ALTERED CA2-ONSET ALZHEIMER-DISEASE( HOMEOSTASIS IN LYMPHOBLASTS FROMPATIENTS WITH LATE)

The authors report calcium (Ca2+) homeostasis features of transformed lymphocytes from patients with late-onset Alzheimer disease and health y age-matched controls. Alzheimer lymphoblasts show higher basal cytos olic-free [Ca2+] than controls. The antibodies anti-immunoglobulin M o r the beta-amyloid (beta-amyloid) peptide fragment 25-35-induced eleva tion of cytosolic-free [Ca2+] was higher in Alzheimer disease lymphobl asts than in control cells. However, the kinetics of Ca2+ replenishmen t of Ca2+-depleted cells shows a higher accumulation of cytosolic Ca2 in Alzheimer disease than in control lymphoblasts, which is better ap preciated when the Ca2+ efflux is inhibited. Thus, the authors conclud ed that Alzheimer disease lymphoblasts have a lower Ca2+ buffering cap acity than normal cells, probably because of changes in availability o r intrinsic functional properties of the intracellular Ca2+-binding st ructures. Aging alters the kinetics of the Ca2+ replenishment in lymph oblasts in a manner that resembles Alzheimer disease. However, unlike Alzheimer disease, aging does not change the maximum cytosolic-free [C a2+], suggesting that the mechanisms underlying the altered Ca2+ homeo stasis in aging and late-onset Alzheimer disease are different.