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The majority of individuals over an age of 60 have hypertension. Elevated blood pressure and older age are associated with very similar changes in brain structure and function. We review the parallel brain changes associated with increasing age and blood pressure. This review focuses on joint associations of aging and elevated blood pressure with neuropsychological function, regional cerebral blood flow responses to cognitive and metabolic challenges, white matter disruptions, grey matter volume, cortical thinning, and neurovascular coupling. Treatment of hypertension ameliorates many of these changes but fails to reverse them. Treatment of hypertension itself appears more successful with better initial brain function. We show evidence that sympathetic and renal influences known to increase blood pressure also impact brain integrity. Possible central mechanisms contributing to the course of hypertension and aging are then suggested. An emphasis is placed on psychologically relevant factors: stress, cardiovascular reactions to stress, and diet/obesity. The contribution of some of these factors to biological aging remains unclear and may provide a starting point for defining the independent and interacting effects of aging and increasing blood pressure on the brain., (© 2020 Society for Psychophysiological Research.)

Stressor-evoked cardiovascular reactivity, trait positive emotionality, and negative emotionality are all associated with cardiovascular disease. It is unknown, however, whether cardiovascular reactivity may constitute a pathway by which trait positive or negative emotionality relates to disease risk. Accordingly, this study modeled the cross-sectional relationships between trait positive and negative emotionality, stressor-evoked cardiovascular reactivity, and severity of a subclinical vascular marker of cardiovascular risk, carotid artery intima-media thickness (CA-IMT). The sample consisted of healthy, midlife adults free from clinical cardiovascular disease (N = 286; ages 30-54; 50% female). Trait positive and negative emotionality were measured by three questionnaires. Heart rate and blood pressure reactivity were assessed across three stressor tasks. CA-IMT was assessed by ultrasonography. Latent factors of positive and negative emotionality, blood pressure reactivity, heart rate reactivity, and CA-IMT were created using structural equation modeling. Greater negative emotionality was marginally associated with more CA-IMT (β = .21; p = .049), but lower blood pressure reactivity (β = -.19; p = .03). However, heightened blood pressure (β = .21; p = .03), but not heart rate reactivity (β = -.05; p = .75), associated with greater CA-IMT. Positive emotionality was uncorrelated with cardiovascular reactivity (blood pressure: β = -.04; p = .61; heart rate: β = .16; p = .11) and CA-IMT (β = .16; p = .07). Although trait negative emotionality associates with a known marker of cardiovascular disease risk, independent of positive emotionality, it is unlikely to occur via a stressor-evoked cardiovascular reactivity pathway., (© 2020 Society for Psychophysiological Research.)

Exaggerated cardiovascular reactivity to acute psychological stress is associated with an increased risk of developing cardiovascular disease. The amygdala and hippocampus have been implicated in centrally mediating stressor-evoked cardiovascular reactivity. However, little is known about the associations of amygdala and hippocampus morphology with stressor-evoked cardiovascular reactivity. Forty (M age = 19.05, SD = 0.22 years) healthy young women completed two separate testing sessions. Session 1 assessed multiple parameters of cardiovascular physiology at rest and during a validated psychological stress task (Paced Auditory Serial Addition Test), using electrocardiography, Doppler echocardiography, and blood pressure monitoring. In Session 2, 1 year later, structural MRI was conducted. Brain structural volumes were computed using automated segmentation methods. Regression analyses, following Benjamini-Hochberg correction, showed that greater heart rate and cardiac output reactivity were associated with reduced amygdala and hippocampus gray matter volume. Systolic blood pressure reactivity was associated with reduced hippocampus volume. In contrast, no associations between diastolic blood pressure, mean arterial blood pressure, stroke volume, or total peripheral resistance reactivity with amygdala or hippocampus volumes were apparent. Comparison analyses examining insula volume found no significant associations. Some indicators of greater stressor-evoked cardiovascular reactivity associate with reduced amygdala and hippocampus gray matter volume, but the mechanisms of this association warrant further study., (© 2018 The Authors. Psychophysiology published by Wiley Periodicals, Inc. on behalf of Society for Psychophysiological Research.)

