Abstract: The present invention relates to a peptide and its analogs that selectively inhibit the Nav1.7 sodium channel. The present invention also relates to pharmaceutical compositions useful for treating or preventing a disorder responsive to the blockade of sodium ion channels, especially Nav1.7 sodium ion channels. The present invention further provides methods of treating a disorder responsive to the blockade of sodium channels, and particularly Nav1.7 sodium channels, in a mammal suffering from excess activity of the channels, compositions and methods for providing analgesia by administering a peptide of the invention.

Abstract: The present invention relates to methods and kits for diagnosing multiple sclerosis (MS) in a subject. Particularly, the present invention relates to methods and kits for diagnosing a subtype of MS in a subject, the subtype selected from relapsing-remitting MS (RRMS), secondary progressive MS (SPMS), primary progressive MS (PPMS) and a pathologic sub-type of MS lesions selected from Pattern I and Pattern II MS lesion.

Abstract: A method of producing a conformational specific binding partner of a GPCR, the method comprising: a) providing a mutant GPCR of a parent GPCR, wherein the mutant GPCR has increased stability in a particular conformation relative to the parent GPCR; b) providing a test compound; c) determining whether the test compound binds to the mutant GPCR when residing in a particular conformation; and d) isolating a test compound that binds to the mutant GPCR when residing in the particular formation. Methods of producing GPCRs with increased stability relative to a parent GPCR are also disclosed.

Abstract: Antibodies, particularly human antibodies, are disclosed having activity in treatment of demyelinating diseases and diseases of the central nervous system. Neuromodulatory agents are provided comprising a material selected from the group consisting of an antibody capable of binding structures or cells in the central nervous system, a peptide analog, and active fragments, monomers and combinations thereof having one or more of the following characteristics: capable of inducing remyelination; binding to neural tissue; promoting Ca++ signaling with oligodendrocytes; and promoting cellular proliferation of glial cells. Amino acid and DNA sequences of exemplary antibodies are disclosed. Methods are described for treating demyelinating diseases, and diseases of the central nervous system, using polyclonal IgM antibodies and human monoclonal antibodies sHIgm22(LYM 22), sHIgm46(LYM46) ebvHIgM MSI19D10, CB2bG8, AKJR4, CB2iE12, CB2iE7, MSI19E5 and MSI10E10, and active fragments thereof.

Abstract: The invention provides methods of diagnosing or determining a cause of an autoimmune encephalitis or an epilepsy in a subject and of diagnosing a tumor in a subject, comprising the step of testing a biological sample of the subject for an antibody to LGI1. This invention further provides methods of treating an autoimmune encephalitis or an epilepsy, comprising the steps of detecting an antibody to LGI1 and treating a tumor associated with the disease.

Abstract: Provided herein are methods for alleviating symptoms in a subject having a neurodegenerative disorder, comprising administering to the subject an effective amount of an isolated binding molecule which specifically binds to semaphorin-4D (SEMA4D) or to its Plexin-B1 or Plexin-B2 receptors.

Abstract: The invention demonstrates that, contrary to apoptotic rabies virus G proteins, certain non-apoptotic rabies virus G proteins, such as the G protein of the CVS-NIV strain, have a neurite outgrowth promoting effect. The invention further demonstrates that this neurite outgrowth promoting effect is due to the cytoplasmic tail of the non-apoptotic rabies virus G proteins, more particularly to their PDZ-BS, which shows a single-point mutation compared to the one of apoptotic rabies virus G proteins. The invention provides methods for inducing and/or stimulating neurite outgrowth, which are useful in inducing neuron differentiation, for example for the treatment of a neoplasm of the nervous system, as well as in regenerating impaired neurons, for example for the treatment of a neurodegenerative disease, disorder or condition or in the treatment of a microbial infection, or in protecting neurons from neurotoxic agents or oxidative stress.

Abstract: A vaccine or immunogenic composition comprising at least two fragments of proprotein convertase subtilisin/kexin type 9 (PCSK9) where one fragment contains at least 9 consecutive residues of residues 153 to 165 of PCSK9 and the other fragment contains at least 9 consecutive residues 209 to 222 of the PCSK9 (SEQ ID NO:9). Methods of treatment for hyperlipidemia, hypercholesterolemia, and atherosclerosis involving administering this vaccine.

Abstract: Methods for treating neurodegenerative disorders, including Parkinson's disease, are provided. The methods comprise administrating a therapeutically effective amount of oxytocin or oxytocin analogs to alleviate one or more symptoms of Parkinson's disease. Methods for determining the effectiveness of oxytocin therapy by itself or in addition to one or more adjunctive therapies in alleviating one or more symptoms of Parkinson's disease are also discussed.

Abstract: Provided herein are ligand dimers, compositions thereof, as well as methods of their use. The ligand dimers provided can comprise at least one ligand to a Her receptor and can be used to force dimerization of specific receptor pairs. The forced dimerization of specific receptor pairs can be used to control (e.g., promote or inhibit) signaling, and, therefore, the ligand dimers provided can also be used in various forms of treatment in which such signaling control is beneficial to a subject. It follows that methods for controlling signaling are provided as are various methods of treatment.

