The M1-muscarinic acetylcholine (M1) receptor is the target of choice but has been hampered by adverse effects. An alternative approach is to directly activate cholinergic receptors responsible for learning and memory. Current therapies for Alzheimer’s disease seek to correct for defective cholinergic transmission by preventing the breakdown of acetylcholine through inhibition of acetylcholinesterase, these however have limited clinical efficacy.
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