A reliable finding from the physical pain literature is that individuals with higher resting (i.e., tonic) blood pressure experience relatively less pain in response to nociceptive stimuli. Converging lines of evidence suggest that biological factors that influence the experience of physical pain may also relate to social pain. An open question, however, is whether higher blood pressure per se is a biological factor associated with lower sensitivity to social pain. This possible association was tested in three studies. Consistent with prior findings on physical pain, higher resting blood pressure was associated with lower self-reported sensitivity to social pain across individuals (Study 1 r = -.303, Study 2 r = -.262, -.246), even after adjusting for confounding factors related to blood pressure (Study 3 r = -.222). Findings suggest a previously unknown biological correlate of sensitivity to social pain, providing further evidence for possible shared substrates for physical and social pain., (Copyright © 2018 Elsevier B.V. All rights reserved.)

Background: Individuals who exhibit large-magnitude blood pressure (BP) reactions to acute psychological stressors are at risk for hypertension and premature death by cardiovascular disease. This study tested whether a multivariate pattern of stressor-evoked brain activity could reliably predict individual differences in BP reactivity, providing novel evidence for a candidate neurophysiological source of stress-related cardiovascular risk., Methods and Results: Community-dwelling adults (N=310; 30-51 years; 153 women) underwent functional magnetic resonance imaging with concurrent BP monitoring while completing a standardized battery of stressor tasks. Across individuals, the battery evoked an increase systolic and diastolic BP relative to a nonstressor baseline period (M ∆systolic BP/∆diastolic BP=4.3/1.9 mm Hg [95% confidence interval=3.7-5.0/1.4-2.3 mm Hg]). Using cross-validation and machine learning approaches, including dimensionality reduction and linear shrinkage models, a multivariate pattern of stressor-evoked functional magnetic resonance imaging activity was identified in a training subsample (N=206). This multivariate pattern reliably predicted both systolic BP ( r =0.32; P <0.005) and diastolic BP ( r =0.25; P <0.01) reactivity in an independent subsample used for testing and replication (N=104). Brain areas encompassed by the pattern that were strongly predictive included those implicated in psychological stressor processing and cardiovascular responding through autonomic pathways, including the medial prefrontal cortex, anterior cingulate cortex, and insula., Conclusions: A novel multivariate pattern of stressor-evoked brain activity may comprise a phenotype that partly accounts for individual differences in BP reactivity, a stress-related cardiovascular risk factor., (© 2017 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley.)

Objective: Elevated blood pressure and the Apolipoprotein ε4 allele (APOE ε4) are independent risk factors for Alzheimer's disease. We sought to determine whether the combined presence of the APOE ε4 allele and elevated blood pressure is associated with lower cognitive performance in cognitively healthy middle-aged adults., Methods: A total of 975 participants aged 30-54 (mean age = 44.47) were genotyped for APOE. Cardiometabolic risk factors including blood pressure, lipids, and glucose were assessed and cognitive function was measured using the Trail Making Test and the Visual Reproduction and Logical Memory subtests from the Wechsler Memory Scale., Results: Multivariable regression analysis showed that the association between APOE ε4 and episodic memory performance varied as a function of systolic blood pressure (SBP), such that elevated SBP was predictive of poorer episodic memory performance only in APOE ε4 carriers (β = -.092; t = -2.614; p = .009). Notably, this association was apparent at prehypertensive levels (≥130 mmHg), even after adjusting for physical activity, depression, smoking, and other cardiometabolic risk factors., Conclusions: The joint presence of APOE ε4 and elevated SBP, even at prehypertensive levels, is associated with lower cognitive performance in healthy, middle-aged adults. Results of this study suggest that the combination of APOE ε4 and elevated SBP may synergistically compromise memory function well before the appearance of clinically significant impairments. Interventions targeting blood pressure control in APOE ε4 carriers during midlife should be studied as a possible means to reduce the risk of cognitive decline in genetically susceptible samples., ((c) 2015 APA, all rights reserved).)

