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: Agents that reduce the level of a tau gene product in a cell, e.g., in a neuron, include antisense nucleic acids. For example, antisense nucleic acids can be used to down-regulate expression of a tau gene in a cell (e.g., in a neuron). The antisense sequence is complementary to the mRNA of the targeted gene (e.g., tau), and inhibits expression of the targeted gene products. Suitable oligonucleotides can be chemically modified from the native phosphodiester structure, in order to increase their intracellular stability and binding affinity. A number of such modifications have been described in the literature, which modifications alter the chemistry of the backbone, sugars, or heterocyclic bases.

Abstract: The present invention relates to the intrathecal (IT) administration of recombinant enzyme to treat lysosomal storage disorders. In an exemplary embodiment, intrathecal administration of human ?-L-iduronidase (rhIDU) injections in MPS I affected animals resulted in significant enzyme uptake, significant rh-iduronidase activity in brain and meninges and a decrease of glycosaminoglycan (GAG) storage in cells of MPS I subjects to that of normal subjects. Intrathecal administration proved more effective than intravenous treatment at alleviating MPS I symptoms, indicating it is a useful method of treating lysosomal storage disorders.

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: The present invention relates to methods for modulating the activity of one or more neurotrophins, such as neural growth factor (NGF), brain derived neurotrophic factor (BDNF), neurotrophin-3, and neurotrophin-4 (NT-4), in an animal and methods for treatment of a disease or disorder in an individual by modulation of neurotrophin activity. The modulation is carried out by interfering with binding between a neurotrophin and a receptor of the Vps10p-domain receptor family or modulating the expression of a receptor of the Vps10p-domain receptor family. Methods for screening for agents capable of modulating neurotrophin activity and agents selected using these screening methods are also disclosed, as are methods for determining the effect of an agent on one or more neurotrophins in cells. The present invention also pertains to methods for modulating the transport of one or more neurotrophins.

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 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: 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: Cyclic tetrapeptides that are kappa opioid receptor (KOR) antagonists can be used in therapeutic applications for treating, inhibiting, and/or preventing drug addiction, drug use, or drug seeking behavior in a subject. This can include subjects that have a history of drug addiction. The drug can be selected from cocaine, alcohol, amphetamines, methamphetamines, nicotine, opiate, or combinations thereof. These cyclic tetrapeptides can also be useful for treating, inhibiting, and/or preventing stress-induced drug seeking behavior.

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 of using CPAP equipment to sense cardiogenic oscillations in a patient's airflow, and to monitor and treat the patient's cardiac condition. The apparatus diagnoses cardiac morbidity conditions, such as the existence of arrhythmias or other cardiac abnormalities, and influences and optimizes cardiac stroke volume. The apparatus further monitors pulse-transit time, changes in the heart pre-ejection period, and the duration of the cardiac cycle.

Abstract: The present invention relates to a method for suppressing neuroendocrine disease. The therapy employs use of a non-cytotoxic protease, which is targeted to a neuroendocrine tumor cell, preferably via a somatostatin or cortistatin receptor, a GHRH receptor, a ghrelin receptor, a bombesin receptor, a urotensin receptor a melanin-concentrating hormone receptor 1; a KiSS-1 receptor or a prolactin-releasing peptide receptor. When so delivered, the protease is internalized and inhibits secretion from said tumor cell. The present invention also relates to polypeptides and nucleic acids for use in said methods.

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: 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: A method may include administering botulinum toxin to a tissue of a patient and administering a neuropeptide of the CRF family to the tissue of the patient. In some examples, the botulinum toxin is periodically administered to the tissue of the patient and/or the neuropeptide of the CRF family is periodically administered to the tissue of the patient. The periods with which the botulinum toxin and the neuropeptide of the CRF family are administered may be the same or may be different. In some examples, the botulinum toxin and the neuropeptide of the CRF family are administered to the tissue at substantially the same time, while in other embodiments, the botulinum toxin and the neuropeptide of the CRF family are administered to the tissue at different times.

Abstract: Methods useful for effecting prophylaxis or treatment of amyloidosis, including AA Amyloidosis and AL amyloidosis, by administering peptides comprising neoepitopes, such as AA fragments from a C-terminal region of AA, and antibodies specific for neoepitopes of aggregated amyloid proteins, for example, antibodies specific for the C-terminal region of AA fibrils. Antibodies for inhibition of formation and/or increasing clearance of amyloid deposits in a patient thus effecting prophylaxis or treating amyloid disease.

Abstract: Embodiments of the invention are directed to compositions and methods related to Tau oligomers and Tau oligomer specific antibodies.

Abstract: The present invention features methods and compositions for the generation and use of conformation-specific anti-bodies or fragments thereof.