Reduced Acetylcholine Synthesis in Alzheimer’s Disease is a Clinically Relevant Change

Abstract

There are many causes of the clinical state of dementia. Excluding those patients with symptoms associated with tumors, infections (including Creutzfeldt-Jacob disease caused by a slow virus), vascular disease and the rare dementias (Huntington’s chorea and Pick’s disease), there remains a large group whose brains are atrophied and show an excess of senile degeneration (senile plaques and neurofibrillary degeneration) in the neocortex and hippocampus. When the condition occurs before the age of 65 years it is known as “presenile dementia” or Alzheimer’s disease; after this age it has been called “senile dementia” or senile dementia of Alzheimer’s type. There is no good reason on neuropathological grounds (10, 29) to maintain this distinction. The disease is generally accepted to be the commonest organic cause of intellectual deterioration (8) and is increasing in prevalence (16). There is still considerable uncertainty about its pathogenesis and little is known about its etiology. The first systematic examination of the incidence of senile degeneration in a “population” is described by Corsellis (9), who studied patients that died in Runwell Psychiatric Hospital (Essex, U.K.).