Researchers here mine patient data in order to demonstrate that type 2 diabetes combines with the age-related stiffening of blood vessels to produce greater structural damage in the brain, leading to a more rapid cognitive decline. This correlation between stiffening and damage was not observed in non-diabetic patients. This is an interesting result, as a reasonable view of the consequence of blood vessel stiffening with age is that it will produce increased blood pressure and consequence pressure damage to delicate tissues regardless of other factors. The authors conclude that the most likely explanation is that diabetes makes this process significantly worse, and thus more easily identified in patient data.
Cerebrovascular dysfunction has been proposed as a possible mechanism underlying cognitive impairment in the context of type 2 diabetes mellitus (DM). Although magnetic resonance imaging (MRI) evidence of cerebrovascular disease, such as white matter hyperintensities (WMH), is often observed in DM, the vascular dynamics underlying this pathology remain unclear. Thus, we assessed the independent and combined effects of DM status and different vascular hemodynamic measures (i.e., systolic, diastolic, and mean arterial blood pressure and pulse pressure index [PPi]) on WMH burden in cognitively unimpaired (CU) older adults and those with mild cognitive impairment (MCI).
559 older adults (mean age: 72.4 years) from the Alzheimer's Disease Neuroimaging Initiative were categorized into those with diabetes (DM+; CU = 43, MCI = 34) or without diabetes (DM-; CU = 279; MCI = 203). Participants underwent BP assessment, from which all vascular hemodynamic measures were derived. The presence of DM, but not PPi values, was independently associated with greater WMH burden overall after adjusting for covariates. Higher PPi values predicted greater WMH burden in the DM group only. No significant interactions were observed in the CU group.
Results indicate that higher PPi values are positively associated with WMH burden in diabetic older adults with MCI, but not their non-diabetic or CU counterparts. Our findings suggest that arterial stiffening and reduced vascular compliance may have a role in development of cerebrovascular pathology within the context of DM in individuals at risk for future cognitive decline. Given the specificity of these findings to MCI, future exploration of the sensitivity of earlier brain markers of vascular insufficiency (i.e., prior to macrostructural white matter changes) to the effects of DM and arterial stiffness/reduced vascular compliance in CU individuals is warranted.