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From the Departments of Pathology and Neurology and The R.F. Kennedy Center for Research in Mental Retardation and Human Development, Albert Einstein College of Medicine, Bronx, NY.
Address correspondence and reprint requests to Dr. Dennis W. Dickson, Mayo Clinic Jacksonville, 4500 San Pablo Road, Jacksonville, FL 32224.
Diabetics have impaired cognitive performance relative to age-matched control subjects, but the pathologic basis for this impairment is unknown. Because Alzheimer-type lesions, including both senile plaques and neurofibrillary tangles, contain glycated proteins and glycation is known to be increased in diabetes, we hypothesized that cognitive impairment in diabetes may be due in part to increased Alzheimer-type pathology. We measured the amount of Alzheimer-type pathology in postmortem brains of diabetics and age-matched control subjects with sensitive and specific histofluorescent and immunocytochemical methods. As expected, there were strong correlations between severity of senile plaques and neurofibrillary degeneration and age and also a strong correlation between the pathologic measures. On the other hand, there was no significant difference between diabetics and control subjects with respect to severity of Alzheimer-type pathology, on average, or with respect to age. This finding was true for diabetics with and without insulin dependence. The results confirm reports showing that diabetes is not a risk factor for Alzheimer-type pathology and suggest that factors other than Alzheimer's disease are responsible for cognitive impairment in diabetics.
Supported by National Institute on Aging grants AG06803 and AG03949.
Received January 2, 1997. Accepted in final form May 20, 1997.
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