Skip to main content

Neuronal nicotinic acetylcholine receptors serve as sensitive targets that mediate -amyloid neurotoxicity

Buy Article:

$51.00 plus tax (Refund Policy)

Abstract:

Abstract

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.

Keywords: Alzheimer's disease; neurodegeneration; nicotinic acetylcholine receptor; -amyloid peptides

Document Type: Research Article

DOI: http://dx.doi.org/10.1111/j.1745-7254.2006.00430.x

Affiliations: Division of Neurology, Barrow Neurological Institute, St Joseph's Hospital and Medical Center, Phoenix, Arizona 85013, USA

Publication date: October 1, 2006

bsc/aphs/2006/00000027/00000010/art00001
dcterms_title,dcterms_description,pub_keyword
6
5
20
40
5

Access Key

Free Content
Free content
New Content
New content
Open Access Content
Open access content
Subscribed Content
Subscribed content
Free Trial Content
Free trial content
Cookie Policy
X
Cookie Policy
ingentaconnect website makes use of cookies so as to keep track of data that you have filled in. I am Happy with this Find out more