Abstract: The invention provides compositions and methods relating to bioactive peptide analogs of PEDF.

Abstract: Nitration shielding peptides that reduce or prevent nitration of a protein of interest are disclosed. The peptide can serve as molecular sink for nitrating agents, block access of the nitrating agents to the target tyrosine on the protein of interest, serve as substrate for the nitrating agent (i.e., provide an alternative nitratable tyrosine residue), provide a nitrating agent neutralizing moiety such as antioxidant, or a combination thereof. The nitration shielding peptide can be a fusion protein that includes one or more additional domains such a protein transduction domain, a targeting signal, a purification tag, or any combination thereof. Exemplary nitration shielding peptides for reducing nitration of RhoA and PKG-1?, and methods of use thereof for treating pathologies, disease, and disorders associated with nitration of RhoA and PKG-1?, respectively are also provided.

Abstract: The invention provides methods for treating inflammatory diseases by administering to the subject an effective amount of an agent that provides alpha B-crystallin activity, where the dose is effective to suppress or prevent initiation, progression, or relapses of disease, including the progression of established disease. In some embodiments, the methods of the invention comprise administering to a subject having a pre-existing inflammatory disease condition, an effective amount of alpha B-crystallin protein, to suppress or prevent relapses of the disease.

Abstract: The invention herein related to methods and compositions for treating nervous system disorders. The methods comprise administration of antibodies directed towards peptides that bind to receptors important in disease progression, thus attenuating the disease.

Abstract: The present disclosure generally relates to the use of des-aspartate-angiotensin I and/or its derivatives in medicine. In particular, the present invention relates to the use of des-aspartate-angiotensin I and/or its derivatives for the treatment and/or prophylaxis of inflammatory diseases or pathologies, for inducing anti-inflammatory actions and/or reducing inflammation, and/or for treatment of inflammation-related conditions.

Abstract: The present disclosure provides methods of treating a tauopathy, involving administering an anti-Tau antibody. The present disclosure also provides anti-Tau antibodies, and formulations comprising same, for use in the methods.

Abstract: The present disclosure provides methods of treating a tauopathy, involving administering an anti-Tau antibody. The present disclosure also provides anti-Tau antibodies, and formulations comprising same, for use in the methods.

Abstract: Provided are a composition and an external application for promoting muscle differentiation or improving muscle mass containing an amino acid derivative promoting muscle cell differentiation, a composition and an external application for alleviating muscle function deterioration caused by muscle damage and recovering damaged muscle containing the same, or a pharmaceutical composition and an external application for treating or improving a muscle deterioration disease containing the same.

Abstract: The present invention relates to a dosing regimen for use in the treatment of stroke. More particularly, the invention relates to the administration of two doses of anti-MAG antibodies for the treatment of ischemic and/or haemorrhagic stroke.

Abstract: Provided herein are methods and compositions for treating a subject suffering from a deficiency in ?-L-Iduronidase in the CNS. The methods include systemic administration of a bifunctional fusion antibody comprising an antibody to a human insulin receptor and an ?-L-Iduronidase. A therapeutically effective systemic dose is based on the specific CNS uptake characteristics of human insulin receptor antibody-?-L-Iduronidase fusion antibodies as described herein.

Abstract: Various agents are described to denerve, modulate, or otherwise affect the renal nerves and other neural tissue. Also, various delivery devices are described to deliver an agent locally to the renal nerves. The delivery devices are positioned in the renal artery and penetrate into the wall of the renal artery to deliver the agent to the renal nerves. The delivery devices may be used to deliver the agent according to longitudinal position, radial position, and depth of the renal nerves relative to the renal artery. In addition, various methods are described to denervate, modulate, or otherwise affect the renal nerves and other neural tissue.

Abstract: The invention provides an expression system for producing Caveolin-1 in neuronal cells or neural stem cells comprising a neuron-specific regulatory element and a nucleic acid sequence encoding Caveolin-1.

Abstract: Antibodies and fragments thereof have high affinity for human ?-synuclein protofibrils and low binding of ?-synuclein monomers, wherein the antibodies or fragments have specified Complementarity Determining Region (CDR) sequences. Compositions comprise such an antibody or fragment and methods of detecting ?-synuclein protofibrils use such an antibody or fragment. In further embodiments, methods of preventing, delaying onset of or treating a neurodegenerative disorder with ?-synuclein pathology comprise administering such an antibody or fragment, and such an antibody or fragment is used in the manufacture of a pharmaceutical composition for treatment of a neurodegenerative disorder with ?-synuclein pathology. Such an antibody or fragment is used in the diagnosis or monitoring of the development of a neurodegenerative disorder with ?-synuclein pathology, and in methods for reducing or inhibiting ?-synuclein aggregation by administration of such an antibody or fragment.