We examined the reliability of measures of fMRI, subjective, and cardiovascular reactions to standardized versions of a Stroop color-word task and a multisource interference task. A sample of 14 men and 12 women (30-49 years old) completed the tasks on two occasions, separated by a median of 88 days. The reliability of fMRI BOLD signal changes in brain areas engaged by the tasks was moderate, and aggregating fMRI BOLD signal changes across the tasks improved test-retest reliability metrics. These metrics included voxel-wise intraclass correlation coefficients (ICCs) and overlap ratio statistics. Task-aggregated ratings of subjective arousal, valence, and control, as well as cardiovascular reactions evoked by the tasks showed ICCs of 0.57 to 0.87 (ps < .001), indicating moderate-to-strong reliability. These findings support using these tasks as a battery for fMRI studies of cardiovascular reactivity., (Copyright © 2012 Society for Psychophysiological Research.)

Exaggerated cardiovascular reactivity to stress is a risk factor for cardiovascular disease. Further, individual differences in stressor-evoked cardiovascular reactivity covary with the functionality of corticolimbic brain systems, particularly areas of the cingulate cortex. What remains unclear, however, is how individual differences in personality traits interact with cingulate functionality in the prediction of stressor-evoked cardiovascular reactivity. Accordingly, we tested the associations between (i) a particular personality trait, Agreeableness, which is associated with emotional reactions to conflict, (ii) resting state functional connectivity within the cingulate cortex, and (iii) stressor-evoked blood pressure (BP) reactivity. Participants (N=39, 19 men, aged 20-37 years) completed a resting functional connectivity MRI protocol, followed by two standardized stressor tasks that engaged conflict processing and evoked BP reactivity. Agreeableness covaried positively with BP reactivity across individuals. Moreover, connectivity analyses demonstrated that a more positive functional connectivity between the posterior cingulate (BA31) and the perigenual anterior cingulate (BA32) covaried positively with Agreeableness and with BP reactivity. Finally, statistical mediation analyses demonstrated that BA31-BA32 connectivity mediated the covariation between Agreeableness and BP reactivity. Functional connectivity within the cingulate appears to link Agreeableness and a risk factor for cardiovascular disease, stressor-evoked BP reactivity., (Published by Elsevier Inc.)

An individual's tendency to show exaggerated or otherwise dysregulated cardiovascular reactions to acute stressors has long been associated with increased risk for clinical and preclinical endpoints of coronary heart disease (CHD). However, the 'brain-body' pathways that link stressor-evoked cardiovascular reactions to CHD risk remain uncertain. This review summarizes emerging neuroimaging research indicating that individual differences in stressor-evoked blood pressure reactivity (a particular form of cardiovascular reactivity) are associated with activation patterns in corticolimbic brain areas that are jointly involved in processing stressors and regulating the cardiovascular system. As supported empirically by activation likelihood estimates derived from a meta-analysis, these corticolimbic areas include divisions of the cingulate cortex, insula, and amygdala--as well as networked cortical and subcortical areas involved in mobilizing hemodynamic and metabolic support for stress-related behavioral responding. Contextually, the research reviewed here illustrates how behavioral medicine and health neuroscience methods can be integrated to help characterize the 'brain-body' pathways that mechanistically link stressful experiences with CHD risk.

Individuals who express relatively large-magnitude or "exaggerated" blood pressure (BP) reactions to behavioral stressors are presumably at increased risk for cardiovascular disease. As shown by recent neuroimaging studies, individuals who express exaggerated stressor-evoked BP reactivity also express heightened neural activity in corticolimbic brain areas that centrally regulate the cardiovascular system. These studies, however, have exclusively examined BP reactivity and concomitant neural activity during stressor exposure. If exaggerated BP reactivity originates in part from a centrally regulated and dispositional cardiovascular response tendency, then heightened resting (prestressor) corticolimbic activity may predict the subsequent expression of exaggerated stressor-evoked BP reactivity. To test this hypothesis, perfusion MRI was used to quantify resting regional cerebral blood flow (an indirect metabolic measure of neural activity) in men (n=19) and women (n=20) aged 20 to 37 years who subsequently performed cognitive stressor tasks to evoke BP reactivity. Individuals who expressed larger task-induced rises in systolic and diastolic BP also expressed higher resting regional cerebral blood flow in 4 functionally related corticolimbic areas: the dorsal and perigenual anterior cingulate, medial prefrontal, and insular cortices. Specifically, resting regional cerebral blood flow in these areas accounted, respectively, for 40% and 31% of the variance in systolic (P=0.001) and diastolic (P=0.008) BP reactivity, after accounting for total resting cerebral blood flow, resting BP, task performance, and task-related ratings of unpleasantness, arousal, and perceived psychological control. Heightened resting corticolimbic activity may represent a neurobiological correlate of an individual's predisposition for exaggerated stressor-evoked BP reactivity and possibly related cardiovascular risk.

