Abstract: Methods and compositions are provided for preventing or inhibiting neuronal degeneration, or for promoting nerve regeneration, in the central nervous system (CNS) or peripheral nervous system (PNS), or for protecting nerves from glutamate toxicity, which comprises administering to an individual in need thereof an effective amount of the copolymer poly-Glu,Tyr.

Abstract: Methods and compositions are provided for treatment of neurodegenerative diseases in which there is accumulation of misfolded and/or aggregated proteins, excluding prion diseases. In particular, the invention relates to treatment of the neurodegenerative diseases Huntington's disease (HD), Alzheimer's disease (AD) or Parkinson's disease (PD), by administration of an agent selected from the group consisting of (i) Copolymer 1, (ii) a Copolymer 1-related peptide, (iii) a Copolymer 1-related polypeptide, and (iv) T cells activated with (i), (ii) or (iii).

Abstract: A vaccine for reducing disease progression, and/or protection of motor nerve degeneration, and/or protection from glutamate toxicity in motor neurone disease (MND), particularly amyotrophic lateral sclerosis (ALS), patients, comprising an active agent selected from the group consisting of Cop 1, a Cop 1-related peptide, a Cop 1-related polypeptide, and poly-Glu, Tyr. The active agent is preferably Cop 1 or poly-Glu, Tyr, and can be administered with or without an adjuvant.

Abstract: The invention provides an eye-drop vaccine for therapeutic immunization of a mammal comprising Copolymer 1, a Copolymer 1-related peptide, or a Copolymer 1-related polypeptide, for treating neuronal degeneration caused by an injury or disease, disorder or condition in the central nervous system (CNS) or peripheral nervous system (PNS), for preventing or inhibiting neuronal secondary degeneration which may otherwise follow primary injury in the CNS, for promoting nerve regeneration in the CNS or in the PNS after an injury, disease, disorder or condition or for protecting CNS and PNS cells from glutamate toxicity.

Abstract: Oligosaccharides, and in particular disaccharides, which are degradation products of chondroitin sulfate proteoglycan are effective for use in treating, inhibiting, or ameliorating the effects of injuries or diseases or disorders that result in or are caused by neuronal degeneration or of disorders resulting in mental and cognitive dysfunction.

Abstract: Pharmaceutical compositions and methods for preventing or inhibiting neuronal degeneration, or for promoting nerve regeneration, in the central nervous system (CNS) or peripheral nervous system (PNS), in the treatment of an injury, disorder or disease of the CNS or PNS, comprise antigen-presenting cells, preferably dendritic cells, that have been pulsed with an agent selected from the group consisting of: (a) a nervous system (NS)-specific antigen or an analog thereof; (b) a peptide derived from an NS-specific antigen or from an analog thereof, or an analog or derivative of said peptide; (c) a copolymer selected from the group consisting of Copolymer 1, a Copolymer 1-related peptide or polypeptide, and poly-Glu<50> Tyr<50>; and (d) a non-self antigen.

Abstract: An agent selected from: (a) a pathogenic self-antigen associated with a T-cell-mediated specific autoimmune disease of an organ; (b) a peptide which sequence is comprised within the sequence of (a); (c) a peptide obtained by modification of (b), by replacement of one or more amino acid residues by different amino acid residues, said modified peptide still being capable of recognizing the T-cell receptor recognized by the parent peptide but with less affinity; (d) a nucleotide sequence encoding (a), (b), or (c); and (e) T cells activated by a pathogenic self-antigen of (a), a peptide of (b), or a modified peptide of (c), can be used for treatment of a non-autoimmune disease, disorder or injury in said organ. For example, uveitogenic antigens or peptides thereof can be used for treatment of a non-autoimmune disease, disorder or injury in the eye.

Abstract: A vaccine for reducing disease progression, and/or protection of motor nerve degeneration, and/or protection from glutamate toxicity in motor neurone disease (MND), particularly amyotrophic lateral sclerosis (ALS), patients, comprising an active agent selected from the group consisting of Cop 1, a Cop 1-related peptide, a Cop 1-related polypeptide, and poly-Glu, Tyr. The active agent is preferably Cop 1 or poly-Glu, Tyr, and can be administered with or without an adjuvant.

Abstract: Methods are provided for treating injury to or disease of the central or peripheral nervous system. In one embodiment, treatment is effected by administering activated T cells that recognize an antigen of Cop 1 or a Cop 1-related peptide or polypeptide to promote nerve regeneration or to prevent or inhibit neuronal degeneration within the nervous system. In another embodiment, treatment involves administering Cop 1 or a Cop 1-related peptide or polypeptide to promote nerve regeneration or to prevent or inhibit neuronal degeneration in the nervous system, either the central nervous system or the peripheral nervous system. The activated T cells, which have been activated by the presence of Cop 1 or a Cop 1-related peptide or polypeptide, can be administered alone or in combination with Cop 1 or a Cop 1-related peptide or polypeptide.

Abstract: Methods are provided for treating injury to or disease of the central or peripheral nervous system. In one embodiment, treatment is effected by administering activated T cells that recognize an antigen of Cop 1 or a Cop 1-related peptide or polypeptide to promote nerve regeneration or to prevent or inhibit neuronal degeneration within the nervous system. In another embodiment, treatment involves administering Cop 1 or a Cop 1-related peptide or polypeptide to promote nerve regeneration or to prevent or inhibit neuronal degeneration in the nervous system, either the central nervous system or the peripheral nervous system. The activated T cells, which have been activated by the presence of Cop 1 or a Cop 1-related peptide or polypeptide, can be administered alone or in combination with Cop 1 or a Cop 1-related peptide or polypeptide.

