Alzheimer's disease and non-insulin-dependent diabetes mellitus: common features do not make common bedfellows.

A lzheimer's Disease (AD) and non-insulin-dependent diabetes mellitus (NIDDM) are two of the most common and devastating health problems afflicting older adults. AD and NIDDM share a number of common features. Both conditions can have an enormous impact on a patient's quality of life, and both are associated with substantial health care costs. AD and NIDDM both have names that contain little useful information. AD is named after an obscure pathologist primarily to avoid use of a term that would convey directly its devastating impact on cognitive functioning. NIDDM is a non name that obscures the reality that many patients with NIDDM are in fact treated with insulin. Furthermore, a substantial proportion of patients with NIDDM rarely or never have significant amounts of sugar in their urine, certainly not enough to give their urine the sweet taste which is the basis for the name diabetes mellitus. Both AD and NIDDM are subjects of intensive investigation by the scientific community, and substantial resources of relevant NIH institutes are committed to support research about them. Perhaps my only tangible qualification to write about both disorders is that I serve on the advisory board of two NIH-supported Center grants at the University of Michigan: the Michigan Diabetes Research and Training Center and the Michigan Alzheimer's Disease Research Center. At this time, a major research emphasis both in NIDDM and in AD is the search for genetic markers for these conditions, since both have a genetic predisposition. Specific genetic defects have now been identified in a small number of families with NIDDM! and with AD. The information obtained thus far suggests that there may be considerable heterogeneity in the genetic factors which contribute to both of these conditions. The importance of genetic markers to advance understanding of these disorders relates, in part, to the difficulty in establishing the clinical phenotype for both NIDDM and AD. Thus, studies relating clinical phenotype to genotypic markers are particularly important. In this issue of the Journal of the American Geriatrics Society, Nielson et al. have used apolipoprotein-E genotyping to correlate with the clinical phenotype in 265 dementia patients participating in a University-based Alzheimer's Disease Research Center Clinic." Included in this population were 15 patients who also had diabetes mellitus by history. In confirmation of findings from other studies (reference 4 and others referenced by Nielson et al.), they found a high prevalence rate of apo-E4 and a low prevalence rate of apo-E2 in patients meeting criteria for possible or probable AD. Patients with other clinical types of dementia and those dementia patients with diabetes mellitus