This Article Full Text (PDF) References Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Saved Citations Download to citation manager Request Permissions Request Reprints Add to My Marked Citations Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Citing Articles via Scopus Google Scholar Articles by Foster, T. C. Articles by Kumar, A. Search for Related Content PubMed PubMed Citation Articles by Foster, T. C. Articles by Kumar, A. Social Bookmarking                         What's this?

Calcium Dysregulation in the Aging Brain

Department of Molecular and Biomedical Pharmacology, University of Kentucky, Lexington, Kentucky, Tfoster{at}pop.uky.edu

Ashok Kumar

Department of Molecular and Biomedical Pharmacology, University of Kentucky, Lexington, Kentucky

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 Ca²⁺-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 Ca²⁺-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.

Key Words: Aging • Calcium • Hippocampus • Memory • Synaptic plasticity

The Neuroscientist, Vol. 8, No. 4, 297-301 (2002)
DOI: 10.1177/107385840200800404


CiteULike    Complore    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter    What's this?

This article has been cited by other articles:

				R. M. Uranga, N. M. Giusto, and G. A. Salvador Iron-Induced Oxidative Injury Differentially Regulates PI3K/Akt/GSK3{beta} Pathway in Synaptic Endings from Adult and Aged Rats Toxicol. Sci., October 1, 2009; 111(2): 331 - 344. [Abstract] [Full Text] [PDF]

				K. Boric, P. Munoz, M. Gallagher, and A. Kirkwood Potential Adaptive Function for Altered Long-Term Potentiation Mechanisms in Aging Hippocampus J. Neurosci., August 6, 2008; 28(32): 8034 - 8039. [Abstract] [Full Text] [PDF]

				S. Chen, J. Nilsen, and R. D. Brinton Dose and Temporal Pattern of Estrogen Exposure Determines Neuroprotective Outcome in Hippocampal Neurons: Therapeutic Implications Endocrinology, November 1, 2006; 147(11): 5303 - 5313. [Abstract] [Full Text] [PDF]

				G. F. Reis, M. B. Lee, A. S. Huang, and K. D. Parfitt Adenylate Cyclase-Mediated Forms of Neuronal Plasticity in Hippocampal Area CA1 Are Reduced With Aging J Neurophysiol, June 1, 2005; 93(6): 3381 - 3389. [Abstract] [Full Text] [PDF]

				A. Kumar and T. C. Foster Enhanced Long-Term Potentiation During Aging Is Masked by Processes Involving Intracellular Calcium Stores J Neurophysiol, June 1, 2004; 91(6): 2437 - 2444. [Abstract] [Full Text] [PDF]

				G. F. Reis, M. B. Lee, A. S. Huang, and K. D. Parfitt Adenylate Cyclase-Mediated Forms of Neuronal Plasticity in Hippocampal Area CA1 Are Reduced With Aging J Neurophysiol, June 1, 2005; 93(6): 3381 - 3389. [Abstract] [Full Text] [PDF]