Cognitive impairment is common in heart failure (HF) and believed to be the result of cerebral hypoperfusion and subsequent brain changes including white matter hyperintensities (WMH). The current study examined the association between cerebral blood flow and WMH in HF patients and the relationship of WMH to cognitive impairment. Sixty-nine patients with HF completed the mini mental state examination (MMSE), echocardiogram, transcranial Doppler sonography (TCD) for cerebral blood flow velocity of the middle cerebral artery and brain magnetic resonance imaging (MRI). Multivariable hierarchical regression analyses controlling for medical and demographic characteristics as well as intracranial volume showed reduced cerebral blood flow velocity of the middle cerebral artery was associated with greater WMH (β = −.34, p = .02). Follow up regression analyses adjusting for the same medical and demographic factors in addition to cerebral perfusion also revealed marginal significance between increased WMH and poorer performance on the MMSE (β = −.26, p = .05). This study suggests that reduced cerebral perfusion is associated with greater WMH in older adults with HF. Our findings support the widely proposed mechanism of cognitive impairment in HF patients and prospective studies are needed to confirm our findings.

Background Clinically significant cognitive impairment is found in a subset of patients undergoing bariatric surgery. These difficulties could contribute to reduced adherence to postsurgical lifestyle changes and decreased weight loss. Objectives The current study is the first to prospectively examine the independent contribution of cognitive function to weight loss following bariatric surgery. Executive function/attention and verbal memory at baseline were expected to negatively predict percent excess weight loss (%EWL) and body mass index (BMI) at follow-up. Setting Three sites of the Longitudinal Assessment of Bariatric Surgery (LABS) parent project were used: Columbia, Cornell, and Neuropsychiatric Research Institute Methods Eighty-four individuals enrolled in the LABS project undergoing bariatric surgery completed cognitive evaluation at baseline. BMI and %EWL were calculated at 12-week and 12-month post-surgery follow-ups. Results Clinical impairment in task performance was most prominent in tasks associated with verbal recall and recognition (14.3–15.5% of the sample) and perseverative errors (15.5%). After accounting for demographic and medical variables, baseline tests of attention/executive function and memory predicted BMI and %EWL at 12 months, but not at 12 weeks. Conclusions Results demonstrate that baseline cognition predicts greater %EWL and lower BMI 12 months following bariatric surgery. Further work is needed to clarify the degree to which cognition contributes to adherence, and the potential mediation of cognition on the relationship between adherence and weight loss in this group.

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HD-tDCS appears well-tolerated and safe with effective sham-control in older adults, even at 3 mA. These data support the use of HD-tDCS in randomized controlled trials and clinical translation efforts.

This review paper will discuss the recent literature examining the relationship between obesity and neurocognitive outcomes, with a particular focus on cognitive changes after bariatric surgery. Obesity is now recognized as an independent risk factor for adverse neurocognitive outcomes, and severely obese persons appear to be at even greater risk. Bariatric surgery is associated with rapid improvements in cognitive function that persist for at least several years, although the mechanisms underlying these improvements are incompletely understood. Assessment of cognitive impairment in bariatric surgery patients is challenging, and improved methods are needed, as poorer performance on neuropsychological tests of memory and executive function leads to poorer clinical weight outcomes. In addition to its clinical importance, further study in this area will provide key insight into obesity-related cognitive dysfunction and clarify the possibility of an obesity paradox for neurological outcomes.