Two distinct patterns of cerebral injury were associated with dementia in autopsy studies, depending on whether or not the subject had diabetes.
In subjects without diabetes, dementia was associated with a greater load of amyloid-β peptide and greater free radical damage. In those with diabetes, dementia was associated with more microvascular infarcts and greater activation of neuroinflammation, said Dr. Joshua A. Sonnen of the department of pathology, University of Washington, Seattle, and his associates (Arch. Neurol. 2009;66:315–22).
These findings suggest that the pathogenesis of dementia differs between patients with diabetes and those without it.
The researchers examined autopsy data from subjects in an ongoing community-based study of brain aging and incident dementia. The subjects included 196 elderly men and women divided into four groups: those who had no diabetes and no dementia (92 cases), those who had diabetes but no dementia (33 cases), those who did not have diabetes but did have dementia (45 cases), and those who had both diabetes and dementia (26 cases).
Subjects with both diabetes and dementia died with a lower burden of amyloid-β peptide in brain parenchyma and cerebral blood vessels, compared with those who had dementia but no diabetes. They also showed significantly more deep microvascular injuries, suggesting “the basal-penetrating vessels may be especially vulnerable to damage from diabetes,” the researchers reported.
These subjects also had higher levels of neuroinflammation than did their nondiabetic counterparts, which may be related to their higher numbers of microvascular injuries, the authors wrote.