Individuals who exhibit exaggerated blood pressure reactions to psychological stressors are at risk for hypertension, ventricular hypertrophy, and premature atherosclerosis; however, the neural systems mediating exaggerated blood pressure reactivity and associated cardiovascular risk in humans remain poorly defined. Animal models indicate that the amygdala orchestrates stressor-evoked blood pressure reactions via reciprocal signaling with corticolimbic and brainstem cardiovascular-regulatory circuits. Based on these models, we used a multimodal neuroimaging approach to determine whether human individual differences in stressor-evoked blood pressure reactivity vary with amygdala activation, gray matter volume, and functional connectivity with corticolimbic and brainstem areas implicated in stressor processing and cardiovascular regulation. We monitored mean arterial pressure (MAP) and concurrent functional magnetic resonance imaging BOLD signal changes in healthy young individuals while they completed a Stroop color-word stressor task, validated previously in epidemiological studies of cardiovascular risk. Individuals exhibiting greater stressor-evoked MAP reactivity showed (1) greater amygdala activation, (2) lower amygdala gray matter volume, and (3) stronger positive functional connectivity between the amygdala and perigenual anterior cingulate cortex and brainstem pons. Individual differences in amygdala activation, gray matter volume, and functional connectivity with corticolimbic and brainstem circuits may partly underpin cardiovascular disease risk by impacting stressor-evoked blood pressure reactivity.

Individuals who show exaggerated blood pressure reactions to psychological stressors are at increased risk for hypertension, atherosclerosis, and stroke. We tested whether individuals who show exaggerated stressor-induced blood pressure reactivity also show heightened stressor-induced neural activation in brain areas involved in controlling the cardiovascular system. In a functional MRI study, 46 postmenopausal women (mean age: 68.04; SD: 1.35 years) performed a standardized Stroop color-word interference task that served as a stressor to increase blood pressure. Across individuals, a larger task-induced rise in blood pressure covaried with heightened and correlated patterns of activation in brain areas implicated previously in stress-related cardiovascular control: the perigenual and posterior cingulate cortex, bilateral prefrontal cortex, anterior insula, and cerebellum. Entered as a set in hierarchical regression analyses, activation values in these brain areas uniquely predicted the magnitude of task-induced changes in systolic (DeltaR(2)=0.54; P<0.001) and diastolic (DeltaR(2)=0.27; P<0.05) blood pressure after statistical control for task accuracy and subjective reports of task stress. Heightened stressor-induced activation of cingulate, prefrontal, insular, and cerebellar brain areas may represent a functional neural phenotype that characterizes individuals who are prone to show exaggerated cardiovascular reactivity.

The anterior cingulate cortex presumptively regulates blood pressure reactions to behavioral stressors. There is little evidence in humans, however, that stressor-evoked changes in blood pressure correlate with concurrent changes in anterior cingulate activity. Using fMRI, we tested whether changes in mean arterial blood pressure correlate with ongoing changes in blood oxygen level dependent (BOLD) activation in 9 women and 11 men who completed a stressful Stroop color-word interference task. Higher mean arterial pressure during the Stroop task correlated with greater BOLD activation in two regions of the cingulate cortex (perigenual and mid-anterior) and in other networked brain regions, including the insula, thalamus, and periaqueductal gray. These results support the hypothesis that the anterior cingulate cortex regulates blood pressure reactions to behavioral stressors in humans.