Abstract: There are provided herein novel monoclonal antibodies that selectively bind and/or activate TrkC receptors, pharmaceutical compositions thereof and the use thereof for treating or preventing conditions which require activation of TrkC, such as amyotrophic lateral sclerosis and other neurodegenerative conditions and motor neuron diseases. The monoclonal antibodies are useful to screen for agents that share the same binding epitope on the TrkC receptor.

Abstract: Disclosed is a method for treating relapsing-remitting multiple sclerosis in a patient by administering to the patient autologous, ex vivo-expanded CD4+CD25+Foxp3+CD127low T reg cells when the patient is in remission. Also disclosed is a method of inhibiting the activity of autoimmune, autologous cytotoxic T and B cells in a patient suffering from relapsing-remitting multiple sclerosis, comprising administering a therapeutically effective amount of autologous CD4+CD25+Foxp3+CD127low T reg cells to the patient.

Abstract: Nucleic acid molecule selected from the group consisting of (a) a nucleic acid molecule having a nucleotide sequence shown in SEQ ID: NO 1, (b) a nucleic acid molecule which encodes a peptide having an amino acid sequence shown in SEQ ID: NO 2, (c) a nucleic acid molecule whose complementary strand hybridizes to a nucleic acid molecule according to (a) or (b) and which codes for a peptide which binds to ciliary neurotrophic factor receptor (CNTFR), the peptide binding with lower affinity than ciliary neurotrophic factor to the interleukin-6 receptor (IL-6R), (d) a nucleic acid molecule whose nucleotide sequence differs from the nucleotide sequence of a nucleic acid molecule according to (c) due to the degenerated genetic code, the codon at positions 82-84 of the nucleic acid molecule according to (a) coding for a non-positively charged amino acid, and the peptide at position 28 shown in SEQ ID: NO 2 having a non-positively charged amino acid residue.

Abstract: Disclosed are novel phosphorylation sites identified in LRRK2 and associated with Parkinson's Disease, antibodies that specifically bind to the novel phosphorylation sites, and laboratory and clinical uses thereof.

Abstract: The present application relates to the field of motor neuron diseases, most particularly to amyotrophic lateral sclerosis and spinomuscular atrophy. Provided herein are strategies to improve symptoms and increase survival in patients with these axonopathies by inhibiting signaling mediated by the EphA4 ephrin receptor.

Abstract: The invention is in the field of molecular immunology, more in particular in the field of medical treatment of animals such as humans suffering from unwanted immune reactions. The invention relates to methods for the treatment of unwanted immune reactions and provides means and methods for suppressing an immune response. The present invention relates in particular to regulatory T cells and methods of long-term, culture-expanding, activating and using same in immunotherapy and for the suppression of autoimmune responses, allergies and inflammatory diseases. The invention provides a sia alpha 2,3-conjugated antigen for use in the suppression of an immune response in a patient in need of such a treatment.

Abstract: Provided herein are compositions comprising light-activated chimeric proteins expressed on plasma membranes and methods of using the same to selectively depolarize excitatory or inhibitory neurons.

Abstract: The present invention relates to the discovery that specific human taste receptors in the T2R taste receptor family respond to particular bitter compounds. Also, the invention relates to the discovery of specific hT2R9 alleles and their disparate activity in functional assays with the same biter ligands. The invention further relates to the use of these T2R receptors in assays for identifying ligands that modulate the activation of these taste receptors by specific bitter ligands and related compounds. These compounds may be used as additives and/or removed from foods, beverages, cosmetics and medicinals in order to modify (block) T2R-associated bitter taste. Also T2R ligands may be used as therapeutics to treat and modulate T2R associated gastrointestinal and metabolic functions as well as treat gastrointestinal and metabolic diseases such as eating disorders, food sensing, food absorption, obesity, diabetes, Crohn's disease, celiac disease, et al.

Abstract: A family of novel feline bitter taste receptors, referred to as feline TAS2R (fTAS2R), are disclosed herein. Isolated polynucleotides encoding the novel feline bitter taste receptors and chimeric polypeptides are also disclosed, as are expression vectors and host cells for expression of the novel feline bitter taste receptors. Methods of identifying compounds that bind to the novel feline bitter taste receptors and modulate their activity are disclosed.

Abstract: Newly identified mammalian taste-cell-specific G Protein-Coupled Receptors and the genes encoding said receptors are described. Specifically, T2R taste G Protein-Coupled Receptors that are believed to be involved in bitter taste sensation, and the genes encoding the same, are described, along with methods for isolating such genes and for isolating and expressing such receptors. Methods for representing taste perception of a particular tastant in a mammal are also described, as are methods for generating a novel molecules or combinations of molecules that elicit a predetermined taste perception in a mammal, and methods for simulating one or more tastes.