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Published on: March 23, 2011
Dysregulation of calcium in Alzheimer's disease
1Laboratory of Bio-Physical Methods, Nencki Institute of Experimental Biology, 3 Pasteur St., 02-093 Warsaw, Poland. mbrzyska@nencki.gov.pl.
Abstract:
Multiple efforts has underlined importance of calcium dependent cellular processes in the biochemical characterisation of Alzheimer's disease (AD), suggesting that abnormalities in calcium (Ca2+) homeostasis might be involved in the pathophysiology of the disease. Studies of the pathogenic mutations in presenilins 1 and 2 (PS1 and PS2) and amyloid precursor protein (APP) responsible for early onset familial AD have estabilished central roles for perturbed cellular Ca2+ homeostasis. Studies of apolipoprotein E (ApoE) neurotoxic effects in AD confirmed involvement of Ca(2+)-mediated mechanisms. Futher consequences of Ca2+ alterations in AD underline the importance of the ER and mitochondria as the regulatory sites involved in the pathogenesis of neuronal degeneration. Alterations of Ca2+ homeostasis include cells from peripheral tissues, including lymphocytes and fibroblasts from AD donors.
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