Neuronal Nicotinic Acetylcholine Receptors Serve As Sensitive Targets That Mediate Î²-Amyloid Neurotoxicity
Alzheimer's disease (AD) is the most common form of brain dementia characterized by the accumulation of Î²-amyloid peptides (AÎ²) and loss of forebrain cholinergic neurons. AÎ² accumulation and aggregation are thought to contribute to cholinergic neuronal degeneration, in turn causing learning and memory deficits, but the specific targets that mediate AÎ² neurotoxicity remain elusive. Recently, accumulating lines of evidence have demonstrated that AÎ² directly modulates the function of neuronal nicotinic acetylcholine receptors (nAChRs), which leads to the new hypothesis that neuronal nAChRs may serve as important targets that mediate AÎ² neurotoxicity. In this review, we summarize current studies performed in our laboratory and in others to address the question of how AÎ² modulates neuronal nAChRs, especially nAChR subunit function. Â©2006 CPS and SIMM.
Acta Pharmacologica Sinica
Digital Object Identifier (DOI)
Liu, Qiang and Wu, Jie, "Neuronal Nicotinic Acetylcholine Receptors Serve As Sensitive Targets That Mediate Î²-Amyloid Neurotoxicity" (2006). Translational Neuroscience. 454.