Parasympathetic and sympathetic nervous systems interactively predict change in cognitive functioning in midlife adults.
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ABSTRACT:
SUBMITTER: Knight EL
PROVIDER: S-EPMC7722158 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:OBJECTIVE:A study was undertaken to examine the association between overall cardiovascular health as recently defined by the American Heart Association in young adulthood to middle age and cognitive function in midlife. Overall ideal cardiovascular health incorporates 7 metrics, including the avoidance of overweight or obesity, a healthful diet, nonsmoking, and physical activity, total cholesterol, blood pressure, and fasting glucose at goal levels. METHODS:This analysis of the Coronary Artery Risk Development in Young Adults study, a multicenter community-based study with 25 years of follow-up, included 2,932 participants aged 18 to 30 years at baseline (year 0) who attended follow-up examinations at years 7 and 25. Cardiovascular health metrics were measured at each examination. The Digit Symbol Substitution Test (DSST), modified Stroop test, and Rey Auditory Verbal Learning Test (RAVLT) were completed at year 25. RESULTS:A greater number of ideal cardiovascular metrics in young adulthood and middle age were independently associated with better cognitive function in midlife (p for trend < 0.01, for all). Specifically, each additional ideal metric was associated with 1.32 more symbols on the DSST (95% confidence interval [CI] = 0.93 - 1.71), a 0.77-point lower interference score on the Stroop test (95% CI=-1.03 to -0.45), and 0.12 more words on the RAVLT (95% CI = 0.04 to 0.20). Participants who had ?5 ideal metrics at a greater number of the 3 examinations over the 25-year period exhibited better performance on each cognitive test in middle age (p for trend < 0.01, for all). INTERPRETATION:Ideal cardiovascular health in young adulthood and its maintenance to middle age is associated with better psychomotor speed, executive function, and verbal memory in midlife.
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Project description:Coping Power is an evidence-based preventive intervention for youth with aggressive behavior problems that has traditionally been delivered in small group formats, but because of concerns about potentially diminished effects secondary to aggregation of high-risk youth, an individual format of Coping Power has been developed. The current study examined whether physiological characteristics of the child may provide information about which intervention delivery format works best for that individual. Indicators of sympathetic and parasympathetic nervous system functioning were examined in 360 fourth-grade children (65% male; 76.4% self-reported African-American) who were randomly assigned to Group Coping Power (GCP) or Individual Coping Power (ICP) (Lochman et al. 2015). Longitudinal assessments of teacher- and parent-reported proactive and reactive aggression were collected through a 1-year follow-up. For children with higher initial levels of aggression, those with lower parasympathetic functioning at pre-intervention showed greater reductions in teacher-rated proactive aggression in the ICP condition than the GCP condition. For children with high parasympathetic functioning, there was no differential effect of intervention format. Regardless of intervention format, youth with lower levels of sympathetic functioning at pre-intervention demonstrated greater reductions in teacher-rated proactive aggression. These findings suggest that physiological indicators may be worth considering in future studies examining which youth respond best to specific types of interventions.
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Project description:Exposure to prenatal adversity is associated with aggression later in life. Individual differences in autonomic nervous system (ANS) functioning, specifically nonreciprocal activation of the parasympathetic (PNS) and sympathetic (SNS) nervous systems, increase susceptibility to aggression, especially in the context of adversity. Previous work examining interactions between early adversity and ANS functioning in infancy is scarce and has not examined interaction between PNS and SNS. This study examined whether the PNS and SNS moderate the relation between cumulative prenatal risk and early physical aggression in 124 children (57% male). Cumulative risk (e.g., maternal psychiatric disorder, substance (ab)use, and social adversity) was assessed during pregnancy. Parasympathetic respiratory sinus arrhythmia (RSA) and sympathetic pre-ejection period (PEP) at baseline, in response to and during recovery from emotional challenge were measured at 6 months. Physical aggression and non-physical aggression/oppositional behavior were measured at 30 months. The results showed that cumulative prenatal risk predicted elevated physical aggression and non-physical aggression/oppositional behavior in toddlerhood; however, the effects on physical aggression were moderated by PNS and SNS functioning. Specifically, the effects of cumulative risk on physical aggression were particularly evident in children characterized by low baseline PNS activity and/or by nonreciprocal activity of the PNS and SNS, characterized by decreased activity (i.e., coinhibition) or increased activity (i.e., coactivation) of both systems at baseline and/or in response to emotional challenge. These findings extend our understanding of the interaction between perinatal risk and infant ANS functioning on developmental outcome.
