Source: Bentham Science Publishers.
The ability of protein interactions to modify nAChR function adds a completely new level of complexity to cholinergic signaling in the brain that may be specifically altered in AD. NeuroscienceNews.com image is for illustrative purposes only.
Nicotinic acetylcholine receptors (nAChRs) have been pursued for decades as potential molecular targets to treat cognitive dysfunction in Alzheimer’s disease (AD) due to their demonstrated role in processes underlying cognition such as synaptic facilitation, and theta and gamma wave activity.
Historically, activity at these receptors is facilitated in AD by use of drugs that increase the levels of their endogenous agonist acetylcholine, and more recently nAChR selective ligands have undergone clinical trials.
In this article, we discuss recent findings suggesting that the expression and function of nAChRs in AD may be regulated by direct interactions with specific proteins in the brain, including Lynx proteins, NMDA-receptors and the Wnt/β-catenin pathway, as well as β-amyloid sheets./.../
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