Acetylcholinesterase provides deeper insights into Alzheimer's disease

Med Hypotheses. 1994 Jul;43(1):21-30. doi: 10.1016/0306-9877(94)90045-0.

Abstract

This article reviews the considerable evidence which rejects the cholinergic hypothesis of Alzheimer's disease (AD) and proposes that it is the AChE system of which the lightly stained neurons are located in the entorhinal cortex, the CA1/subiculum of the hippocampus and the amygdala which are the most vulnerable and are the earliest affected in the pathological processes of AD. Changes then spread out to the intermediately stained neurons of the association cortex, until they affect the heavily stained cells of the motor cortex. In general, senile plaque, a hallmark of AD, may be formed from the terminals of AChE-containing neurons. Neurofibrillary tangle, another hallmark of AD, may be formed in the perikarya of AChE-containing cells and bring about the demise of the neuron, thus leading to dementia.

MeSH terms

  • Acetylcholinesterase / cerebrospinal fluid
  • Acetylcholinesterase / deficiency
  • Acetylcholinesterase / physiology*
  • Aged
  • Alzheimer Disease / enzymology
  • Alzheimer Disease / etiology*
  • Alzheimer Disease / pathology
  • Brain / enzymology
  • Choline O-Acetyltransferase / physiology
  • Dementia / enzymology
  • Dementia / etiology
  • Humans
  • Middle Aged
  • Models, Biological*
  • Neurofibrillary Tangles / enzymology
  • Neurofibrillary Tangles / pathology
  • Neurotransmitter Agents / physiology
  • Risk Factors

Substances

  • Neurotransmitter Agents
  • Choline O-Acetyltransferase
  • Acetylcholinesterase