Background: Cerebral hypoperfusion accompanies heart failure (HF) and is associated with reduced cognitive performance. Obesity is prevalent in persons with HF and is also a likely contributor to cognitive function, as it has been independently linked to cognitive impairment in healthy individuals. The current study examined the association between obesity and cognitive performance among older adults with HF and whether obesity interacts with cerebral hypoperfusion to exacerbate cognitive impairment.
Methods: Patients with HF (n = 99, 67.46 ± 11.36 years of age) completed neuropsychological testing and impedance cardiography. Cerebral blood flow velocity (CBF-V) measured by transcranial Doppler sonography quantified cerebral perfusion and body mass index (BMI) operationalized obesity.
Results: A hierarchical regression analysis showed that lower CBF-V was associated with reduced performance on tests of attention/executive function and memory. Elevated BMI was independently associated with reduced attention/executive function and language test performance. Notably, a significant interaction between CBF-V and BMI indicated that a combination of hypoperfusion and high BMI has an especially adverse influence on attention/executive function in HF patients.
Conclusions: The current findings suggest that cerebral hypoperfusion and obesity interact to impair cognitive performance in persons with HF. These results may have important clinical implications, as HF patients who are at high risk for cerebral hypoperfusion may benefit from weight reduction.
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http://dx.doi.org/10.1159/000343222 | DOI Listing |
Aging Dis
December 2024
Central Laboratory, Xuanwu Hospital, Capital Medical University, Beijing, China.
Vascular cognitive impairment and dementia (VCID), resulting from chronic cerebral hypoperfusion, represent the second most prevalent form of dementia globally. Aerobic exercise is widely acknowledged as an effective intervention for various cognitive disorders. This study utilized a bilateral common carotid artery stenosis (BCAS) model to investigate whether aerobic exercise promotes cognitive recovery through the Annexin-A1 (ANXA1)/mitogen-activated protein kinase (MAPK) axis in BCAS mice.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Alzheimer's Center at Lewis Katz School of Medicine, Temple University, Philadelphia, PA, USA.
Background: Brain endothelial cell (EC) stress, including that induced by vascular amyloid β (Aβ) deposits in cerebral amyloid angiopathy (CAA) and Alzheimer's disease (AD), contributes to cerebral blood flow impairment, blood brain barrier (BBB) damage, neurovascular unit dysfunction, microhemorrhages and hypoperfusion, precipitating neurodegeneration and neuroinflammation processes. Epidemiological and experimental evidence suggests that hyperhomocysteinemia (Hhcy) contributes to increasing AD risk as well as CAA pathology. However, the cellular and molecular mechanisms through which Aβ and Hhcy drive EC and BBB dysfunction, whether the molecular effects of these challenges are additive or independent, and possible therapeutic strategies, remain to be determined.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Oregon, Eugene, OR, USA.
Background: Stiffening of the large arteries is a hallmark feature of vascular aging and is associated with cognitive impairment and Alzheimer's disease pathology. Increased large artery stiffness leads to higher-than-normal pulse pressure in the cerebral circulation, damaging endothelial cells. It is known that short-term exposure to stiffer large arteries causes cerebral artery endothelial dysfunction and hypoperfusion in young mice.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Indiana University School of Medicine, Stark Neurosciences Research Institute, Department of Neurology, Indianapolis, IN, USA.
Background: Cerebral Amyloid Angiopathy (CAA) occurs at the intersection of Alzheimer's disease and vascular contributions to cognitive impairment and dementia (VCID). In the human brain it occurs when amyloid beta (Aβ) aggregates in small/medium-sized cerebral blood vessels, which contribute to hypoperfusion and cognitive decline by altering vascular function and integrity. The current study seeks to track the progression of CAA and associated neuroinflammation and glial cell changes in Tg2576 mice.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Miami, Coral Gables, FL, USA.
Background: Despite being the second most common form of dementia, vascular contributions of Frontotemporal Dementia are understudied. Recent data from patients and preliminary experiments have indicated that in progranulin-deficient mice, an increased number of cortical capillaries are stalled, and cerebral blood flow is reduced. Here, we examined the underlying mechanism contributing to microvascular dysfunction in FTD.
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