Abstract: The disclosure pertains to epitopes identified in A-beta including conformational epitopes, antibodies thereto and methods of making and using immunogens and antibodies specific thereto.

Abstract: The present invention relates to a novel use of NCKAP1 gene in neurodegenerative diseases. More specifically, the present invention relates to a marker composition for predicting the prognosis of a neurodegenerative disease, comprising a NCKAP1 protein or a gene encoding same, a composition and a kit for predicting the prognosis of a neurodegenerative disease, which comprises a formulation for measuring the level of the protein or an mRNA of the gene encoding same, and a pharmaceutical composition for preventing or treating neurodegenerative disease, comprising the protein or the gene encoding same as an active ingredient.

Abstract: Disclosed is a fusion protein containing a brain-derived neurotrophic factor (BDNF). The fusion protein is a fusion protein of BDNF and a specific range of human anti-transferrin receptor antibody, which makes BDNF administered into the blood able to pass through the blood-brain barrier.

Abstract: The disclosure pertains to conformational epitopes in A-beta, antibodies thereto and methods of making and using immunogens and antibodies specific thereto.

Abstract: The present invention relates to amino acid sequences that can bind to serum albumin. In particular, the present invention relates to immunoglobulin single variable domains, and in particular heavy-chain immunoglobulin single variable domains, that can bind to serum albumin. The invention also relates to proteins, polypeptides and other constructs, compounds, molecules or chemical entities that comprise at least one of the immunoglobulin single variable domains binding to serum albumin that are described herein.

Abstract: The present invention is directed to a fusion protein comprising a light chain region of a Clostridial neurotoxin and a heavy chain region of a Clostridial neurotoxin, where the light and heavy chain regions are linked by a disulfide bond. The fusion protein also has a single chain antibody positioned upstream of the light chain region, where the single chain antibody possesses antigen-binding activity. Also disclosed are therapeutic agents, treatment methods, propeptide fusions, isolated nucleic acid molecules, expression systems, host cells, and methods of expressing fusion proteins.

Abstract: The present invention relates to neutralizing antibodies of the human pituitary adenylate cyclase activating polypeptide type I receptor (PAC1) and pharmaceutical compositions comprising such antibodies. Methods of treating or preventing headache conditions, such as migraine and cluster headache, using the neutralizing antibodies are also described.

Abstract: Novel therapeutic agents, particularly those capable of activating (GPR)124/RECK/Frizzled/lipoprotein receptor-related protein (LRP)-mediated Wnt signaling, while not activating Frizzled/LRP-mediated Wnt signaling in the absence of RECK and/or GPR124. The agents are particularly useful for the prevention or treatment of neurovascular disorders or central nervous system (CNS) disorders including neurovascular dysfunction.

Abstract: Methods and materials for treating and preventing autoimmune diseases, in particular, multiple sclerosis (MS) including small peptides are capable of interacting with CD40, thereby altering and/or modulating the ability of CD40 to interact with CD154, which apparently affects inflammation; and/or the use of such peptides in reducing the inflammatory response, and in particular, the autoimmune inflammatory response; and/or the use of such short peptides to prevent or reverse autoimmune disease, and particularly, multiple sclerosis, in individuals; and/or methods and materials for detecting T-cells that express CD40 (Th40 cells). Also provided are kits for reducing inflammation, treating autoimmune diseases, or detecting Th40 cells. Additionally, methods and apparatuses to administer the peptide are provided.

Abstract: The disclosure pertains to methods of treating or preventing a disease or condition associated with and/or induced by soluble A-beta oligomer such as Alzheimer's disease by administering to a subject in need thereof conformation specific and/or selective antibodies or binding fragments thereof and related products.

Abstract: There is provided in the present application a pharmaceutically acceptable salt of a polypeptide and a pharmaceutical composition comprising the same, wherein the polypeptide comprises the amino acid sequence YEKLLDTEI (SEQ ID NO:1) or a functional variant thereof.

Abstract: Provided are compounds reducing SAICAR accumulation, and applications. On the basis of existing protein structure data and small molecule structure data, calculations and analysis are performed using software to screen and obtain compounds capable of effectively interfering with PAICS activity, reducing SAICAR synthesis, and ultimately reducing SAICAR accumulation, in order to achieve the goal of treating or improving ADSL deficiency. A better effect in the treatment or improvement of ADSL deficiency is expected from the joint use of at least two of the described compounds.

Abstract: A brain-penetrating composition of amyloid-ß binding peptide is disclosed. This may be useful in the treatment of Alzheimer's disease, for example as a bifunctional molecule, comprising a blood-brain barrier crossing antibody and an amyloid-ß targeting peptide linked via an Fc fragment that is able to transmigrate across the blood-brain barrier into the brain, and compositions comprising same. Methods of using this composition for treating Alzheimer's disease are disclosed.

