The cholinergic hypothesis

The cholinergic hypothesis of AD, now some 40 years old, resulted from the discovery of reduced choline acetyltransferase activity, the enzyme that synthesizes acetylcholine (ACh), and basal forebrain cholinergic neurons in postmortem AD brain.12 These findings led to the hypothesis that dementia resulted from cholinergic neuron dysfunction and/or loss. This hypothesis was supported by animal studies in which cholinergic neuron loss or dysfunction impaired tasks requiring memory or cognitive abilities. The exact relationship between cholinergic dysfunction and dementia is unclear; however, it is generally accepted that cholinergic systems are involved in both cognitive (e.g., attention and memory) and noncognitive (e.g., apathy, depression, pychosis, aggression, and sleep disturbances) behaviors that manifest during AD progression. Patients with MCI have increased choline acetyltransferase activity in the frontal cortex and hippocampus at autopsy, suggesting that upregulation of this enzyme may be a compensatory change occurring early in disease to counteract progression to AD.13

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