementia (FTD), but not TDP-43 associated with amyotrophic lateral sclerosis (ALS) or TDP-43 associated with healthy human brain tissue, and antibodies, antibody fragments and binding agents that specifically recognize TDP-43 associated with ALS, but not TDP-43 associated FTD or TDP-43 associated with healthy human brain tissue.

Abstract: The present invention is directed to novel Anti-TNF? antibody binding compounds and methods of using the same. Anti-TNF? antibody binding compounds of the invention comprise novel heavy chain immunoglobulin polypeptides of portions thereof. In some embodiments, the invention also includes pharmaceutical compositions comprising at least one Anti-TNF? antibody binding compound. The invention further provides the use of an Anti-TNF? antibody binding compound of the invention in the preparation of a medicament for the therapeutic and/or prophylactic treatment of a disorder.

Abstract: Described herein are chemically defined, adherent culture protocols for generating functional motor neurons characteristic of diverse hindbrain and spinal cord regions, with high efficiency.

Abstract: The present description relates to methods for clinically assessing Parkinson's disease in a subject using erythrocyte-derived extracellular vesicles (EEV) as a biomarker.

Abstract: Provided herein are compositions, kits, methods and systems related to administering a structure that crosses the blood brain barrier (BBB) along with a monosaccharide, either simultaneously or consecutively. The structure may be, for example an antibody or fusion antibody that binds to an insulin receptor.

Abstract: Methods for inhibiting degeneration of a neuron, methods of treating a neurological/neurodegenerative disease, methods of modulating the directional growth of a neuron, and methods of interfering with the interaction of Wnt and Ryk are provided herein. Also provided are isolated anti-Ryk antibodies and antibody fragments that specifically bind to a binding domain of Wnt.

Abstract: This invention demonstrates the formation of a novel polarized membrane lipid raft signaling module in neurons, in response to several diverse neurotoxic stimuli. This polarization occurs well before neurons commit to die, and is an early mechanism in death signaling. The formation of this signaling module is dependent on cholesterol for its formation and provides a mechanistic explanation for the protective effects of cholesterol depleting drugs in several non-neural models of cell death. As such, the formation of the signaling module lends itself as a novel screen for the identification of new drugs and therapeutics which would retard its formation and protect against neuronal injury and death.

Abstract: An object is to provide a neuron cultivation device which promptly develops bundles of axons extending from neurons in vitro. A device for cultivating neuron with axon, the device comprising a cultivation plate and a plurality of modules arranged in the cultivation plate. Each of the modules includes at least one of first chambers receivable of cell bodies of neurons at least one of second chambers, and at least one of channels receivable of a bundle of axon extended from the cell bodies. The channels connect the first chambers and the second chambers. Bottom ends of the first chambers, the second chambers and the channels are closed and top ends of the first chambers and the second chambers are open.

Abstract: Disclosed are methods and compositions for selectively targeting sites of traumatic brain injury (TBI). A brain injury-specific 4-amino acid peptide (sequence CAQK), identified by in vivo phage display screening in mice with acute brain injury, shows selective binding to mouse and human brain injury lesions, and when systemically injected, specifically homes to sites of injury in penetrating and non-penetrating (controlled cortical impact) brain injury models. Also disclosed are methods and compositions for delivering therapeutic compounds to such sites. CAQK-coated nanoparticles containing silencing oligonucleotides provide an alternative to local delivery of therapeutics, which is invasive and can add complications to the injury.

Abstract: Self assembling peptides in combination with infectious and non-infectious proteins as inhibitors and diagnostic tools in transmissible spongiform encephalopathies and amyloid producing neuorodegenerative diseases are described herein.

Abstract: Methods for producing new neurons in the brain in vivo are provided according to aspects of the present invention which include introducing NeuroD1 into a glial cell, particularly into a reactive astrocyte or NG2 cell, thereby “converting” the reactive glial cell to a neuron. Methods of producing a neuronal phenotype in a glial cell are provided according to aspects of the present invention which include expressing exogenous NeuroD1 in the glial cell, wherein expressing exogenous NeuroD1 includes delivering an expression vector, such as a viral expression vector, including a nucleic acid encoding the exogenous NeuroD1 to the glial cell.

Abstract: The present invention relates to the use of multiple doses of Cladribine combined with beta interferon for the treatment of multiple sclerosis in patients who are refractory to at least one conventional therapy.

Abstract: Described are molecules specifically binding to human islet amyloid polypeptide (hIAPP) also known as amylin, particularly human-derived antibodies as well as fragments, derivatives and variants thereof for antagonizing islet amyloid polypeptide (IAPP) induced ?-cell damage and impaired glucose tolerance which are symptoms typically associated with diabetes mellitus type 2 (T2D).