Differences between white matter hyperintensities lesion load across allostatic load risk in cognitive complaint subjects

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AbstractBackgroundChronic exposure to stress, quantified by allostatic load (AL), has been postulated as a cause of structural brain changes in the context of dementia. White matter hyperintensities (WMH), detected in MRI FLAIR, are a common brain abnormality representing small vessel disease or degenerative changes in the brain. Here, we studied differences in tract‐specific WMH volume across three risk levels of AL in Chilean subjects with cognitive complaint, to explore links between chronic stress exposure and prodromal steps of dementia.MethodThe study included 135 subjects with cognitive complaint from a chilean cohort. Based in MoCA test, subjects were classified in mild cognitive impairment (MCI) (47) and subjective cognitive complaint (SCC) (88). To measure AL, we employed 15 metabolic, cardiovascular and immunity biomarkers, and the scores were classified in low, medium, and high risk levels of AL. WMH were calculated with Lesion Segmentation Toolbox, in SPM 12, and segmented according to John Hopkins University (JHU) and Human Connectome (HCP) atlases. To explore differences in tract‐specific WMH volume per risk level AL, we used a Kruskal Wallis test in each cognitive group (SCC and MCI). In significant tracts, a U Mann ‐ Whitney test was performed to establish the paired AL risk groups with significance.ResultIn the MCI group, we found a higher tract‐specific WMH load as a function of AL risk level in 10 tracts of the JHU atlas, and in 31 tracts of the HCP atlas. Differences were observed between low and medium‐risk of AL, with medium‐risk group showing a higher WMH load than low‐risk group.ConclusionWe observed significative differences in tract‐specific WMH lesion between low and medium risk of AL, only in MCI. It is according with literature that show the WMH burden could be associated with cognitive deficit, but not it’s risk. In this study, we further establish a link between chronic stress exposure and WM structural changes in early stages of neurocognitive disorders. We suggest that AL is a global measurement that could mediate the relation between vascular or neurodegenerative factors to WMH origin. Use of neurodegenerative and cardiovascular biomarkers can be useful to explore this mediation.