Abstract: The present invention relates to compositions and methods for treating neurodegeneration and neurodegenerative diseases associated with axonal degeneration. Neurodegeneration and neurodegenerative diseases associated with axonal degeneration are treated with therapies comprising SARM1 inhibitors such as SARM1 antisense oligonucleotides.

Abstract: The present disclosure relates to methods of treating neurodegeneration and neurodegenerative diseases comprising administering to a subject in need thereof a combination of a SARM1 inhibitor and NAD+ or a NAD+ precursor.

Abstract: The present disclosure relates to methods of treating neurodegeneration and neurodegenerative diseases comprising administering to a subject in need thereof a combination of a SARM1 inhibitor and a neuroprotective agent.

Abstract: The present invention relates to compositions and methods for treating neurodegeneration and neurodegenerative diseases associated with axonal degeneration. Neurodegeneration and neurodegenerative diseases associated with axonal degeneration are treated with therapies comprising SARM1 inhibitors such as SARM1 antisense oligonucleotides.

Abstract: The present disclosure relates to methods of treating neurodegeneration and neurodegenerative diseases comprising administering to a subject in need thereof a combination of a SARM1 inhibitor and NAD+ or a NAD+ precursor.

Abstract: The present disclosure relates to methods of treating neurodegeneration and neurodegenerative diseases comprising administering to a subject in need thereof a combination of a SARM1 inhibitor and a neuroprotective agent.

Abstract: This disclosure relates to the use of anti-?-synuclein antibody to diagnose an elevated level of ?-synuclein in the brain. Specifically, the disclosure relates to the method of assessing the levels of ?-synuclein in a blood plasma or CSF following administration to the test subject of an anti-?-synuclein antibody or antigen-binding fragment thereof, which can bind ?-synuclein with sufficient activity to alter the net efflux of ?-synuclein from brain to blood, or from brain to CSF.

Abstract: This disclosure relates to the use of anti-?-synuclein antibody to diagnose an elevated level of ?-synuclein in the brain. Specifically, the disclosure relates to the method of assessing the levels of ?-synuclein in a blood plasma or CSF following administration to the test subject of an anti-?-synuclein antibody or antigen-binding fragment thereof, which can bind ?-synuclein with sufficient activity to alter the net efflux of ?-synuclein from brain to blood, or from brain to CSF.

Abstract: This disclosure relates to the use of anti-A? antibody or antigen-binding fragment thereof to reduce brain amyloid plaques, or minimizes the occurrence of microhemorrhage during chronic dosing of an anti-A? antibody or antigen-binding fragment thereof. For example, the disclosure relates to the method of reducing brain amyloid plaques, comprising administering to a subject an anti-A? antibody or antigen-binding fragment thereof that binds to the same epitope as BIIB037 antibody, wherein the administration can reduce amyloid plaques in brain without affecting vascular amyloid, and wherein BIIB037 antibody binds to an epitope comprising amino acids 3-6 of A?.

Abstract: This disclosure relates to the use of anti-?-synuclein antibody to diagnose an elevated level of ?-synuclein in the brain. Specifically, the disclosure relates to the method of assessing the levels of ?-synuclein in a blood plasma or CSF following administration to the test subject of an anti-?-synuclein antibody or antigen-binding fragment thereof, which can bind ?-synuclein with sufficient activity to alter the net efflux of ?-synuclein from brain to blood, or from brain to CSF.

Abstract: It is shown here that hedgehog polypeptides possess novel activities beyond phenotype specification. Using cultures derived from the embryonic day 14.5 (E14.5) rat ventral mesencephalon, we show that hedgehog is also trophic for dopaminergic neurons and other neurons which are sensitive to exotoxicity.

Abstract: It is shown here that hedgehog polypeptides possess novel activities beyond phenotype specification. Using cultures derived from the embryonic day 14.5 (E14.5) rat ventral mesencephalon, we show that hedgehog is also trophic for dopaminergic neurons and other neurons which are sensitive to exotoxicity.

Abstract: It is shown here that hedgehog polypeptides possess novel activities beyond phenotype specification. Using cultures derived from the embryonic day 14.5 (E14.5) rat ventral mesencephalon, we show that hedgehog is also trophic for dopaminergic neurons and other neurons which are sensitive to exotoxicity.