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The overall goal of this study was to evaluate the molecular and behavioral consequences of modulating the M1 muscarinic receptor in a mouse model that mimics Alzheimer disease (AD). The researchers’ rationale came from prior reports that selective stimulation of this receptor in cultured cells altered processing of the amyloid precursor protein by reducing levels of the toxic amyloid-β42 (Aβ42) fragment. Two pharmacologic treatments — the selective M1 agonist AF267B and the M1 antagonist dicyclomine — were tested on triple-transgenic mutant mice that progressively develop many of the pathologic features of AD, including amyloid plaques, neuronal tau aggregates, cholinergic dysfunction, and cognitive impairments.
The investigators found that…