Abstract: The invention provides an antibody or antigen binding fragments thereof that binds to 3pE A? and methods of making and using the antibody or antigen binding fragment thereof, including use for formulations, administration and kits. The antibody and antigen binding fragments thereof and methods disclosed are useful for diagnosis, prognosis and treatment of Alzheimer's disease or other ?-amyloid-related diseases.

Abstract: The disclosure provides methods of preventing or treating Friedreich's ataxia in a mammalian subject, reducing risk factors, signs and/or symptoms associated with Friedreich's ataxia, and/or reducing the likelihood or severity of Friedreich's ataxia. The methods comprise administering to the subject an effective amount of an aromatic-cationic peptide to e.g., reduce oxidative stress, increase mitochondrial metabolism, or a combination thereof.

Abstract: The present invention provides for a novel peptide and method for treating polyglutamine (polyQ) diseases. Also disclosed are related compositions and kits for therapeutic use in the treatment of polyQ diseases.

Abstract: Disclosed herein are monoclonal antibodies targeting specific tau epitopes, particularly, microtubule binding domain region 2 or region 4. Also disclosed herein are antibodies or antigen binding fragments thereof that specifically recognize a tau epitope consisting of the amino acid sequence of SEQ ID NO: 9 or 11. Also disclosed herein are methods of detecting tau protein in a subject, comprising performing an assay using the antibodies or antigen binding fragments thereof on the subject or on a biological sample obtained from the subject. Assay kits containing the disclosed antibodies are also provided. Further, methods of treating or preventing a tauopathy in a subject by administering to the subject tau antibodies or antigen-binding fragments thereof are provided.

Abstract: A method of treating a synucleinopathy with a peptide (C)DQPVLPD (SEQ ID NO: 59), (C)DMPVLPD (SEQ ID NO: 60), (C)DSPVLPD (SEQ ID NO: 61), (C)DQPVLPDN (SEQ ID NO: 64), (C)DMPVLPDN (SEQ ID NO: 65), (C)DSPVLPDN (SEQ ID NO: 66), (C)HDRPVTPD (SEQ ID NO: 70), (C)DRPVTPD (SEQ ID NO: 71), (C)DVPVLPD (SEQ ID NO: 72), (C)DTPVYPD (SEQ ID NO: 73), (C)DTPVIPD (SEQ ID NO: 74), (C)HDRPVTPDN (SEQ ID NO: 75), (C)DRPVTPDN (SEQ ID NO: 76), (C)DVPVLPDN (SEQ ID NO: 78), (C)DTPVYPDN (SEQ ID NO: 79), (C)DQPVLPDG (SEQ ID NO: 81), (C)DMPVLPDG (SEQ ID NO: 82), (C)DSPVLPDG (SEQ ID NO: 83), (C)DHPVHPDS (SEQ ID NO: 86), (C)DMPVSPDR (SEQ ID NO: 87), (C)DRPVYPDI (SEQ ID NO: 90), (C)DHPVTPDR (SEQ ID NO: 91), (C)DTPVLPDS (SEQ ID NO: 93), (C)DMPVTPDT (SEQ ID NO: 94), (C)DAPVTPDT (SEQ ID NO: 95), (C)DSPVVPDN (SEQ ID NO: 96), (C)DLPVTPDR (SEQ ID NO: 97), (C)DSPVHPDT (SEQ ID NO: 98), (C)DAPVRPDS (SEQ ID NO: 99), (C)DMPVWPDG (SEQ ID NO: 100), (C)DRPVQPDR (SEQ ID NO: 102), (C)YDRPVQPDR (SEQ ID NO: 103), (C)DMPVDADN (SEQ ID NO: 105), DQPVLPD(C) (SE

Abstract: Disclosed herein are methods for promoting neuronal outgrowth in a subject with a neuronal lesion in their CNS by administering effective amounts of a pro-regenerative OPN fragment, optionally with IGF1 and/or BDNF. A voltage gated potassium channel blocker can also be administered. Pharmaceutical compositions, devices for administration, and kits are also disclosed.

Abstract: The present disclosure provides pharmaceutical compositions comprising rationally designed peptide analogs of the p65-TAD binding region of GILZ to selectively sequester activated p65. Structural and functional analyses suggest that select GILZ analog (GA) bind p65-TAD with optimum affinity, exhibit an estimated half minimal lethal dose comparable to known peptide drugs and suppress A?1-42 induced cytotoxicity. Furthermore, the present disclosure provides uses and methods of using the pharmaceutical compositions, and uses and methods of using pharmaceutical formulations comprising the pharmaceutical compositions, for the treatment of neurodegenerative diseases such as Alzheimer's Disease, Parkinson's Disease, multiple sclerosis, and amyotrophic lateral sclerosis (ALS).