Type 2 diabetes mellitus, brain atrophy, and cognitive decline

Abstract

ObjectiveTo study longitudinal relationships between type 2 diabetes mellitus (T2DM), cortical thickness, and cognitive function in older people with normal cognition, mild cognitive impairment, and Alzheimer disease (AD).MethodsThe sample was derived from the Alzheimer's Disease Neuroimaging Initiative cohort who underwent brain MRI and cognitive tests annually for 5 years. Presence of T2DM was based on fasting blood glucose ≥7.0mml/L or the use of glucose-lowering agents. We used latent growth curve modeling to explore longitudinal relationships between T2DM, cortical thickness, and cognitive function, adjusting for relevant covariates and testing for interactions.ResultsThere were 124 people with T2DM (mean age 75.5 years, SD 6.2) and 693 without T2DM (mean age 75.1 years, SD 6.9) with at least 1 MRI available. AD and lower cortical thickness at study entry was associated with a lower chance of having a MRI available at each follow-up phase (all p < 0.001). T2DM was associated with lower baseline cortical thickness (p = 0.01). We found no direct effect of T2DM on decline in cortical thickness or cognitive function, but there was an indirect pathway linking T2DM and cognitive decline via baseline cortical thickness (β = −0.17, p = 0.022). There was an interaction between T2DM and education whereby the negative effect of T2DM on baseline cortical thickness was reduced in those with greater education (β = 0.34, p = 0.037). These associations changed minimally when adjusted for baseline cognitive diagnosis.ConclusionsIn an older cohort with low cerebrovascular disease burden, T2DM contributes to cognitive decline via neurodegeneration. Prior brain and cognitive reserve may protect against this effect.

Cognitive reserve and midlife vascular risk: Cognitive and clinical outcomes

“…A number of cross-sectional studies across the clinical spectrum (i.e., cognitively normal, MCI, and dementia) suggest that higher levels of CR may reduce the impact of WMH load [18][19][20][21][22] or vascular risk factors [23][24][25][26][27][28] on cognitive performance, at least for some cognitive domains. However, few longitudinal studies have examined this issue [29][30][31][32][33] and to our knowledge, none were conducted among individuals who were primarily middle aged and cognitively normal at baseline. Moreover, studies among cognitively normal older individuals (mean baseline age 70-80 years) have been characterized by short follow-up periods (mean 2.5-5 years) and produced mixed results.…”

Effects of Possible Osteoporotic Conditions on the Recurrence of Chronic Subdural Hematoma

“…Exudation due to capillary vasculopathy caused by diabetes or well-developed neovascularization of the neomembrane in diabetes patients may play an important role in the recurrence of CSDH (27). It has also been reported that type 2 diabetes is associated with an increased risk of brain atrophy (28,29). The cerebral atrophy induced by type 2 diabetes is naturally thought to be associated with the recurrence of CSDH as described above.…”

Review of the Effect of Natural Compounds and Extracts on Neurodegeneration in Animal Models of Diabetes Mellitus

“…The mechanisms implicated have not been completely elucidated; however, cognitive impairment, vascular dementia, Alzheimer’s disease, stroke or anxiety/depression have been related to diabetes [1,11]. In this sense, the diabetic brain (with controlled or uncontrolled hyperglycemia) show brain injury with a wide profile of micro and macrostructural changes, leading to neurodegeneration, neurovascular deterioration, neuroinflammation and progressive cognition dysfunction [12,13,14,15,16,17,18,19]. However, the study of central complications associated with T2D has been probably hampered by the difficulty of the measurements [2], the lack of ideal animal models, or the fact that T2D is a complex disorder and, therefore, it is likely that multiple different, synergistic processes may interact to promote central alterations.…”