Axon degeneration: molecular mechanisms of a self-destruction pathway.
Axon degeneration is a characteristic event in many neurodegenerative conditions including stroke, glaucoma, and motor neuropathies. However, the molecular pathways that regulate this process remain unclear. Axon loss in chronic neurodegenerative diseases share many morphological features with those in acute injuries, and expression of the Wallerian degeneration slow (WldS) transgene delays nerve degeneration in both events, indicating a common mechanism of axonal self-destruction in traumatic injuries and degenerative diseases. A proposed model of axon degeneration is that nerve insults lead to impaired delivery or expression of a local axonal survival factor, which results in increased intra-axonal calcium levels and calcium-dependent cytoskeletal breakdown.
Department of Neurobiology, Stanford University School of Medicine, Stanford, CA 94305, USA. jtw@stanford.edu
Jack T
JT
Wang
Zachary A
ZA
Medress
Ben A
BA
Barres
D001369:Axons / Q000378:metabolism / Q000473:pathology / Q000502:physiology*; D002118:Calcium / Q000378:metabolism; D020013:Calcium Signaling; D020930:MAP Kinase Kinase Kinases / Q000378:metabolism / Q000502:physiology; D009410:Nerve Degeneration / Q000235:genetics / Q000378:metabolism*; D046988:Proteasome Endopeptidase Complex / Q000378:metabolism / Q000502:physiology; D013997:Time Factors; D014452:Ubiquitins / Q000378:metabolism / Q000502:physiology
D014452:Ubiquitins; D020930:MAP Kinase Kinase Kinases; D046988:Proteasome Endopeptidase Complex; D002118:Calcium