Apoptotic mechanisms in Alzheimer neurofibrillary degeneration: cause or effect?
Increasing evidence suggests that selective neuronal loss in neurodegenerative diseases involves activation of cysteine aspartyl proteases (caspases), which initiate and execute apoptosis. In Alzheimer disease both extracellular amyloid deposits and intracellular amyloid beta protein may activate caspases, leading to cleavage of nuclear and cytoskeletal proteins, including tau protein. Proteolysis of tau may be critical to neurofibrillary degeneration, which correlates with dementia.
Dickson
Dennis W
DW
Department of Pathology, Mayo Clinic College of Medicine, Jacksonville, Florida 32224, USA. dickson.dennis@mayo.edu
D000544:Alzheimer Disease / Q000209:etiology / Q000235:genetics / Q000473:pathology*; D016229:Amyloid beta-Peptides / Q000502:physiology; D017209:Apoptosis / Q000502:physiology*; D006801:Humans; D008959:Models, Neurological; D008967:Molecular Biology; D009410:Nerve Degeneration / Q000473:pathology*; D016874:Neurofibrillary Tangles / Q000473:pathology*
D016229:Amyloid beta-Peptides