Altered glycosylation of acetylcholinesterase in the Alzheimer’s disease brain: involvement of α7 nicotinic acetylcholine receptors

Although it is generally accepted that the accumulation of amyloid β (Aβ) in the brain is an important step in the pathogenesis of Alzheimer’s disease (AD), the mechanism by which Aβ causes neuronal dysfunction is poorly understood. The cognitive loss that occurs in AD is more likely to be caused by changes in synaptic plasticity than by non-specific neurotoxicity or cell loss.1 For this reason, there is a need to examine the effects of Aβ on biochemical mechanisms that regulate synaptic plasticity.