Exploring Brain Connectivity and White Matter Hyperintensities in Older Diabetic Individuals

Published on March 25, 2022

Imagine your brain’s white matter like a vast highway network, connecting different regions of the brain. In older individuals with diabetes and low vitamin B12, this highway system can get disrupted, leading to an increased load of white matter hyperintensities (WMHs). But what impact do these WMHs have on cognition? This study delves into the intricate details of cortical short-range fiber connectivity and its association with deep brain WMHs in older diabetic individuals. It turns out that the short-range fibers near the surface of the brain might actually strengthen as a response to the degeneration happening deeper within. The study also highlights the role of vitamin B12 deficiency in influencing these changes. Interestingly, as time progressed, researchers observed an increase in fiber density in the frontal cortices of the brain, indicating potential brain plasticity. However, this increase was not influenced by vitamin B12 supplementation alone. There’s still more to uncover about these fascinating connections between diabetes, WMHs, and brain plasticity. Dive into the research to uncover new insights!

Although previous studies have indicated that older people with diabetes mellitus (DM) had an approximately two times larger white matter hyperintensity (WMH) load than those without DM, the influence of WMHs on cognition is uncertain and inconsistent in the literature. It is unclear whether the short-range fibers in the juxtacortical region, traditionally considered to be spared from WMH pathology, are enhanced as an adaptive response to deep WM degeneration in older diabetic people with normal cognition. Moreover, the specific effect of vitamin B12 deficiency, commonly accompanied by DM, remains to be investigated. This study implemented a specialized analysis of the superficial cortical short-range fiber connectivity density (SFiCD) based on a data-driven framework in 70 older individuals with DM and low serum vitamin B12. Moreover, the effects of time and vitamin B12 supplementation were assessed based on a randomized placebo-controlled trial in 59 individuals. The results demonstrated a higher SFiCD in diabetic individuals with a higher deep WMH load. Additionally, a significant interaction between DWMH load and homocysteine on SFiCD was found. During the 27-month follow-up period, a longitudinal increase in the SFiCD was observed in the bilateral frontal cortices. However, the observed longitudinal SFiCD change was not dependent on vitamin B12 supplementation; thus, the specific reason for the longitudinal cortical short fiber densification may need further study. Overall, these findings may help us better understand the neurobiology of brain plasticity in older patients with DM, as well as the interplay among DM, WMH, and vitamin B12 deficiency.

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