Abstract: Methods and compositions are provided for preventing or inhibiting neuronal degeneration, or for promoting nerve regeneration, in the central nervous system (CNS) or peripheral nervous system (PNS), or for protecting CNS cells from glutamate toxicity, comprising an effective amount of an agent selected from the group consisting of (a) poly-Glu,Tyr and (b) T cells which have been activated by poly-Glue,Tyr.

Abstract: Compositions and methods to promote nerve regeneration or to confer neuroprotection and prevent or inhibit neuronal degeneration within the nervous system, either the central nervous system or the peripheral nervous system, are provided. Treatment involves administering NS-specific activated T cells, or an NS-specific antigen or analog thereof, a peptide derived therefrom or an analog or derivative of said peptide, or a nucleotide sequence encoding said antigen or peptide, or any combination thereof.

Abstract: Methods and compositions are provided for preventing or inhibiting neuronal degeneration, or for promoting nerve regeneration, in the central nervous system (CNS) or peripheral nervous system (PNS), or for protecting nerves from glutamate toxicity, which comprises administering to an individual in need thereof an effective amount of the copolymer poly-Glu,Tyr.

Abstract: Compositions are provided for promoting nerve regeneration or reducing or inhibiting degeneration in the CNS or PNS to ameliorate the effects of injury or disease, comprising an active ingredient selected from: (a) a peptide obtained by modification of a self-peptide derived from a CNS-specific antigen, which modification consists in the replacement of one or more amino acid residues of the self-peptide by different amino acid residues, said modified CNS peptide still being capable of recognizing the T-cell receptor recognized by the self-peptide but with less affinity; (b) a nucleotide sequence encoding said peptide; (c) T cells activated by said peptide; and (d) any combination of (a)-(c). The peptide is preferably obtained by modification of the self-peptide p87-99 of MBP, more preferably, by replacing lysine 91 with glycine (G91) or alanine (A91) or by replacing proline 96 with alanine (A96).

Abstract: The present invention is directed to a central nervous system-derived heat stable immune privilege factor which exerts an inhibitory effect on macrophage migration and/or macrophage phagocytic activity. In addition, the factor exerts an inhibitory effect on the ability of macrophages and T cells to adhere to extracellular matrix and/or fibronectin. The invention is also directed to the isolation and methods for use of this immune privilege factor for the inhibition of inflammation in the central nervous system generally and at specific lesions in the central nervous system.

Abstract: The present invention discloses compositions and methods for the treatment of injury or disease of the nervous system CNS. In a particular embodiment, the invention provides methods of treatment using non-recombinant activated antiself T-cells that recognize an antigen of the NS or a peptide derived therefrom or a derivative thereof to promote nerve regeneration or to prevent or inhibit axonal degeneration within the NS. The invention also provides methods of treatment using a NS-specific antigen or peptide derived therefrom or a derivative thereof or a nucleotide sequence encoding said antigen or peptide to promote nerve regeneration or to prevent or inhibit axonal degeneration in NS, i.e., the CNS and/or PNS. The NS-specific antiself activated T-cells may be administered alone or in combination with NS-specific antigen or peptide derived therefrom or a derivative thereof or a nucleotide sequence encoding said antigen or peptide or any combination thereof.

Abstract: Methods and compositions are provided for preventing or inhibiting neuronal degeneration, or for promoting nerve regeneration, in the central nervous system (CNS) or peripheral nervous system (PNS), or for protecting CNS cells from glutamate toxicity, comprising an effective amount of an agent selected from the group consisting of (a) poly-Glu,Tyr and (b) T cells which have been activated by poly-Glue,Tyr.

Abstract: Compositions and methods to promote nerve regeneration or to confer neuroprotection and prevent or inhibit neuronal degeneration within the nervous system, eiteher the central nervous system or the peripheral nervous system, are provided. Treatment involves administering NS-specific activated T cells, or an NS-specific antigen or analog thereof, a peptide derived therefrom or an analog or derivative of said peptide, or a nucleotide sequence encoding said antigen or peptide, or any combination thereof.

Abstract: Methods are provided for treating injury to or disease of the central or peripheral nervous system. In one embodiment, treatment is effected by administering activated T cells that recognize an antigen of Cop 1 or a Cop 1-related peptide or polypeptide to promote nerve regeneration or to prevent or inhibit neuronal degeneration within the nervous system. In another embodiment, treatment involves administering Cop 1 or a Cop 1-related peptide or polypeptide to promote nerve regeneration or to prevent or inhibit neuronal degeneration in the nervous system, either the central nervous system or the peripheral nervous system. The activated T cells, which have been activated by the presence of Cop 1 or a Cop 1-related peptide or polypeptide, can be administered alone or in combination with Cop 1 or a Cop 1-related peptide or polypeptide.

Abstract: Methods and compositions are disclosed for the use of allogeneic mononuclear phagocytes to promote axonal regeneration in the central nervous system of a mammal. In one embodiment, allogeneic mononuclear phagocytes are cultured together with stimulatory tissue, such as skin, dermis or at least one nerve segment, and are subsequently administered into the central nervous system of a mammal at or near a site of injury or disease. In an alternative embodiment, autologous monocytes, preferably stimulated autologous monocytes, are administered into the central nervous system of a mammal at or near a site of injury or disease. CNS administration of mononuclear phagocytes may optionally be combined with administration of an adjuvant factor (e.g. aFGF) to the CNS, anti-inflammatory therapy of the mammal, or both. Methods for screening stimulatory tissue and cells and methods and compositions for cryopreserved allogeneic mononuclear phagocytes are also disclosed.