Neuronal Nicotinic Acetylcholine Receptors Serve As Sensitive Targets That Mediate β-Amyloid Neurotoxicity
Department
neurobiology
Document Type
Article
Abstract
Alzheimer's disease (AD) is the most common form of brain dementia characterized by the accumulation of β-amyloid peptides (Aβ) and loss of forebrain cholinergic neurons. Aβ accumulation and aggregation are thought to contribute to cholinergic neuronal degeneration, in turn causing learning and memory deficits, but the specific targets that mediate Aβ neurotoxicity remain elusive. Recently, accumulating lines of evidence have demonstrated that Aβ 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 Aβ neurotoxicity. In this review, we summarize current studies performed in our laboratory and in others to address the question of how Aβ modulates neuronal nAChRs, especially nAChR subunit function. ©2006 CPS and SIMM.
Publication Date
10-1-2006
Publication Title
Acta Pharmacologica Sinica
ISSN
16714083
Volume
27
Issue
10
First Page
1277
Last Page
1286
Digital Object Identifier (DOI)
10.1111/j.1745-7254.2006.00430.x
Recommended Citation
Liu, Qiang and Wu, Jie, "Neuronal Nicotinic Acetylcholine Receptors Serve As Sensitive Targets That Mediate β-Amyloid Neurotoxicity" (2006). Translational Neuroscience. 454.
https://scholar.barrowneuro.org/neurobiology/454