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Aging, senile dementia, and the intralaminar microchemistry of cerebral cortex

Department of Neurology, Lexington Veterans Administration Medical Center (Dr. DeKosky) and University of Kentucky (Drs. DeKosky and Bass), and the Sanders-Brown Research Center on Aging (Drs. DeKosky and Bass), Lexington, KY.

We compared the microchemical architecture of right frontal isocortex from patients with senile dementia and age-matched and younger controls. Neuronal connectivity within deep lamina of the cortical column (Brodmann area 9) tended to decline in normal aging and was profoundly depleted in senile dementia. In both aging and senile dementia, there was a significant 20% loss of total cells (neurons and glia) in cortical layers III to VI. In senile dementia, marked diminution of total ganglioside sialic acid per neuron and galactocerebroside per cell in the lower lamina far exceeded alterations associated with aging itself. This structural loss may imply deafferentation of the cortex, owing to loss of projections from subcortical areas such as nucleus basalis. Selective vulnerability of axodendritic arborization of neurons in lower lamina may be correlated to the impaired cognitive functions of senile dementia.

Address correspondence and reprint requests to Dr. DeKosky, Department of Neurology (127), Lexington Veterans Administration Medical Center, Lexington, KY 40511.

This research was supported by Research Grant No. N.S. 16009 from the NINCDS and the Research Service of the Veterans Administration. Dr. DeKosky is the recipient of a Teacher Investigator Development Award (No. NS00444) from the NINCDS.

Accepted for publication April 1, 1982.

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