Alzheimer's disease is one of the most common forms of
dementia in the elderly. One of its hallmarks is the abnormal aggregation and deposition of β-
amyloid (Aβ). Endogenous and exogenous
metal ions seem to influence β-
amyloid folding process, aggregation and deposition. Besides these variables other elements appear to affect β-
amyloid behavior, such as
cholesterol. The physiological concentration of
cholesterol in the cerebrospinal fluid (CSF) was used in order to determine the extent in which Aβ and Aβ-
metal complexes in vitro aggregation and their toxicity on human
neuroblastoma cell cultures is affected.
Cholesterol did not appear to influence Aβ and Aβ-
metal complexes aggregation, but it was effective in protecting
neuroblastoma cells against Aβ complexes' toxicity. The Aβ-Al complex seemed to be the most effective in disrupting and damaging membrane external layer, and simultaneously it appears to increase its toxicity on cell cultures; both of these effects are preventable by
cholesterol. The presence in physiological concentrations of
cholesterol seemed to compensate membrane damage that occurred to
neuroblastoma cells. These findings appear to contradict some data reported in literature. We believe that our results might shed some light on the role played by
cholesterol at physiological concentrations in both cellular balance and membrane protection.