The aim of this study was to evaluate the association between resting baroreflex sensitivity (BRS) and carotid intima-media thickness (IMT), a putative marker of subclinical atherosclerosis. Participants were 64 men and 18 women (median age, 57 years; range, 40 to 70 years), who did not have a previous history of coronary artery disease or treatment for hypertension. Resting BRS was measured during a 9-min baseline period using the noninvasive sequence technique; carotid IMT was subsequently determined using ultrasonography. Hierarchical multiple regression analyses showed that greater IMT in the carotid bulb (an area with a high density of baroreceptors) was associated with reduced BRS. These findings remained after adjusting BRS for resting mean arterial pressure, age, body mass index, gender, and smoking history, R2 = 0.06, P = .03. In contrast, IMT in the common and internal carotid regions (areas with presumably lower baroreceptor densities) did not account for a significant proportion of the variance in BRS. These results suggest that subclinical atherosclerosis, specifically in a region with high baroreceptor density, is associated with a reduced sensitivity of the baroreflex.

A reliable finding from the physical pain literature is that individuals with higher resting (i.e., tonic) blood pressure experience relatively less pain in response to nociceptive stimuli. Converging lines of evidence suggest that biological factors that influence the experience of physical pain may also relate to social pain. An open question, however, is whether higher blood pressure per se is a biological factor associated with lower sensitivity to social pain. This possible association was tested in three studies. Consistent with prior findings on physical pain, higher resting blood pressure was associated with lower self-reported sensitivity to social pain across individuals (Study 1 r = -.303, Study 2 r = -.262, -.246), even after adjusting for confounding factors related to blood pressure (Study 3 r = -.222). Findings suggest a previously unknown biological correlate of sensitivity to social pain, providing further evidence for possible shared substrates for physical and social pain.

Threats to social connectedness in the form of social and societal rejection, and the permanent loss of social bonds, are inevitable and common sources of social pain. However, sensitivity to social pain, also known as algesia, differs across individuals and contexts. Such sensitivity has implications for health, well-being, and the maintenance of social connection over time. What biological factors predict differences in sensitivity to social pain? Based on long-standing translational perspectives and emerging findings, the current review highlights blood pressure as a novel predictor of sensitivity to social pain: Higher resting blood pressure appears to relate to lower sensitivity to social pain. Despite evidence for this association, possible psychobiological bases and moderating influences are not yet established. Moreover, although higher blood pressure may afford tolerance for life's many pains, the health-related implications and trade-offs of such an effect are unknown. [ABSTRACT FROM AUTHOR]

Background: Several personality traits increase the risk for atherosclerotic cardiovascular disease. Because many of these traits are correlated, their associations with disease risk could reflect shared variance, rather than unique contributions of each trait. We examined a higher‐order personality trait of Stability as related to preclinical atherosclerosis and tested whether any such relationship might be explained by correlated variation in cardiometabolic risk factors. Method: Among 798 community volunteers, lower‐order traits of Neuroticism, Agreeableness, and Conscientiousness were modeled as latent variables (from self‐ and informant ratings) and used to estimate the second‐order factor, Stability. Cardiometabolic risk was similarly modeled from indicators of glycemic control, blood pressure, adiposity, and lipids. Carotid artery atherosclerosis was measured as intima‐media thickness (IMT) by duplex ultrasonography. Result: A structural equation model incorporating direct and indirect effects showed lower Stability associated with greater IMT, and this relationship was accounted for by the indirect pathway via cardiometabolic risk. Secondary analyses showed that: (1) Neuroticism, Agreeableness, and Conscientiousness were unrelated to IMT independent of Stability; and (2) Stability predicted variation in IMT when estimated from informant‐, but not self‐rated, traits. Conclusion: Personality traits may associate with atherosclerotic burden through their shared, rather than unique, variance, as reflected in Stability. [ABSTRACT FROM AUTHOR]

