Fibroblasts and lymphocytes from Alzheimer patients are resistant to beta-amyloid-induced increase in the intracellular calcium concentration.
A major neuropathological finding in Alzheimer's disease (AD) is the presence of senile plaques in certain regions in the brain. The plaques contain extracellular deposits of beta-amyloid peptide (beta AP). Destabilization of intracellular calcium homeostasis in neurons, caused by beta AP, plays a central role in AD pathogenesis. In the present study, the authors report ionic alterations of lymphocytes and fibroblasts harvested from sporadic AD patients and from age-matched controls. Intracellular free calcium level ([Ca2+]i) of human cells, labeled with Fura-2AM, was determined by dual wavelength spectrofluorimetry. Basal [Ca2+]i appeared to be higher in AD lymphocytes when compared to control ones. Resting [Ca2+]i of AD fibroblasts, however, has proven to be lower than that seen with control cells. Exposure of cells to beta AP resulted in the elevation of the [Ca2+]i in both control cell types, however, that of AD lymphocytes and fibroblasts did not differ considerably.
D000368:Aged; D000544:Alzheimer Disease / Q000378:metabolism*; D016229:Amyloid beta-Peptides / Q000494:pharmacology*; D002118:Calcium / Q000378:metabolism*; D002478:Cells, Cultured; D005347:Fibroblasts / Q000187:drug effects* / Q000378:metabolism; D006801:Humans; D007424:Intracellular Fluid / Q000187:drug effects / Q000378:metabolism*; D008214:Lymphocytes / Q000187:drug effects* / Q000378:metabolism; D008875:Middle Aged; D010446:Peptide Fragments / Q000494:pharmacology*
D016229:Amyloid beta-Peptides; D010446:Peptide Fragments; C075222:amyloid beta-protein (1-42); D002118:Calcium