Abstract: The present invention provides a method for identifying compounds which modulate the interaction of Nogo and Nogo receptor (NgR). The present invention also provides compounds that modulate the interaction of Nogo and Nogo receptor (NgR), the use of such compounds and compositions in the treatment or amelioration of conditions diseases or disorders, such as spinal cord injury, traumatic brain injury, stroke, multiple sclerosis, ALS, Huntington's disease, Alzheimer's disease, Parkinson's disease, epilepsy, Schizophrenia or schizoaffective disorders.

Abstract: The invention provides compositions and methods for interfering with Nogo-receptor mediated signaling and mediating axonal growth. The invention also provides methods for treating central nervous system diseases, disorders or injuries.

Abstract: The invention provides methods of inhbiting suppression of long term potentiation, improving acute memory retention and spatial memory performance and treating Alzheimer's disease by administration of a PrPc antagonist or combinations thereof. Additionally, this invention provides pharmaceutical kits comprising, and methods for making and using, such combinittions, as well as methods of identifying molecules that could function as PrPc antagonists.

Abstract: 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.

Abstract: 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.

Abstract: The invention relates generally to genes that encode proteins that inhibit axonal growth. The invention relates specifically to genes encoding NgR protein homologs in humans and mice. The invention also includes compositions and methods for modulating the expression and activity of Nogo and the NgR proteins. Specifically, the invention includes peptides, proteins and antibodies that 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.

Abstract: Nogo, MAG, and OMgp are myelin-derived proteins that bind to a neuronal Nogo-66 Receptor (NgR) to limit axonal regeneration after CNS injury. Nogo-A protein may play the most prominent role in vivo, perhaps because its action is mediated both by NgR and by other receptors. Here, we extend our previous analysis of Nogo-A and NgR functional domains. In addition to a NgR-dependent Nogo-66 inhibitory domain and a NgR-independent Amino-Nogo-A specific domain, we identify a third Nogo-A specific domain that binds to NgR with nanomolar affinity. This third domain of 19 amino acids (aa) does not alter cell spreading or axonal outgrowth. Ala-scanning mutagenesis of surface residues in NgR partially distinguishes ligand binding sites for the two Nogo domains and for MAG, OMgp and Lingo-1. Fusion of the two NgR-binding Nogo-A domains creates a ligand with ten-fold enhanced affinity for NgR and converts a NgR antagonist peptide to an agonist.

Abstract: The invention provides compositions and methods for interfering with Nogo-receptor mediated signaling and mediating axonal growth. The invention also provides methods for treating central nervous system diseases, disorders or injuries.

Abstract: 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.

Abstract: 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.

Abstract: 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.

Abstract: The present invention provides polynucleotides, polypeptides, pharmaceutical compositions, and methods for modulation of nerve growth and regeneration.

Abstract: The invention relates generally to genes that encode proteins that inhibit axonal growth. The invention relates specifically to genes encoding NgR protein homologs in humans and mice. The invention also includes compositions and methods for modulating the expression and activity of Nogo and the NgR proteins. Specifically, the invention includes peptides, proteins and antibodies that 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.

Abstract: 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.

Abstract: The invention relates generally to genes that encode proteins that inhibit axonal growth. The invention relates specifically to genes encoding NgR protein homologs in humans and mice. The invention also includes compositions and methods for modulating the expression and activity of Nogo and the NgR proteins. Specifically, the invention includes peptides, proteins and antibodies that 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.

Abstract: 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.

Abstract: Disclosed are Nogo receptor proteins and biologically active Nogo (ligand) protein fragments. Also disclosed are compositions and methods for modulating the expression or activity of the Nogo and Nogo receptor 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.

Abstract: Inhibition of nerve growth normally helps to prevent aberrant pathway or target selection, but also prevents needed regeneration in the mammalian central nervous system. The responsible inhibitory ligands are unknown, but pertussis toxin-sensitive G proteins, which are enriched in growth cones, appear to be involved in causing the responding growth cones to collapse. GAP-43 is an intracellular protein that can amplify the response to the stimulation of G protein-coupled receptors. We have attempted to modify the sensitivity of nerves to inhibitory signals by the use of GAP-43 peptides. The peptide corresponding to the native amino terminus sequence stimulates G.sub.o and enhances the growth cone collapse induced by inhibitory ligands. Modification of two critical cysteines generates peptides which inhibit G.sub.o and which markedly reduce the degree of inhibitor-mediated growth cone collapse.