Alzheimer's disease
- 1 March 1962
- journal article
- research article
- Published by Wolters Kluwer Health in Neurology
- Vol. 12 (3) , 213
- https://doi.org/10.1212/wnl.12.3.213
Abstract
The case of a 35-year-old white male in whom mental deterioration began to develop at the age of 31 is presented. His father also died after a disorder that resulted in slow, progressive mental deterioration. A diagnosis of Alzheimer''s disease was established by biopsy of the cerebrum. Enzyme-histo-chemical studies of senile plaques were done in biopsy material. The findings were correlated with data obtained by conventional technics. The early phase of development of senile plaques was characterized by increased activity of diphosphopyridine nucleotide diaphorase and succinic dehydrogenase and increased number of mitochondria. Alkaline phosphatase increased only in the plaques localized in the superficial part of the molecular layer. These changes represented an accentuation of the normal local enzymatic patterns. The development of the plaque was followed by astrocytic hypertrophy; these cells likewise showed increased oxidative enzyme activity. The late phase was charactdrized by central degeneration, with loss of oxidative enzymatic activity and of mitochondria. The deposition of fat or high molecular carbohydrates was dependent on central degeneration. These plaques were invaded by microglia cells with very strong acid phosphatase activity. This late degenerative phase was the one conventionally recognized as senile plaques. Senile plaques, thus, began as zones of increased enzymatic activity. Their size and the central degeneration were explained on the basis of scarce capillarization, since 92% of all plaques lacked capillaries.Keywords
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