Calcium dysregulation in the aging brain.
The idea that age-related cognitive decline is associated with disruption of calcium (Ca2+) homeostasis has been investigated over the past two decades. Much of this work has focused on the hippocampus because hippocampal-dependent memory is age sensitive. It is now well established that Ca(2+)-dependent processes such as susceptibility to neurotoxicity, the afterhyperpolarization amplitude, induction of synaptic plasticity, and long-term potentiation and long-term depression are altered with age. Recent work has identified changes in Ca2+ signaling pathways that may underlie the development of these biological markers of aging. This review considers recent findings concerning interactions between the various Ca(2+)-dependent processes, with special emphasis on the role of altered Ca2+ regulation and disruption of Ca2+ signaling pathways in mediating the expression of biological and behavioral markers of brain aging.
Foster
Thomas C
TC
University of Kentucky, College of Medicine, Department of Molecular and Biomedical Pharmacology, Lexington, KY 40536, USA. Tfoster@pop.uky.edu
Kumar
Ashok
A
D000375:Aging / Q000378:metabolism* / Q000502:physiology; D000818:Animals; D015415:Biomarkers / Q000032:analysis; D001921:Brain / Q000378:metabolism* / Q000502:physiology; D002118:Calcium / Q000378:metabolism*; D015220:Calcium Channels / Q000378:metabolism; D006624:Hippocampus / Q000378:metabolism; D006801:Humans; D017774:Long-Term Potentiation; D036881:Long-Term Synaptic Depression; D008564:Membrane Potentials; D009473:Neuronal Plasticity; D017470:Receptors, Glutamate / Q000378:metabolism; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism; D015398:Signal Transduction
D015415:Biomarkers; D015220:Calcium Channels; D017470:Receptors, Glutamate; D016194:Receptors, N-Methyl-D-Aspartate; D002118:Calcium