Abstract: Compositions and methods for targeting therapeutic agents to neuromuscular junctions are disclosed. Also disclosed are methods for treating diseases and conditions affecting the neuromuscular junction. Compositions include a neuromuscular junction targeting peptide coupled to a therapeutic agent. Compositions may further include a linker peptide. Methods for targeting therapeutic agents to neuromuscular junctions and treating diseases and conditions affecting the neuromuscular junction include administering a composition including a neuromuscular junction targeting peptide coupled to a therapeutic agent.

Abstract: Described herein are variant, recombinant ?-glucocerebrosidase proteins characterized as having increased stability relative to recombinant wild-type ?-glucocerebrosidase. Also provided herein are variant, recombinant ?-glucocerebrosidase proteins characterized as retaining more catalytic activity relative to recombinant wild-type ?-glucocerebrosidase. Further described herein are variant, recombinant ?-glucocerebrosidase proteins that can have amino acid variations at one or more of the following positions: 316, 317, 321 and 145. Methods of making the variant, recombinant ?-glucocerebrosidase proteins are also described as well as methods of treating patients having lysosomal storage diseases.

Abstract: The present application provides synthetic modified peptides of five to seven natural or non-natural amino acids as well as pharmaceutical compositions comprising them, for use in the treatment a disease or disorder presenting behavioral abnormalities associated with impairment of sensory gating function, depression or cognitive impairment, particularly schizophrenia and Alzheimer's disease.

Abstract: The present invention relates to a composition including stem cell-derived microvesicles as an active ingredient for promoting neurogenesis. The stem cell-derived microvesicles according to the present invention can promote neurogenesis and migration of nerves and also promote angiogenesis in vascular endothelial cells, and thus can be usefully used in treatment of neurological damage.

Abstract: The present invention provides novel PAR lderived cytoprotective oligopeptides or polypeptides which typically contain at least the first 4 N-terminal residues that are substantially identical to the corresponding N-terminal residues of Met1-Arg46 deleted human PAR 1 sequence. These cytoprotective oligopeptides or polypeptides are capable of activating PAR 1 and promoting PAR 1 cytoprotective signaling activities. The invention also provides engineered cells or transgenic non-human animals which harbor in their genome an altered PAR 1 gene that is resistant to cleavage at Arg41 and/or Arg46 residues. Additionally provided in the invention are methods of screening candidate compounds to identity additional cytoprotective compounds or cytoprotective proteases. The invention further provides therapeutic use or methods of employing a PAR 1 derived cytoprotective oligopeptide or polypeptide to treat conditions associated with tissue injuries or undesired apoptosis.

Abstract: Provided are compositions and methods for treating or preventing nausea and vomiting in patients undergoing chemotherapy, radiotherapy, or surgery.

Abstract: The present application provides novel compounds of the Formula (I), pharmaceutical compositions comprising such compounds and methods for using such compounds as tools for biological studies or as agents or drugs for modulating Protease Activated Receptor-2 (PAR2) and for treating a subject at risk of—or susceptible to—a disease or disorder, or having a disease or disorder associated with undesirable PAR2 activity.

Abstract: Human-derived fibroblast cells with copy number variation for alpha-synuclein, and methods of use thereof, are provided. For example, compositions and methods for high through-put screening of potential therapies for neurodegenerative disease such as Parkinson's disease are provided.

Abstract: The present invention relates to a method of treating or preventing transthyretin amyloidosis, pharmaceutical composition for use in said treatment or prevention, as well as to a diagnostic method and a kit.

Abstract: A method of treating Parkinson's disease in humans is disclosed, wherein glial cell-line derive neurotrophic factor (GDNF) is chronically administered directly to one or both putamen of a human in need of treatment thereof via convection-enhanced infusion using at least one implantable pump and at least one catheter. In one aspect of the present invention the GDNF is infused directly into one or both putamen through one or more indwelling intraparenchymal multiport brain catheters connected to one or more implantable pumps wherein the flow rate is pulsed.

Abstract: The present invention relates to the therapeutic use of the carboxy-terminal domain of the heavy chain of the tetanus toxin for the treatment of amyotrophic lateral sclerosis (ALS).

Abstract: A method of treating Parkinson's disease in humans is disclosed, wherein glial cell-line derive neurotrophic factor (GDNF) is chronically administered directly to one or both putamen of a human in need of treatment thereof via convection-enhanced infusion using at least one implantable pump and at least one catheter. In one aspect of the present invention the GDNF is infused directly into one or both putamen through one or more indwelling intraparenchymal mutitiport brain catheters connected to one or moreimplantable pumps wherein the flow rate is pulsed.

Abstract: This invention relates to a vaccine for preventing or treating tautopathy, comprising a vector, as an active ingredient, comprising a nucleic acid encoding a mutant tau protein linked to a secretion signal sequence, wherein the vaccine is capable of inducing an antibody against an (optionally phosphorylated) tau protein in a subject in a more sustained manner compared with a case where the mutant tau protein is administered directly.

