The journals of gerontology. Series A, Biological sciences and medical sciences最新文献

Background: Walking automaticity facilitates maintenance of gait speed without prefrontal cortex (PFC) resources. Brain aging may cause shifts to attentional gait with greater engagement of the PFC. Nigrostriatal dopaminergic integrity likely facilitates walking automaticity and gait speed during attentional dual-tasks.

Methods: Older adults (n = 201; age = 74.9; 63.2% women, gait speed = 1.10 m/s) completed a dual-task protocol of saying every other letter of the alphabet while walking. PFC activation was measured by functional near-infrared spectroscopy. Four groups were defined based on PFC activation (increased during dual-task, PFC+, or not, PFC-) and gait speed performance (maintained during dual-task, gait+, or slowed, gait-). To compare nigrostriatal dopaminergic integrity across groups, we assessed binding of the type-2 vesicular monoamine transporter density in the sensorimotor and associative striatum using [11C]-(+)-a-dihydrotetrabenazine (DTBZ) positron emission tomography. Multinomial regression estimated adjusted associations of DTBZ binding with group membership. We hypothesized that DTBZ binding was highest for those who maintained gait speed without additional PFC activation when switching from single- to dual-task (PFC-/gait+; ie, highest gait automaticity).

Results: In bivariate analyses, the PFC-/gait+ group had the highest DTBZ binding in the sensorimotor striatum (P = .05); binding in the associative striatum was similar across groups (P = .1). Results were similar in adjusted regression analyses; DTBZ binding in sensorimotor striatum was associated with lower likelihood to be in the PFC-/gait- (odds ratio [OR] = 0.28; 95% CI, 0.08-0.94) or the PFC+/gait+ (OR = 0.29; 95% CI, 0.10-0.84) groups compared to PFC-/gait+ reference group.

Conclusion: These results provide support for dopaminergic involvement in sustaining gait automaticity at older ages.

Background: Research on cognition and pain is limited in Low and Middle-income Countries (LMICs) and understanding how chronic conditions and pain treatment may moderate this association is underexplored. This study aimed to explore the relationship between pain and cognition and the moderating effect of hypertension, diabetes, HIV, pain treatment, and depressive symptoms.

Methods: We analyzed data from 3803 individuals enrolled in the HAALSI study, a longitudinal population study of older adults in Agincourt, South Africa. Pain was measured with the Brief Pain Inventory. Cognition was assessed using a composite of orientation questions, a memory test, and the Trails Making Test B. Chronic conditions were assessed using biological measures, and depressive symptoms were measured using the CES-D scale. Linear regression models were used to investigate the relationship.

Results: Baseline and longitudinal pain were significantly associated with poorer episodic memory (ß = -0.17 [P < .001]; ß = -0.18 [P < .001]). Hypertension amplified the negative effect of pain on episodic memory, while diabetes and HIV did not moderate the relationship between pain and cognition (ß = -0.10 [.006]). Pain treatment was associated with poorer cognitive performance. Depressive symptoms moderated the relationship between pain and both cognition and executive function (EF) (P = .02). The negative effect of pain on episodic memory was observed in individuals with both acute and persisting pain, while it only affected EF in those with acute pain.

Conclusions: These findings highlight the importance of examining factors that may moderate the relationship between pain and cognition and strategies to mitigate the effect pain has on cognition, particularly in LMICs.

