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.
University of Kentucky, College of Medicine, Department of Molecular and Biomedical Pharmacology, Lexington, KY 40536, USA. Tfoster@pop.uky.edu
Thomas C
TC
Foster
Ashok
A
Kumar
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