The amyloid hypothesis has been the most accepted causative theory of Alzheimer's disease during the last decades. Amyloid-beta aggregation is considered a main pathological process and is responsible for neuronal loss and function impairment. In recent studies, it has been shown that acetylcholine can act as a neuroprotective agent against amyloid-beta toxicity by promoting conformational changes in the peptide. Here, the effect of acetylcholine on amyloid-beta mediated phosphorylation of the cytosolic phospholipase A2 is investigated in a human neuroectodermal cell line. The results show that these cells are responsive to amyloid-beta and that, in undifferentiated cells, it induces a 2.5-fold increase of cytosolic phospholipase A2 phosphorylation, but not in long-term treatments. Moreover, acetylcholine treatment on these cells was able to disrupt amyloid-beta effects. Overall, this study reinforces the idea that acetylcholine can have neuroprotective effects on non-cholinergic cells and opens the door to new therapeutic strategies against amyloid-beta mediated toxicity.
Effects of acetylcholine on β-amyloid-induced cPLA2 activation in the TB neuroectodermal cell line: implications for the pathogenesis of Alzheimer’s disease
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