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• Our study is the first to show the effect of cumulative HbA1c (AUC HbA1c) and mean HbA1c over time (HbA1c avg) on dementia. • Prior studies have focused on the diagnosis of T2DM or single-time HbA1c in association with development of dementia, while we examined the effects of long-term cumulative glycemic exposure. • Our study suggests poorly controlled diabetes may increase the risk of developing dementia and shorten the time to onset of dementia based on the levels of AUC HbA1c and HbA1c avg. We examined cumulative effects of long-term glycemic exposure in patients with type 2 diabetes mellitus (T2DM) on the development of dementia. The study involved 20,487 records of patients with T2DM identified in the electronic medical record at Severance Hospital, Korea. Cumulative HbA1c (AUC HbA1c) and mean HbA1c over time (HbA1c avg) as measures of long-term glycemic exposure were compared for the development of dementia and the time to dementia. AUC HbA1c and HbA1c avg were significantly higher in patients who later developed dementia than in those who did not (AUC HbA1c : 56.2 ± 26.4 vs. 52.1 ± 26.1 %Year; HbA1c avg : 7.3 ± 1.0 vs. 7.0 ± 1.0%). Odds ratio of dementia increased when HbA1c avg was 7.2% (55 mmol/mol) or above, and when AUC HbA1c was 42 %Year (e.g., HbA1c 7.0% maintained for 6 years) or above. Among those who developed dementia, as HbA1c avg increased, the time to dementia onset decreased (β = -380.6 days, 95% confidence interval [CI]: −416.2 to −345.0). Our results indicate poorly controlled T2DM was associated with an increased risk of developing dementia, as measured by AUC HbA1c and HbA1c avg. Higher cumulative glycemic exposure may lead to developing dementia in a shorter time. [ABSTRACT FROM AUTHOR]

Background/Objectives Although hypertension is known to be a risk factor for AD, the effects of hypertension on brain function in AD patients are not well understood. We investigated alterations in resting-state functional connectivity according to the presence of hypertension in AD patients by using a method of correlation analysis based on a seed region in the posterior cingulate cortex (PCC). We also determined whether differences in resting-state connectivity were associated with gray matter atrophy. Methods Thirty-seven AD patients (18 patients with hypertension and 19 patients without hypertension) underwent the resting-state functional magnetic resonance imaging. We obtained the PCC maps by a temporal correlation method, to identify alterations in the functional connectivity of the PCC in hypertensive group relative to non-hypertensive group. Voxel-based morphometry analysis was also applied to adjust the confounding effect of gray matter atrophy. Results We detected a decreased connectivity to the PCC in the regions of subgenual anterior cingulated cortex (ACC) in hypertensive group relative to non-hypertensive group. However, we observed a pattern of increased connectivity between the PCC and the left inferior parietal cortex in hypertensive group. After correction for gray matter atrophy, all detected regions still remained significant. Conclusions Altered connectivity in AD patients with hypertension suggests the possibility that hypertension impairs resting-state functional connectivity of the AD brain, inducing a compensational process outside the impaired networks or disequilibrium in brain connectivity. This finding may account for an additional contribution of hypertension to the pathophysiology of AD. [ABSTRACT FROM AUTHOR]