Abstract: We have discovered that LRG-47 (also called p47 GTPase), plays a central role in the pathogenesis of multiple sclerosis, and that inhibition of LRG-47 activity by anti-LRG-47 antibodies or of LRG-47 expression by siRNA dramatically reduce the pathology and symptoms of multiple sclerosis. Certain embodiments of the invention are directed to the therapeutic use of anti-LRG-47 antibodies (mouse or rabbit or other antibodies that are humanized or human antibodies to LRG-47, preferably antibodies made against human LRG-47) or siRNA or antisense nucleotides that specifically hybridize with the gene or mRNA or cDNA encoding human LRG-47 to treat or prevent multiple sclerosis and other autoimmune diseases that are T-cell-mediated. Other embodiments are directed to methods for the diagnosis of multiple sclerosis or to determining the aggressiveness of multiple sclerosis by determining the amount of human LRG-47 or LRG-47 mRNA in a biological sample from the patient.

Abstract: This invention includes, in part, methods of preparing acetylated Huntingtin (Htt) polypeptides, acetylated Htt polypeptide antigens, and antibodies that specifically recognize acetylated epitopes on Htt polypeptides. The invention also relates, in part, to the preparation and use of antibodies that specifically recognize and bind to acetylated epitopes on acetylated Htt polypeptides when an acetylated residue on the Htt polypeptide is a lysine that corresponds to K444 residue of full-length, wild-type Htt polypeptide. In some aspects, the invention includes hybridoma cell lines that produce antibodies that specifically bind acetylated Htt polypeptide and also includes antibodies and antigen-binding fragments thereof produced using polypeptides of the invention.

Abstract: The present invention provide purified Flt4 receptor tyrosine kinase polypeptides and fragments thereof, polynucleotides encoding such polypeptides, antibodies that specifically bind such polypeptides, and uses therefor.

Abstract: The subject invention relates to isolated proteins, particularly monoclonal antibodies, which bind to the Nogo-66 receptor. Specifically, these antibodies have the ability to inhibit the binding of the natural ligand of the Nogo-66 receptor and neutralize the Nogo-66 receptor. These antibodies or portions thereof of the invention are useful for detecting NgR and for inhibiting NgR activity, for example in a human suffering from a disorder in which NgR or Nogo-66 activity is detrimental.

Abstract: This invention relates to methods for promoting reinnervation of auditory hair cells, specifically, by inhibiting Repulsive Guidance Molecule a (RGMa), a repulsive axonal guidance molecule that is expressed in the cochlea, or its receptor, neogenin.

Abstract: The invention provides methods of treating diseases, disorsers or injuries involving demyelination and dysmyelination, including multiple sclerosis, by the administration of a Sema6A polypeptide.

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: The present invention is directed to a method for early, non-invasive, rapid, efficient, reliable and accurate diagnose of Alzheimer's disease. The present invention particularly addresses obtaining blood samples, and stabilizing platelets from healthy persons and patients with probable cognitive impairment and/or Alzheimer's disease; extracting proteins from the platelets; identifying both monomeric and oligomeric tau proteins in the platelets with at least two monoclonal antibodies against the tau proteins, quantifying the amounts of the identified tau proteins, and comparing the amounts and protein profiles of the tau molecular species in the platelets of the healthy person and the patient.

Abstract: The subject invention pertains to compositions and methods for promoting repair of damaged nerve tissue. The compositions and methods of the subject invention can be employed to restore the continuity of nerve interrupted by disease, traumatic events or surgical procedures. Compositions of the subject invention comprise one or more chondroitin sulfate proteoglycan (CSPG)-degrading enzymes that promote axonal penetration into damaged nerve tissue. The invention also concerns methods for promoting repair of damaged nerve tissue using the present compositions and nerve tissue treated according to such methods. The invention also pertains to kits for nerve repair.

Abstract: Disclosed herein are systems and methods for contributing to the local treatment of pain. More specifically, the disclosed systems and methods contribute to the local treatment pain by inhibiting the NF?B family of transcription factors.

Abstract: Disclosed are methods of enhancing cognitive impairment in a patient wherein the cognitive impairment is due to ADDL neurotoxicity. The methods employ non-peptidic compounds having a molecular weight of less than 1000 and which can antagonize against formation of neurotoxic ADDLs from A?1-42 monomers.

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 provide purified Flt4 receptor tyrosine kinase polypeptides and fragments thereof, polynucleotides encoding such polypeptides, antibodies that specifically bind such polypeptides, and uses therefor.

Abstract: The present invention relates to a method for the isolation of proteins that comprise disulfide bonds in their native conformation. Essentially, a method of the present invention makes use of reducing agents such as ?-mercaptoethanol or dithiothreitol in protein isolation methods obsolete. A method of the present invention is particularly suitable for the isolation of precursor proteins such as proinsulin from recombinant cells.

Abstract: A method is described for producing protein compositions having reduced amounts of O-linked glycosylation. The method includes producing the protein in cells cultured in the presence of an inhibitor of Pmt-mediated O-linked glycosylation and/or in the presence of one or more ?-1,2-mannosidases.

Abstract: Novel anti-NRP1 antibodies and variants thereof having unique structural and functional characteristics are disclosed. Also provided are uses of the antibodies in research, diagnostic and therapeutic applications.

Abstract: The present invention relates to the diagnosis of neurological disorders, more specifically to the diagnosis of multiple sclerosis. A biomarker panel is provided which can be used to detect if a subject has multiple sclerosis. Also described are methods of identification of such biomarkers.

Abstract: The invention relates to a method of preparing heteromultimeric polypeptides such as bispecific antibodies, bispecific immunoadhesins, heteromultimers and antibody-immunoadhesin chimeras. Generally, the method involves introducing a protuberance at the interface of a first polypeptide and a corresponding cavity in the interface of a second polypeptide, such that the protuberance can be positioned in the cavity so as to promote heteromultimer formation and hinder homomultimer formation. The protuberance and cavity can be made by synthetic means such as altering the nucleic acid encoding the polypeptides or by peptide synthesis.

Abstract: Endogenous Sp35 is a negative regulator for neuronal survival, axon regeneration, oligodendrocyte differentiation and myelination. Molecules that block endogenous Sp35 function, such anti-Sp35 antibodies can be used as therapeutics for the treatment of neuron and oligodendrocyte dysfunction. The present invention provides antibodies specific for Sp35, and methods of using such antibodies as antagonists of endogenous Sp35 function. The invention further provides specific hybridoma and phage library-derived monoclonal antibodies, nucleic acids encoding these antibodies, and vectors and host cells comprising these antibodies. The invention further provides methods of promoting oligodendrocyte survival and myelination in a vertebrate, comprising administering to a vertebrate in need of such treatment an effective amount of an anti-Sp35 antibody.

Abstract: Peptide sequences that specifically bind infectious prion protein for the generation of antibodies and therapeutic agents are disclosed herein.