In response to the COVID‐19 pandemic, prior studies have modified the Trier Social Stress Test to be conducted remotely. The current study aimed to extend these studies to test whether a remote Trier Social Stress Test (rTSST) can elicit (a) affective, (b) blood pressure, and (c) heart rate responses relative to a control condition and whether these responses were reliable when assessed 1 week later. Participants (N = 99, 19.7 ± 3.5 years, 55% female) were randomized to a control or stress condition. Participants received blood pressure monitors in person. Controls completed easier versions of the tasks with a single, friendly researcher. Stress participants performed more difficult versions of the task in front of two judges who participants believed were rating their performance. Blood pressure and heart rate were measured every 2 min throughout, while affect was assessed at baseline, after the final task, and following recovery. The rTSST was feasible to administer with minimal technical issues reported. Participants reported lower positive affect and higher negative affect during the tasks in the stress condition relative to controls. Similarly, stress participants had higher cardiovascular responses during the tasks relative to controls, except that blood pressure was not elevated during mental arithmetic in stress participants relative to controls. Cardiovascular responses demonstrated good test–retest reliability when assessed 1 week later, especially when computed using area under the curve methods. Overall, a rTSST can be used to elicit affective and cardiovascular reactivity and provides an opportunity to increase the accessibility of research participation among diverse populations. We demonstrate that the Trier Social Stress Test can evoke both affective and cardiovascular (heart rate and blood pressure) responses when delivered online and remotely. This protocol can be administered during the COVID‐19 pandemic and could be used to include underserved and other populations that may have less accessibility to participate in research protocols. [ABSTRACT FROM AUTHOR]

Social pain is a common experience that has potent implications for health. However, individuals differ in their sensitivity to social pain. Recent evidence suggests that sensitivity to social pain varies according to a biological factor that modulates sensitivity to physical pain: resting (tonic) blood pressure. The current studies extended this evidence by testing whether blood pressure relates to sensitivity to imagined (Study 1: N = 762, 51% female adults) and acute (Study 2, preregistered: N = 204, 57% female adults) experiences of social pain and whether associations extend to general emotional responding (Studies 1–3; Study 3: N = 162, 59% female adults). In line with prior evidence, results showed that higher resting blood pressure was associated with lower sensitivity to social pain. Moreover, associations regarding blood pressure and sensitivity to social pain did not appear to be explained by individual differences in general emotional responding. Findings appear to be compatible with the interpretation that social and physical pain share similar cardiovascular correlates and may be modulated by convergent interoceptive pathways. [ABSTRACT FROM AUTHOR]

Pulse wave velocity (PWV) is a common measure of arterial stiffness. Non‐invasive methods to measure PWV are widely used in biomedical studies of aging and cardiovascular disease, but they are rarely used in psychophysiology. Barriers to wider use include the prohibitive costs of specialized equipment and need for trained technicians (e.g., ultrasonographers). Here, we describe an impedance cardiography method to measure PWV. By this method, impedance signals are dually collected from the thorax and calf. Combined with ensemble averaging of vascular signals, this dual impedance cardiography (d‐ICG) method allows for the measurement of aortic flow onset and the arrival time of peripheral pulse waveforms to compute PWV. In a community sample of adults (aged 19–78 years), PWV measured with d‐ICG exhibited a strong positive correlation with age. Moreover, age‐specific mean PWV values were within the normative reference intervals established by large scale studies using other techniques. PWV derived from d‐ICG exhibited high test‐retest reliability across several days, as well as excellent inter‐rater reliability. Last, PWV exhibited expected associations with known cardiovascular disease risk factors and indicators of autonomic cardiovascular control. d‐ICG is an inexpensive and reliable method to assess arterial stiffness. Impact Statement: We describe a relatively low‐cost and reliable methodology based on impedance cardiography to assess arterial pulse wave velocity. Pulse wave velocity is an important index of arterial stiffness that is strongly related to increased age and other risk factors for cardiovascular disease, as well as aspects of cerebrovascular health and cognitive function. This methodology lends itself to broader use in psychophysiology, behavioral medicine, and allied fields of study. [ABSTRACT FROM AUTHOR]

BACKGROUND Adiposity and elevated blood pressure (BP) are associated with brain structure abnormalities, but whether these effects are independent is unknown. We tested whether associations between adiposity and white matter integrity were explained by elevated BP. METHODS A sample of 209 middle-aged adults underwent diffusion tensor imaging to quantify indirect metrics of white matter structural integrity. These included putative markers of global white matter integrity (fractional anisotropy (FA)), axonal integrity (axial diffusivity), and myelin integrity (radial diffusivity). Participants were either normotensive or prehypertensive. RESULTS After adjusting for age and sex, regression analyses showed that waist circumference was associated with FA (β = -0.15, P < 0.05) and axial diffusivity (β = -0.24, P < 0.001), and mean arterial pressure (MAP) was associated with FA (β = -0.21, P < 0.05). Direct and indirect effect analyses showed that waist circumference was indirectly associated with whole brain FA through MAP (β = -0.06), and directly related to whole brain axial diffusivity, independent of MAP (β = -0.24). Examination of specific white matter tracts yielded similar results; waist circumference was indirectly related to FA through MAP and radial diffusivity, and directly related to axial diffusivity, independent of MAP. Supplemental analyses using body mass index, systolic BP, and diastolic BP also yielded similar results. CONCLUSION These findings suggest at least 2 mechanisms explain the adiposity and white matter association: one pathway through elevated BP impacting global white matter integrity and reducing integrity of the myelin sheath, and at least one other adiposity-specific pathway decreasing axonal integrity. [ABSTRACT FROM AUTHOR]

