Aging, senile dementia, and the intralaminar microchemistry of cerebral cortex.
We compared the microchemical architecture or 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.
D000328:Adult; D000368:Aged; D000375:Aging; D002540:Cerebral Cortex / Q000032:analysis* / Q000166:cytology; D004247:DNA / Q000032:analysis; D003704:Dementia / Q000503:physiopathology*; D005699:Galactosylceramides / Q000032:analysis; D006801:Humans; D008875:Middle Aged; D009457:Neuroglia / Q000166:cytology; D009474:Neurons / Q000166:cytology / Q000648:ultrastructure; D012313:RNA / Q000032:analysis; D014018:Tissue Distribution
D005699:Galactosylceramides; D012313:RNA; D004247:DNA