Abstract: The invention provides a cyclic polypeptide of Formula I (SEQ ID NO: 1): X1-R-X3-X4-L-S-X7-X8-X9-X10-X11-X12-X13??I or an amide, an ester or a salt thereof, or a bioconjugate thereof, wherein X1, X3, X4, X7, X8, X9, X10, X11, X12 and X13 are defined herein. The polypeptides are agonist of the APJ receptor.

Abstract: The present invention provides therapeutic modalities for the treatment of an ischemic event (e.g., stroke) that creates or embodies a risk of neurological damage in CNS sites by administration of a thrombopoietin receptor ligand.

Abstract: The present invention relates to a myostatin inhibitor comprising extracellular water-soluble domains of delta-like 1 homolog (DLK1) as active ingredients. More particularly, the present invention relates to a composition for inhibiting myostatin activity, comprising, as active ingredients, extracellular water-soluble domains of DLK1 or a deletion mutant of extracellular water-soluble domains of DLK1. The myostatin inhibitor of the present invention is bonded to the myostatin or activin receptor type IIB so as to inhibit the action mechanism of the myostatin, to thereby promote myogenesis and prevent differentiation into fat cells. Therefore, the myostatin inhibitor of the present invention may be used in preventing and treating diseases such as muscular dysplasia that requires differentiation to muscular cells, or metabolic diseases.

Abstract: The invention provides a bioconjugates comprising a synthetic polypeptide of Formula I? (SEQ ID NO: 1): or an amide, an ester or a salt thereof, wherein X1, X2, X3, X4, X5, X6, X7, X8, X9, X10, X11, X12 and X13 are defined herein and a half-life extending moiety wherein the peptide and the half-life extending moiety are covalently linked or fuse, optionally via a linker. The polypeptides are agonist of the APJ receptor.

Abstract: The instant invention provides soluble fusion protein complexes and IL-15 variants that have therapeutic and diagnostic use, and methods for making such proteins. The instant invention additionally provides methods of stimulating or suppressing immune responses in a mammal using the fusion protein complexes and IL-15 variants of the invention.

Abstract: The invention relates to compositions and methods for treating or preventing vascular dementia in a mammal comprising mucosal administration of an amount of E-selectin polypeptide sufficient to induce bystander immune tolerance in the mammal. Another aspect of the invention relates to compositions useful for treating or preventing vascular dementia.

Abstract: The present invention relates to a treatment of an autoimmune demyelinating disease/disorder. Also included in the present invention is the use of bone marrow stromal cells for the treatment of multiple sclerosis (MS).

Abstract: An object of the present invention is to provide a safe and effective method for enhancing an immune response and a medicament for preventing or treating Alzheimer disease comprising amyloid ? peptide that induces an enhanced immune response. An amyloid ? peptide or a portion thereof with addition or insertion of cysteine and a method for enhancing an immune response using the peptide or a method for enhancing an immune response using the peptide together with an adjuvant. A medicament for preventing or treating Alzheimer disease comprising an amyloid ? peptide or a portion thereof that induces an enhanced immune response. A DNA vaccine, that may have the same effect, comprising the gene encoding an amyloid ? peptide or a portion thereof that induces an enhanced immune response with addition or insertion of cysteine.

Abstract: The invention provides animal models and clinical trials for assessing agents for potential use in treating and effecting prophylaxis stroke and other neurological diseases, particularly those mediated at least in part by excitoxitity. The invention also provides preferred dosage and infusion regimes and pharmaceutical compositions for clinical application of such agents.

Abstract: In its various embodiments, the invention provides myelin basic proteins and fragments of that interfere with the fibrillization of peptides implicated in the amyloidoses, especially the amyloid-b eta peptide associated with Alzheimer's disease (“AD”) and cerebral amyloid angiopathy (“CAA”). Some embodiments provide methods of identifying additional interfering fragments. Others provide methods of identifying substances that modulate the interference. Further embodiments provide methods of preventing amyloidoses, especially AD and CAA by administering myelin basic proteins or fragments thereof.

Abstract: Embodiments of the present disclosure provide for aligned nanofibrous polymer matrix structure, structures incorporating aligned nanofibrous polymer matrix structures, methods of using aligned nanofibrous polymer matrix structures, methods of making aligned nanofibrous polymer matrix structures, and the like.