The polyvagal theory states that social behavior is linked to cardiac vagal control. This theory has been tested widely in infants and children, but less so in adults. Thus, we examined if resting or stress-related changes in high-frequency heart rate variability (HF-HRV; a presumed index of vagal control) varied with social functioning in 50 healthy women (mean age 68 years). After completing assessments of social functioning, women were exposed to laboratory stressors with concurrent psychophysiological monitoring. Although stressor-induced suppression of HF-HRV was common, women with less stressor-induced suppression of HF-HRV reported more positive social functioning. Resting HF-HRV was not related to social functioning. These findings are at apparent odds with the polyvagal theory; however, they complement prior work suggesting that emotional self-regulation could plausibly modulate cardiac vagal control in association with social functioning. [ABSTRACT FROM AUTHOR]

Background: Converging animal findings suggest that higher peripheral levels of inflammation are associated with activation of central inflammatory mechanisms that result in hippocampal neurodegeneration and related impairment of memory function. We have recently shown, consistent with animal findings, an inverse association between peripheral levels of interleukin-6 (IL-6), a relatively stable marker of systemic inflammation, and memory function in mid-life adults. In the current study, we extend this work to test whether systemic inflammation is associated with reduced grey matter volume of the hippocampus. Methods: For this purpose, we used a computational structural neuroimaging method (optimized voxel-based morphometry) to evaluate the relationship between plasma IL-6 levels and hippocampal grey matter volume in a sample of 76 relatively healthy community volunteers ages 30–54. Results: Peripheral levels of IL-6 covaried inversely with hippocampal grey matter volume, and this relationship persisted after accounting for several possible confounders, including age, gender, race, years of education, percent body fat, blood pressure, smoking, physical activity, hours of sleep, alcohol use, and total grey matter volume. Conclusions: To our knowledge, this is the first report of a relationship between a peripheral marker of IL-6 and hippocampal grey matter volume, raising the possibility that low-grade systemic inflammation could plausibly presage subclinical cognitive decline in part via structural neural pathways. [Copyright &y& Elsevier]

Abstract: Hypertension is a risk factor for diffuse brain atrophy. Yet, there is little evidence that higher blood pressure predicts focal brain atrophy, as indicated by a lower volume of regional brain tissue. This voxel-based morphometry study tested (a) whether higher blood pressure predicts lower regional grey or white matter volume and (b) whether a blood-pressure-related reduction in regional brain tissue volume predicts poorer neuropsychological test performance. Participants were 76 men (M age = 61.33, SD = 4.95 years) and 58 women (M age = 59.86, SD = 5.10 years) without a cardiovascular, cerebrovascular, or neuropsychiatric disease. Results showed that among men, higher resting systolic blood pressure predicted lower grey matter volume in the supplementary motor area and adjacent superior frontal gyrus, the anterior cingulate cortex, and middle temporal gyrus. Among men, lower grey matter volume in the supplementary motor area also predicted a slower time to complete the Trail Making Part B Test of executive control and a poorer recall of items from the Four-word Short-term Memory Test of working memory. These relationships were independent of age, total brain tissue volume, educational history, severity of carotid atherosclerosis, and the extent of periventricular and subcortical white matter lesions. Among women, no statistically significant relationships were found between blood pressure, regional brain tissue volume, and cognitive function. These findings suggest a functional relationship among men between higher blood pressure, lower regional grey matter volume, and poorer cognitive function that is independent of other risk factors and confounding medical conditions. [Copyright &y& Elsevier]