42 results about "Nogo Receptors" patented technology

The present invention relates to antibodies and related molecules that specifically bind to the Nogo receptor (NogoR). Such antibodies have uses, for example, in the treatment of spinal cord injury, brain trauma, paralysis, degenerative nervous system diseases, and stroke. The invention also relates to nucleic acid molecules encoding anti-NogoR antibodies, vectors and host cells containing these nucleic acids, and methods for producing the same.

The present invention relates to antibodies and related molecules that specifically bind to the Nogo receptor (NogoR). Such antibodies have uses, for example, in the treatment of spinal cord injury, brain trauma, paralysis, degenerative nervous system diseases, and stroke. The invention also relates to nucleic acid molecules encoding anti-NogoR antibodies, vectors and host cells containing these nucleic acids, and methods for producing the same.

Disclosed are immunogenic Nogo receptor-1 polypeptides, Nogo receptor-1 antibodies, antigen-binding fragments thereof, soluble Nogo receptors and fusion proteins thereof and nucleic acids encoding the same. Also disclosed are compositions comprising, and methods for making and using, such Nogo receptor antibodies, antigen-binding fragments thereof, soluble Nogo receptors and fusion proteins thereof and nucleic acids encoding the same.

Disclosed are NgR proteins and biologically active Nogo (ligand) protein fragments. Also disclosed are compositions and methods for modulating the expression or activity of the Nogo and NgR protein. Also disclosed are peptides which block Nogo-mediated inhibition of axonal extension. The compositions and methods of the invention are useful in the treatment of cranial or cerebral trauma, spinal cord injury, stroke or a demyelinating disease.

This invention relates to compounds, compositions, and methods useful for modulating NOGO and/or NOGO receptor gene expression using short interfering nucleic acid (siNA) molecules. This invention also relates to compounds, compositions, and methods useful for modulating the expression and activity of other genes involved in pathways of NOGO and/or NOGO receptor gene expression and/or activity by RNA interference (RNAi) using small nucleic acid molecules. In particular, the instant invention features small nucleic acid molecules, such as short interfering nucleic acid (siNA), short interfering RNA (siRNA), double-stranded RNA (dsRNA), micro-RNA (miRNA), and short hairpin RNA (shRNA) molecules and methods used to modulate the expression of NOGO and/or NOGO receptor genes, such as NOGO-A, NOGO-B, NOGO-C, NOGO-66 receptor, NI-35, NI-220, NI-250, myelin-associated glycoprotein, tenascin-R, and NG-2

The present invention is based on the discovery that suppressing the activity of the Nogo receptor (NgR) alone does not result in extensive axon regeneration unless the intrinsic growth program of neurons is also activated Accordingly, the present invention is directed to methods of stimulating axon regeneration using a combination therapy wherein agents that inhibit NgR activity or downstream pathways activated by inhibitory signals are combined with agents that activate the growth pathway of neurons (e.g. polypeptide growth factors, activators of macrophages, purine nucleosides, or hexoses).

Disclosed are immunogenic Nogo receptor-1 polypeptides, Nogo receptor-1 antibodies, antigen-binding fragments thereof, soluble Nogo receptors and fusion proteins thereof and nucleic acids encoding the same. Also disclosed are Nogo receptor antagonist polynucleotides. Also disclosed are compositions comprising, and methods for making and using, such Nogo receptor antibodies, antigen-binding fragments thereof, soluble Nogo receptors and fusion proteins thereof, nucleic acids encoding the same and antagonist polynucleotides.

Inhibitors of Nogo Receptor (NgR)-p75 binding are used to reduce NgR-p75 binding mediated axon growth inhibition. Mixtures of NgR and p75 are used in pharmaceutical screens to characterize agents as inhibiting binding of NgR to p75 and promoting axon regeneration.

The present invention is based on the discovery that suppressing the activity of the Nogo receptor (NgR) alone does not result in extensive axon regeneration unless the intrinsic growth program of neurons is also activated. Accordingly, the present invention is directed to methods of stimulating axon regeneration using a combination therapy wherein agents that inhibit NgR activity or downstream pathways activated by inhibitory signals are combined with agents that activate the growth pathway of neurons (e.g. polypeptide growth factors, activators of macrophages, purine nucleosides, or hexoses).