Abstract: The present invention provides peptide-based peroxidase inhibitors having the formula AA1-AA2-AA3, wherein AA1 is a positively charged, negatively charged or neutral amino acid, AA2 is a redox active amino acid, and AA3 is an amino acid possessing a reducing potential such that AA3 is capable of undergoing a redox reaction with a radical of amino acid AA2 or a retro or retro-inverso analog thereof. The result of such a combination is a highly effective inhibitor of peroxidase activity that has potent anti-inflammatory properties in widely diverse models of vascular disease and injury. Exemplary tripeptides effectively inhibit peroxidase mediated LDL oxidation, increase vasodilation in SCD mice, inhibit eosinophil infiltration and collagen deposition in asthma mice, inhibit acute lung injury, and decrease ischemic injury of the heart.

Abstract: New liposomes are described, comprising: (i) phosphatidic acid and/or cardiolipin; (ii) apolipoprotein E (ApoE) or derivatives thereof. The so modified liposomes, administered systemically, obtain a dramatic in-vivo reduction of the amyloid plaque in the central nervous system, allowing an effective treatment of neurodegenerative diseases, in particular Alzheimer's disease.

Abstract: In certain embodiments compositions are provided that comprise a pentapeptide comprising the formula: C1-X2-X3-X4-C5 where C1 and C5 are independently selected cysteines or cysteine analogues, or other amino acids with sidechains suitable for cyclization, where the cysteines or cysteine analogs are attached to each other by a linkage that does not comprise X2, X3, and X4; where X2, X3, and X4 are independently selected amino acids; and the peptide, when administered to a cell alters APP signaling and/or switches APP processing from aberrant to normal. The compositions mitigate amyloid plaque formation.

Abstract: The invention relates to compounds that can be used, in particular, as structural mimetics of proline-rich peptides and are correspondingly able to bond with proline-rich-motif binding domains (PRM domains) of proteins. The invention further relates to the use of these compounds as pharmaceutically active agents, as well as the use of the pharmaceutically active agents for the treatment of bacterial, neurodegenerative and tumor diseases.

Abstract: The invention provides pharmaceutical compositions and methods of use thereof for preventing or ameliorating disorders of the nervous system. More specifically, the invention provides pharmaceutical compositions, including phosphopeptides that when administered disrupt the physical interaction of TrkB with its signaling effector, phospholipase C?1 (PLC?1). The invention further provides method of treatment comprising administering phosphopeptides that uncouple TrkB from PLC?1 in order to prevent and/or ameliorate nervous system disorders such as epilepsy, anxiety, and seizures.

Abstract: The invention relates to a preparation for improving memory and learning comprising enzymatic protein hydrolyzate of animal nervous tissue, preferably the tissue of spinal cord of animals for slaughter, while the preferred protein being a myelin protein. The invention also relates to composition for use in treatment of memory disorders, in particular age associated memory disorders and learning impairment. Also disclosed is the method for improving memory and learning.

Abstract: Disclosed are compositions and methods related to improving pharmacological properties of bioactive compounds targeting nervous system.

Abstract: Composition containing a chimeric neuregulin polypeptides and method of making such polypeptides are disclosed. The chimeric neuregulin comprises a first moiety of at least 10 amino acids, wherein the first moiety is derived from a first polypeptide; and a second moiety of at least 5 amino acids, wherein the second moiety is derived from a second polypeptide; wherein the first polypeptide is a neuregulin and the chimeric neuregulin exhibits an enhanced binding affinity to integrin, Erb 3, or Erb 4 comparing to that of the first neuregulin.

Abstract: The present invention relates to C5 binding polypeptides, comprising a C5 binding motif, BM, which motif consists of an amino acid sequence selected from i) EX2X3X4A X6X7EID X11LPNL X16X17X18QW X21AFIX23X26LX28D, and ii) an amino acid sequence which has at least 86% identity to the sequence defined in i), wherein the polypeptide binds to C5. The present invention moreover relates to C5 binding polypeptides for use in therapy, such as for use in treatment of a C5 related condition, and to methods of treatments.

Abstract: The present invention provides a novel macrocyclic compound of general Formula (I) having histone deacetylase (HDAC) inhibitory activity, a pharmaceutical composition comprising the compound, and a method useful to treat diseases using the compound.

Abstract: The present invention relates to a method for the treatment of vascular dysfunction, reducing ischemic pain and/or treatment of a vascular disease comprising administering a therapeutically effective amount of Annexin A5 or a functional analogue or variant thereof to a patient in need of such treatment. The vascular dysfunction, ischemic pain and/or vascular disease may be associated with impaired endothelium mediated vasodilatation, a reduced eNOS activity, and/or a reduced NO bioavailability. The patient may be suffering from a disease selected from angina pectoris, ischemic heart disease, peripheral artery disease, systolic hypertension, migraine, type 2 diabetes and erectile dysfunction.

Abstract: The present disclosure provides methods of treating a tauopathy, involving administering an anti-Tau antibody. The present disclosure also provides anti-Tau antibodies, and formulations comprising same, for use in the methods.

Abstract: Compounds derived from a transduction complex that enhance memory in mammals and methods of enhancing memory using said compounds are disclosed.