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 (Ca 2+ ) 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 Ca 2+ homeostasis. Studies of apolipoprotein E (ApoE) neurotoxic effects in AD confirmed involvement of Ca 2+ -mediated mechanisms. Futher consequences of Ca 2+ alterations in AD underline the importance of the ER and mitochondria as the regulatory sites involved in the pathogenesis of neuronal degeneration. Alterations of Ca 2+ homeostasis include cells from peripheral tissues, including lymphocytes and fibroblasts from AD donors.