Small_2012_Neurodegener.Dis_10_76

Amyloid-beta (Abeta)-induced Ca(2+) influx into neurons has been well described since it was first reported almost 20 years ago. Ca(2+) influx can disrupt mechanisms of long-term potentiation and long-term depression and increase neuronal susceptibility to excitotoxicity. Our studies show that Abeta also causes an increase in acetylcholinesterase (AChE) levels and induces AMPA receptor internalization through Ca(2+)-dependent mechanisms. As Abeta-induced Ca(2+) entry may increase neuronal excitability, the increase in AChE and the downregulation of cell surface AMPA receptors may be part of a homeostatic mechanism which maintains normal levels of cholinergic and glutamatergic signaling.