Patients with dementia and diabetes appear to display a different pattern of injuries in their brains than patients with dementia but without diabetes, according to an article posted online Jan. 12 that will appear in the March print issue of Archives of Neurology, one of the JAMA/Archives journals.
“The association between diabetes mellitus and increased risk for dementia in the elderly is well documented,” the authors write as background information in the article. Several possible mechanisms have been proposed for this association, including the direct effects of high blood glucose and insulin, the build-up of beta-amyloid plaques in the brain and the effects of diabetes-related vascular disease on blood vessels in the brain.
Dr. Joshua A. Sonnen, UW senior fellow in pathology, and colleagues studied 196 individuals who were part of the Adult Changes in Thought Study, a community-based dementia investigation managed by the Center for Health Studies at Group Health Cooperative. After the participants died, their brains were autopsied and their cases were divided into four groups based on clinical information: those with diabetes and dementia, those with diabetes but not dementia, those with dementia but not diabetes and those without either disease.
In the 125 patients without dementia, neuropathological and biochemical factors did not differ based on diabetes status. However, among the 71 with dementia, two patterns of injury emerged based on whether the patients had diabetes and received diabetes treatment. Those without diabetes had larger amounts of beta-amyloid buildup and greater free radical damage, whereas those with diabetes had more microvascular infarcts (microscopic injury to small blood vessels in the brain known as arterioles) and more inflammation in neural tissue. This pattern was related to diabetes treatment, in that patients with dementia receiving treatment for diabetes had more microvascular infarcts, and untreated diabetic patients with dementia had beta-amyloid build-up similar to non-diabetic patients with dementia.
“These novel characterizations of two apparently different patterns of injury in dementia depending on diabetes mellitus status may have important etiologic and therapeutic implications,” the authors conclude.
This work was supported by grants from the National Institutes of Health; by the Nancy and Buster Alvord Endowment; and by the U.S. Department of Veterans Affairs.
Dr. Suzanne Craft, professor of psychiatry and behavioral sciences, is the corresponding author for the study. She noted that the results indicate that there may be two different pathways for dementia that would need different treatments.
Other authors are Drs. Eric B. Larson of the UW and Group Health; Kiri Brickell of psychiatry; Paul Crane of Group Health; Thomas Montine of pathology, and Randall Woltjer of Oregon Health and Sciences University.