Neuronal nicotinic acetylcholine receptors serve as sensitive targets that mediate -amyloid neurotoxicity
Alzheimer's disease (AD) is the most common form of brain dementia characterized by the accumulation of -amyloid peptides (A) and loss of forebrain cholinergic neurons. A accumulation and aggregation are thought to contribute to cholinergic neuronal degeneration, in turn causing learning and memory deficits, but the specific targets that mediate A neurotoxicity remain elusive. Recently, accumulating lines of evidence have demonstrated that A 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 A neurotoxicity. In this review, we summarize current studies performed in our laboratory and in others to address the question of how A modulates neuronal nAChRs, especially nAChR subunit function.
Document Type: Research Article
Affiliations: Division of Neurology, Barrow Neurological Institute, St Joseph's Hospital and Medical Center, Phoenix, Arizona 85013, USA
Publication date: October 1, 2006