Interaction between APOE-{varepsilon}4 and HMGB1 is associated with widespread cortical thinning in mild cognitive impairment

Biomarkers which allow for identification of the underlying aetiology of mild cognitive impairment (MCI) are of prognostic importance. In addition to the amyloid-β and hyperphosphorylated tau pathology, genetic factors such as apolipoprotein E (APOE)-4 and neuroinflammation may have additional roles in the pathogenesis of Alzheimer's Disease (AD). In this study, we investigated the influence of APOE-4 status, neuroinflammation as measured by high mobility group box 1 protein (HMGB1), and their interaction effect on cortical thickness in MCI. We hypothesised that the interaction between APOE-4 and HMGB1 would result in a more widespread pattern of cortical thinning compared with either one factor alone.

Fifty-two individuals (27 mild cognitive impairment (MCI) and 25 controls) were recruited from a tertiary neurological centre. MCI was clinically diagnosed using the National Institute on Aging and the Alzheimer's Association workgroup (NIA-AA) criteria.1 They had a Clinical Dementia Rating (CDR) score of 0.5 and had no...

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