Calcium in the initiation, progression and as an effector of Alzheimer's disease pathology.
The cause(s) of sporadic Alzheimer's disease (sAD) are complex and currently poorly understood. They likely result from a combination of genetic, environmental, proteomic and lipidomic factors that crucially occur only in the aged brain. Age-related changes in calcium levels and dynamics have the potential to increase the production and accumulation of both amyloid-beta peptide (Abeta) and tau pathologies in the AD brain, although these two pathologies themselves can induce calcium dyshomeostasis, particularly at synaptic membranes. This review discuses the evidence for a role for calcium dyshomeostasis in the initiation of pathology, as well as the evidence for these pathologies themselves disrupting normal calcium homeostasis, which lead to synaptic and neuronal dysfunction, synaptotoxicity and neuronal loss, underlying the dementia associated with the disease.
Green
Kim N
KN
Department of Neurobiology and Behavior, University of California, Irvine, Irvine, CA 92697-4545, USA. kngreen@uci.edu
D000544:Alzheimer Disease / Q000378:metabolism* / Q000473:pathology / Q000628:therapy*; D000818:Animals; D002118:Calcium / Q000378:metabolism*; D018450:Disease Progression; D006801:Humans
D002118:Calcium