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Project description:Melanocortin 4 receptors (MC4Rs) in the central nervous system are key regulators of energy and glucose homeostasis. Notably, obese patients with MC4R mutations are hyperinsulinemic and resistant to obesity-induced hypertension. Although these effects are probably dependent upon the activity of the autonomic nervous system, the cellular effects of MC4Rs on parasympathetic and sympathetic neurons remain undefined. Here, we show that MC4R agonists inhibit parasympathetic preganglionic neurons in the brainstem. In contrast, MC4R agonists activate sympathetic preganglionic neurons in the spinal cord. Deletion of MC4Rs in cholinergic neurons resulted in elevated levels of insulin. Furthermore, re-expression of MC4Rs specifically in cholinergic neurons (including sympathetic preganglionic neurons) restores obesity-associated hypertension in MC4R null mice. These findings provide a cellular correlate of the autonomic side effects associated with MC4R agonists and demonstrate a role for MC4Rs expressed in cholinergic neurons in the regulation of insulin levels and in the development of obesity-induced hypertension.
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Project description:Variants in transcription factor 7-like 2 (266096218TCF7L2266096218USuser266096218Gene names have been italicized per house style. Please check and confirm whether there are other instances that need to be italicized or instances where italics have been inappropriately applied.) gene have been found strongly associated with an increased risk of type 2 diabetes, as well as with an impairment of glucagon-like peptide-1 (GLP-1) signalling chain. In rats, stimulation of central GLP-1 receptors increases heart rate and activates autonomic regulatory neurons. We aimed to evaluate the potential role of TCF7L2 gene polymorphisms on sympathovagal response in relation to changes in plasma insulin and/or GLP-1 concentration after glucose ingestion. Genotyping was performed for rs12255372 and rs7903146 TCF7L2 gene variants in 250 non-related healthy volunteers (mean age 27±3 years). Consistent with previous reports, both single-nucleotide polymorphisms were in strong linkage disequilibrium (D'=0.87, r(2)=0.76). A subset of 167 patients underwent an oral glucose tolerance test while a continuous recording of heart rate variability was performed. At baseline, no differences in fasting plasma insulin, in GLP-1 levels and in LF/HF (low frequency/high frequency) ratio between the three genotypes were found. Along with glucose ingestion TT subjects had lower INS(AUC) (insulin area under curve), as well as higher LF/HF(AUC) (LF/HF area under curve) values. No difference in GLP-1(AUC) (GLP-1 area under curve) between TCF7L2 gene variants was found. A multivariate analysis including multiple covariates showed that only INS(AUC,) GLP-1(AUC) and TCF7L2 gene variants were independently associated with LF/HF(AUC). In conclusion, TT genotype of rs12255372 and rs7903146 TCF7L2 gene variants is associated with lower insulin secretion and higher cardiosympathetic activity. Moreover, such effect is independent of GLP-1 and insulin plasma concentrations suggesting a potential role of such gene variants in increasing cardiovascular risk through enhanced sympathetic nervous system activity.
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Project description:Type 2 diabetes is associated with dementia risk, but evidence is limited for possible associations of diabetes and prediabetes with cognitive decline.To determine whether diabetes in midlife is associated with 20-year cognitive decline and to characterize long-term cognitive decline across clinical categories of hemoglobin A1c (HbA1c) levels.Prospective cohort study.The community-based ARIC (Atherosclerosis Risk in Communities) study.13,351 black and white adults aged 48 to 67 years at baseline (1990 to 1992).Diabetes was defined by self-reported physician diagnosis or medication use or HbA1c level of 6.5% or greater. Undiagnosed diabetes, prediabetes, and glucose control in persons with diagnosed diabetes were defined by clinical categories of HbA1c level. Delayed word recall, digit symbol substitution, and word fluency tests were used to assess cognitive performance and were summarized with a global Z score.Diabetes in midlife was associated with a 19% greater cognitive decline over 20 years (adjusted global Z-score difference, -0.15 [;95% CI, -0.22 to -0.08];) compared with no diabetes. Cognitive decline was significantly greater among persons with prediabetes (HbA1c level of 5.7% to 6.4%) than among those with an HbA1c level less than 5.7%. Participants with poorly controlled diabetes (HbA1c level ? 7.0%) had greater decline than those whose diabetes was controlled (adjusted global Z-score difference, -0.16; P = 0.071). Longer-duration diabetes was also associated with greater late-life cognitive decline (P for trend < 0.001). Rates of decline did not differ significantly between white and black persons (P for interaction = 0.44).Single HbA1c measurement at baseline, 1 test per cognitive domain, and potential geographic confounding of race comparisons.Diabetes prevention and glucose control in midlife may protect against late-life cognitive decline.National Institutes of Health.
