Vascular health and cognitive function in older adults with cardiovascular disease

Forman, Daniel E.; Cohen, Ronald A.; Hoth, Karin F.; Haley, Andreana P.; Poppas, Athena; Moser, David J.; Gunstad, John; Paul, Robert; Jefferson, Angela L.; Tate, David F.; Ono, Makoto; Wake, Nicole; Gerhard‐Herman, Marie

doi:10.1016/j.artres.2008.01.001

Cited by 25 publications

(18 citation statements)

References 48 publications

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“…IL-2 in particular, could affect endothelial function through increasing blood brain barrier permeability. Unlike other cytokines, IL-2 does not require a saturable transport system to cross the blood brain barrier (Forman, 2008). Thus, IL-2 levels can accumulate more quickly in the brain compared to other cytokines, causing more damage to endothelial cells.…”

Section: Discussionmentioning

confidence: 99%

Inflammation as a mediator of the relationship between cortical thickness and metabolic syndrome

Kaur

Gonzales

Eagan

et al. 2014

Brain Imaging and Behavior

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Objective Metabolic Syndrome (MetS), the clustering of obesity, high blood pressure, and disordered glucose and lipid/lipoprotein metabolism within a single individual, is associated with poorer cognitive function. It has been hypothesized that cognitive impairment in MetS occurs primarily within the context of inflammation. MetS risk factors are also associated with thinning of the cerebral cortex. However, the mechanisms by which MetS and inflammation affect the brain are poorly understood. The present study used statistical mediation to examine the relationship between MetS risk factors, cortical thickness in a priori regions of interest (ROIs) and inflammation. ROIs were chosen from the previous literature. Research Design and Methods Forty-three adults between the ages of 40 and 60 years underwent a health screen, neuropsychological testing and structural magnetic resonance imaging. Serum levels of pro-inflammatory markers (interleukin 1, interleukin 2, interleukin 6 and C-Reactive Protein) were measured using enzyme-linked immunosorbent assays. Results A higher number of MetS risk factors were associated with thinning in the inferior frontal ROI (β=−0.35, p = 0.019) as well as higher levels of serum interleukin 2 (β=0.31, p=0.04). A higher level of serum interleukin 2 was also associated with reduced thickness in the inferior frontal gyrus (β=−0.41, p=0.013). After accounting for the effects of interleukin 2, the number of MetS risk factors was no longer associated with cortical thickness in the inferior frontal gyrus indicating successful statistical mediation. Conclusions The results indicate a potentially important role for inflammation in linking MetS to cortical thinning and cognitive vulnerability.

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Section: Discussionmentioning

confidence: 99%

Inflammation as a mediator of the relationship between cortical thickness and metabolic syndrome

Kaur

Gonzales

Eagan

et al. 2014

Brain Imaging and Behavior

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“…An additional goal of this study was to determine the relationship between M268T and cognition given the established relationship between vascular deterioration and cognitive difficulties [71–73]. Several studies have reported cognitive difficulties among individuals with cardiovascular conditions, independent of a vascular dementia diagnosis [74].…”

Section: 0 Discussionmentioning

confidence: 99%

Neuromarkers of the common angiotensinogen polymorphism in healthy older adults: A comprehensive assessment of white matter integrity and cognition

Salminen

Schofield

Pierce

et al. 2016

Behavioural Brain Research

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The common angiotensinogen (AGT) M268T polymorphism (rs699; historically referred to as M235T) has been identified as a significant risk factor for cerebrovascular pathologies, yet it is unclear if healthy older adults carrying the threonine amino acid variant have a greater risk for white matter damage in specific fiber tracts. Further, the impact of the threonine variant on cognitive function remains unknown. The present study utilized multiple indices of diffusion tensor imaging (DTI) and neuropsychological assessment to examine the integrity of specific white matter tracts and cognition between individuals with homozygous genotypes of M268T (MetMet n = 27, ThrThr n = 27). Differences in subcortical hyperintensity (SH) volume were also examined between groups. Results indicated that the threonine variant was associated with significantly reduced integrity in the superior longitudinal fasciculus (SLF) and the cingulate gyrus segment of the cingulum bundle (cingulum CG) compared to those with the methionine variant, and poorer cognitive performance on tests of attention/processing speed and language. Despite these associations, integrity of these tracts did not significantly mediate relationships between cognition and genetic status, and SH did not differ significantly between groups. Collectively our results suggest that the threonine variant ofM268T is a significant risk factor for abnormalities in specific white matter tracts and cognitive domains in healthy older adults, independent of SH burden.

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“…In particular, excess adipose tissue has negative vascular and metabolic consequences on the body, including increased risk for atherosclerotic heart disease and Type II diabetes (Sharma and Chetty, 2005). Moreover, declines in vascular health lead to executive cognitive dysfunction (e.g., Forman et al, 2008), further supporting the potential role of vascular mechanisms in obesity-cognition associations. One major pathway by which obesity, especially central adiposity, can engender risk for heart disease is through associations with elevated blood pressure (e.g., Krauss et al, 1998).…”

Section: Effects Of Obesity On Neurocognitive Healthmentioning

confidence: 91%

Body–Brain Connections: The Effects of Obesity and Behavioral Interventions on Neurocognitive Aging

Stillman

Weinstein

Marsland

et al. 2017

Front. Aging Neurosci.

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Obesity is a growing public health problem in the United States, particularly in middle-aged and older adults. Although the key factors leading to a population increase in body weight are still under investigation, there is evidence that certain behavioral interventions can mitigate the negative cognitive and brain (“neurocognitive”) health consequences of obesity. The two primary behaviors most often targeted for weight loss are caloric intake and physical activity. These behaviors might have independent, as well as overlapping/synergistic effects on neurocognitive health. To date obesity is often described independently from behavioral interventions in regards to neurocognitive outcomes, yet there is conceptual and mechanistic overlap between these constructs. This review summarizes evidence linking obesity and modifiable behaviors, such as physical activity and diet, with brain morphology (e.g., gray and white matter volume and integrity), brain function (e.g., functional activation and connectivity), and cognitive function across the adult lifespan. In particular, we review evidence bearing on the following question: Are associations between obesity and brain health in aging adults modifiable by behavioral interventions?

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Vascular health and cognitive function in older adults with cardiovascular disease

Cited by 25 publications

References 48 publications

Inflammation as a mediator of the relationship between cortical thickness and metabolic syndrome

Inflammation as a mediator of the relationship between cortical thickness and metabolic syndrome

Neuromarkers of the common angiotensinogen polymorphism in healthy older adults: A comprehensive assessment of white matter integrity and cognition

Body–Brain Connections: The Effects of Obesity and Behavioral Interventions on Neurocognitive Aging

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