Dysregulation of calcium in Alzheimer's disease

• Authors: M. Brzyska , E. Danek
• Languages of publication: EN

Abstracts

EN

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 Ca2+-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.

Keywords

EN

ALZHEIMER'S DISEASE; AMYLOID PRECURSOR PROTEIN; CALCIUM; MITOCHONDRIA; PERIPHERAL CELL

Discipline

• EXPERIMENTAL_BIOLOGY_&_MEDICINE: EXPERIMENTAL BIOLOGY & MEDICINE

• Publisher: Marceli Nencki Institute of Experimental Biology, Polish Academy of Sciences
• Journal: Acta Neurobiologiae Experimentalis
• Year: 2003
• Volume: 63
• Issue: 3
• Pages: 171-183

Contributors

author

M. Brzyska

author

E. Danek

• Document Type: article