Dysregulation of calcium in Alzheimer's disease.
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.
D000544:Alzheimer Disease / Q000378:metabolism*; D016564:Amyloid beta-Protein Precursor / Q000378:metabolism; D001057:Apolipoproteins E / Q000378:metabolism; D002118:Calcium / Q000378:metabolism* / Q000494:pharmacology; D006801:Humans; D008565:Membrane Proteins / Q000502:physiology; D008928:Mitochondria / Q000378:metabolism; D016874:Neurofibrillary Tangles / Q000378:metabolism; D053764:Presenilin-1
D016564:Amyloid beta-Protein Precursor; D001057:Apolipoproteins E; D008565:Membrane Proteins; C508853:PSEN1 protein, human; D053764:Presenilin-1; D002118:Calcium