The Prevalence and Malignancy of Alzheimer Disease

c U s o r t i t t t a a “ w i a t a An accompanying letter to the editor (p 304) provides nother illustration of the malignancy of Alzheimer disease, phenomenon well known to neurologists. Katzman and arasu estimate that the senile form of Alzheimer disease ay rank as the fourth or fifth most common cause of death in he United States. Yet the US vital statistics tables do not list Alzheimer disease,” “senile dementia,” or “senility” as a ause of death, even in the extended list of 263 causes of death. The argument that Alzheimer disease is a major killer ests on the assumption that Alzheimer disease and senile ementia are a single process and should, therefore, be onsidered a single disease. Both Alzheimer disease and enile dementia are progressive dementias with similar hanges in mental and neurological status that are indisinguishable by careful clinical analyses. The pathoogical findings are identical-atrophy of the brain, marked oss of neurons, neurofibrillary tangles, granulovascuolar hanges, and neuritic (senile) plaques. Ultrastructural tudies have established the identity of the neurofibrillary angle with its twisted tubule and the senile plaque with ts amyloid core and degenerating neurites in the brains f patients with Alzheimer disease (under age 65) and enile dementia (over age 65). Most recent ultrastructural nd neurochemical studies indicate that the neurofibrilary tangle in both disorders is characterized by the wisted tubule that represents two neurofilaments joined ogether in a helical fashion with a period of 800 Angtroms. The studies of Tomlinson et al and Blessed et al ave established a quantitative correlation between the egree of dementia and the number of neurofibrillary angles and senile plaques in the cerebral cortex. The vidence on which a distinction between senile dementia nd Alzheimer disease can still be argued is the genetic