Calcium dysregulation in the aging brain. Export

@article{citeulike:942179, abstract = {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.}, address = {University of Kentucky, College of Medicine, Department of Molecular and Biomedical Pharmacology, Lexington, KY 40536, USA. Tfoster@pop.uky.edu}, author = {Foster, T. C. and Kumar, A.}, citeulike-article-id = {942179}, citeulike-linkout-0 = {http://view.ncbi.nlm.nih.gov/pubmed/12194497}, citeulike-linkout-1 = {http://www.hubmed.org/display.cgi?uids=12194497}, issn = {1073-8584}, journal = {Neuroscientist}, keywords = {aging, calcium\_dysregulation}, month = {August}, number = {4}, pages = {297--301}, posted-at = {2006-11-13 22:18:15}, priority = {2}, title = {Calcium dysregulation in the aging brain.}, url = {http://view.ncbi.nlm.nih.gov/pubmed/12194497}, volume = {8}, year = {2002} }

TY - JOUR ID - citeulike:942179 L3 - citeulike-article-id:942179 N2 - 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. IS - 4 JF - Neuroscientist SN - 1073-8584 AD - University of Kentucky, College of Medicine, Department of Molecular and Biomedical Pharmacology, Lexington, KY 40536, USA. Tfoster@pop.uky.edu EP - 301 TI - Calcium dysregulation in the aging brain. VL - 8 SP - 297 KW - aging KW - calcium_dysregulation AU - Foster, TC AU - Kumar, A PY - 2002/08// UR - http://view.ncbi.nlm.nih.gov/pubmed/12194497 ER -