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Project description:IntroductionExisting studies predominantly consider the association of late-life lipid levels and subsequent cognitive change. However, midlife rather than late-life risk factors are often most relevant to cognitive health.MethodsWe quantified the association between measured serum lipids in midlife and subsequent 20-year change in performance on three cognitive tests in 13,997 participants of the Atherosclerosis Risk in Communities study.ResultsElevated total cholesterol, low-density lipoprotein cholesterol, and triglycerides were associated with greater 20-year decline on a test of executive function, sustained attention, and processing speed. Higher total cholesterol and triglycerides were also associated with greater 20-year decline in memory scores and a measure summarizing performance on all three tests. High-density lipoprotein cholesterol was not associated with cognitive change. Results were materially unchanged in sensitivity analyses addressing informative missingness.DiscussionElevated total cholesterol, low-density lipoprotein cholesterol, and triglycerides in midlife were associated with greater 20-year cognitive decline.
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Project description:Previous studies examined midlife risk factors separately for old-age impaired physical and cognitive functioning. We determined the overlap of risk factors for both domains of functioning within the same setting.Biological and behavioral risk factors at age 50 years and cognitive and physical functioning were assessed 18 (SD = 5) years later in the Whitehall II study (N = 6,316). Impaired physical functioning was defined as ?1 limitation on the activities of daily living scale. Impaired cognitive functioning was defined as Mini-Mental State Examination score <27. Two statistical analyses were employed: minimally adjusted analysis (for age, sex, and ethnicity) and mutually adjusted analysis (including all risk factors). Missing data on risk factors were imputed.After confounder adjustment, impaired physical and cognitive functioning at older ages were predicted by hypertension (odds ratios [ORs] 1.80 95% confidence interval [CI] 1.39-2.33 and 1.57 95% CI 1.07-2.31, respectively), poor lung function (1.51 95% CI 1.28-1.78 and 1.31 95% CI 1.08-1.59), and physical inactivity, marginally in the case of cognitive function (1.50 95% CI 1.19-1.90 and 1.27 95% CI 0.99-1.62) at age 50 years. Impaired physical functioning but not cognitive functioning was additionally predicted by depression and higher body mass index (1.72 95% CI 1.46-2.03 and 1.29 95% CI 1.16-1.44, respectively).Several midlife risk factors are associated with impaired physical and cognitive functioning in old age, supporting a unified prevention policy. Analysis of 12 risk factors at age 50 suggests that strategies targeting physical inactivity, hypertension, and poor lung function will reduce impairments in both cognitive and physical functioning in old age.
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Project description:OBJECTIVE:Evidence that the metabolic syndrome is a risk factor for poor cognition is mixed and is focused mainly on the elderly population; rarely is an adjustment made for socioeconomic factors. We examined this association in late midlife, with particular focus on cumulative effects and the role of socioeconomic circumstances. RESEARCH DESIGN AND METHODS:Analyses were performed for 4,150 white participants from the Whitehall II study. Metabolic syndrome, using the National Cholesterol Education Program Adult Treatment Panel III criteria, was assessed three times over the 10-year follow-up (1991-2001). Cognitive function was assessed using a battery of six tests at the end of the follow-up. RESULTS:After adjustment for demographic variables, health behaviors, and health status, participants with persistent metabolic syndrome (at least two of the three screenings) over the 10-year follow-up had lower cognitive performance than participants who never had metabolic syndrome. No significant differences in cognitive function were observed between participants with nonpersistent metabolic syndrome (one of the three screenings) and those who never had metabolic syndrome during the follow-up. Adjustment for adult occupational position attenuated this association by between 41 and 86%, depending on the measure of cognitive function. Adjustment for education had little effect. CONCLUSIONS:Only persistent metabolic syndrome was associated with lower cognitive performance in late midlife. Adult occupational position but not education had a substantial impact on this association; these results highlight the importance of adult socioeconomic circumstances in identifying and targeting risk factors for cognitive aging.
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