| Summary: | Thesis (M.Sc)--Memorial University of Newfoundland, 1995. Medicine Bibliography: leaves [131]-156. Senile plaques are considered by many to be the most consistent neuropathologic feature of Alzheimer's disease, but they are also present in the brains of non-demented, elderly subjects. Recent reports (Sparks et al, 1990, 1993) suggest that non-demented patients with critical coronary artery disease show a higher prevalence of senile plaques than non-demented subjects without heart disease. The present study analyzes 40 autopsy brains which were divided into three groups according to the clinico-pathological findings: an Alzheimer's disease group (n=12), a severe cardiovascular disease group (n=17) and a control group (n=11). The brain areas examined were the middle frontal gyrus, the superior and inferior watershed areas, the hippocampal formation with the transentorhinal cortex, the primary visual cortex, the head of the caudate nucleus and the anterior lobe of the cerebellum. Consecutive sections were stained with cresyl violet, the modified Bielschowsky method and immunohistochemistry for amyloid beta-protein. Senile plaques and neurofibrillary tangles were counted in three and six microscopic fields at X100 and X200 magnification, respectively, and the mean values of the counts were calculated and used for statistical analysis. Patients with severe cardiovascular disease (critical coronary artery disease and/or hypertension) showed a higher prevalence of senile plaques than the non-demented controls. In the cardiovascular disease group senile plaque counts were significantly larger in the inferior watershed area, dentate gyrus, subiculum and transentorhinal cortex. Control and cardiovascular disease patients showed no difference regarding the prevalence and number of neurofibrillary tangles. In the sample examined, cardiovascular disease patients occupied an intermediate position in the spectrum of senile plaque formation between Alzheimer's disease and non-heart disease patients. These results suggest that there might be a cardiovascular component in the genesis of senile plaques and that study of patients with severe cardiovascular disease may help to clarify the origin and evolution of these lesions.
|
|---|