This invention relates to methods of treating diseases involving accumulation of Aβ plaques, including Alzheimer's Disease by the peripheral administration of soluble Nogo receptor polypeptides. The invention also provides methods of increasing the plasma to brain ratio of Aβ peptide and enhancing Aβ peptide clearance via peripheral administration of soluble Nogo receptor polypeptides. This invention also provides methods of improving memory function or inhibiting memory loss via the peripheral administration of soluble Nogo receptor polypeptides. The invention also provides methods of decreasing the size and number of Aβ plaques in a mammal via peripheral administration of soluble Nogo receptor polypeptides.

Disclosed are immunogenic Nogo receptor-1 polypeptides, Nogo receptor-1 antibodies, antigen-binding fragments thereof, soluble Nogo receptors and fusion proteins thereof and nucleic acids encoding the same. Also disclosed are compositions comprising, and methods for making and using, such Nogo receptor antibodies, antigen-binding fragments thereof, soluble Nogo receptors and fusion proteins thereof and nucleic acids encoding the same.

The invention provides methods for promoting regeneration or survival of dopaminergic neurons in a mammal displaying signs or symptoms of dopaminergic neuronal degeneration, including a human with Parkinson's disease, using Nogo receptor antagonists.

The present invention relates to antibodies and related molecules that specifically bind to the Nogo receptor (NogoR). Such antibodies have uses, for example, in the treatment of spinal cord injury, brain trauma, paralysis, degenerative nervous system diseases, and stroke. The invention also relates to nucleic acid molecules encoding anti-NogoR antibodies, vectors and host cells containing these nucleic acids, and methods for producing the same.

Disclosed are methods of treating chronic nervous system diseases or injuries, e.g., chronic spinal cord injury, using Nogo receptor antagonists, including Nogo receptor-1 (NgR1) polypeptides, Nogo receptor-1 antibodies and antigen-binding fragments thereof, soluble Nogo receptors and fusion proteins thereof, and polynucleotides. Also disclosed are methods of noninvasively monitoring axonal growth during and after treatment with an axonal growth promoting agent.

Disclosed are compositions relating to the Nogo receptor (NgR) family as well as fragments, chimeras, and variants thereof. The invention provides polypeptides, nucleic acids, vectors, expression systems, and antibodies and antibody fragments related to the NgRs as well as uses thereof. Such uses include modulation neurite outgrowth in a subject and treatment of central nervous system disorders in a subject, as well as, methods of identifying and screening compounds that can be used for modulating neurite outgrowth in a subject or in treatment of central nervous system disorders in a subject.

The invention discloses a preparation method for TAT-NEP1-40 fusion protein and application in treating the injuries of a central nervous system, CNS. The TAT-NEP1-40 fusion protein is characterized in that the TAT-NEP1-40 fusion protein comprises the protein transduction domain (PTD) of a transactivating transduction protein TAT of the human immunodeficiency virus (HIV) and Nogo extracellular peptide residues 1-40, NEP1-40. The fusion protein retains the selective antagonistic activity of the NEP1-40 to a Nogo receptor, NgR, and has the advantages of high transduction efficiency and easy penetration of BBB and BCSB, thereby overcoming the limitation of the NEP1-40, avoiding the extra injuries on nervous tissues caused by the mode of injecting the NEP1-40 through microinjection or miniature pump implantation, and overcoming the problem that the NEP1-40 can hardly pass BBB and BCSB to reach corresponding biological concentration. The fusion protein can be prepared in a large quantity, has a low cost and high activity, and can be used for treating a plurality of CNS injuries including cerebral ischemia, cerebral anoxia, cerebral hemorrhage, cerebral trauma, spinal core injury, and the like, and promoting the regeneration and functional rehabilitation of nervous tissues.

This inventon relates to compounds, compositions, and methods useful for modulating NOGO and/or NOGO receptor gene expression using short interfering nucleic acid (siNA) molecules. This invention also relates to compounds, compositions, and methods useful for modulating the expression and activity of other genes involved in pathways of NOGO and/or NOGO receptor gene expression and/or activity by RNA interference (RNAi) using small nucleic acid molecules. In particular, the instant invention features small nucleic acid molecules, such as short interfering nucleic acid (siNA), short interfering RNA (siRNA), double-stranded RNA (dsRNA), micro-RNA (miRNA), and short hairpin RNA (shRNA) molecules and methods used to modulate the expression of NOGO and/or NOGO receptor genes, such as NOGO-A, NOGO-B, NOGO-C, NOGO-66 receptor, NI-35, NI-220, NI-250, myelin-associated glycoprotein, tenascin-R, and NG-2