Psoriasis burdens children and adults, but the impact of air pollution and aging is unclear. This study examines the association between air pollution exposure and psoriasis risk, considering the mediating role of biological aging. A prospective cohort study of 284 544 adults (51.3% female, mean age 56.26 ± 8.10 years) from the UK Biobank examined long-term exposure to air pollutants (PM2.5, PM10, PM2.5-10, NO2, and NOX). Biological aging was assessed using phenotypic age algorithms. Cox proportional hazards models were constructed to analyze the relationships with the risk of psoriasis, adjusting for demographic, socioeconomic, and health-related factors. Mediation analysis explored the role of biological aging. During a median follow-up of 15.58 years, 3,446 (1.21%) participants developed psoriasis. After adjusting for all confounders, each ten-unit increase (10 μg/m³) in PM2.5, PM10, NO2, and NOx, corresponded to the significantly increased risk of psoriasis by 95.7% (HR = 1.957, 95% CI 1.435-2.671), 19.7% (HR = 1.197, 95% CI 1.006-1.426), 9.0% (HR = 1.090, 95% CI 1.043-1.138) and 4.4% (HR = 1.044, 95% CI 1.024-1.066), respectively. Moreover, all air pollutants are significantly associated with biologically aging, while each one-year increase in PhenoAge was associated with a 5.0% higher risk of psoriasis (HR = 1.050, 95% CI 1.045-1.056). Finally, accelerated biological aging partially mediated 5.96%-13.86% of these air pollutants. Long-term exposure to air pollution significantly affects psoriasis risk, with biological aging as a partial mediator. Reducing pollution may lower the risk of psoriasis by slowing biological aging.

This perspective examines the impact of Social Determinants of Health (SDoH) on the biological age-related decline and Alzheimer's Disease and Related Dementias (ADRD) biomarker trajectories in U.S. Latino populations, emphasizing the need for comprehensive multilevel research frameworks tailored to the community. We discuss the prevailing SDoH among U.S. Latino communities, including economic, educational, and healthcare access inequities that heighten health risks. Subsequently, we examine the pronounced differences in ADRD prevalence and biomarker trajectories among Latinos, suggesting that the interplay between SDoH and biological markers contributes to ADRD risk and progression. Our perspective reflects on the existing research landscape, noting a substantial gap in studies extending beyond identifying and understanding disparities in ADRD, to research incorporating biomarkers and developing actionable interventions to address broader SDoH. This shift is essential for creating a more holistic approach to ADRD research and devising truly effective strategies to mitigate ADRD disparities and improve brain health for older U.S. Latinos.

Background: Community-based palliative care (CBPC) can improve symptom management and quality of life at reduced costs (through hospitalization prevention) for seriously ill older adults. However, CBPC services are underutilized due to multi-level factors including patient perceptions and lack of systematic methods for providers to identify and communicate the potential value of these services.

Methods: The purpose of this study is to describe the co-design of Right for You? (R4U?) intervention materials and to present pilot test results of feasibility and preliminary effectiveness testing. R4U? was designed to improve how a CBPC program (offered as part of a Medicare Advantage health plan) is presented to seriously ill older adults and their caregivers.

Results: Our findings suggest the co-designed R4U? was acceptable to clinicians and when pilot-tested demonstrated preliminary effectiveness with a seven percentage-point increase in enrollment in the CBPC program during the intervention period (May-September 2024).

Conclusions: Our preliminary findings support the acceptability and feasibility of using tailored R4U? as a way of increasing interest and enrollment in a CBPC program. Additional research is needed to determine if observed increases in CBPC enrollment are sustainable over time and scalable in other settings to improve enrollment in CBPC.

Background: Limited population-based data exist on the association between medication use and changes in phenotypic aging. This study investigated these associations using data from the Baltimore Longitudinal Study of Aging.

Methods: Phenotypic aging (PA) markers were constructed using the Klemera-Doubal method across four domains: body composition (structural and metabolic changes), energetics (energy generation and utilization capacity), homeostatic mechanisms (internal stability maintenance), and neuroplasticity/neurodegeneration (nervous system function and decline). Associations between 27 common drug categories and changes in these PA markers were analyzed using conditional generalized estimating equations (cGEE), focusing on within-individual variation to control for genetics and early-life factors, with additional adjustments for time-varying covariates.

Results: Five drug categories were associated with significant reductions in PA markers. Vitamin D, bisphosphonates, and proton pump inhibitors were linked to decreases in body composition (Beta = -0.73 years, 95% CI: -1.35 to -0.10), energetics (Beta = -2.05, 95% CI: -3.98 to -0.13), and neuroplasticity/neurodegeneration (Beta = -1.00, 95% CI: -2.02 to -0.03), respectively. Thyroid hormones showed reductions in body composition (Beta = -1.75, 95% CI: -3.24 to -0.26) and neuroplasticity/neurodegeneration (Beta = -1.04, 95% CI: -1.96 to -0.12). Thiazides were associated with decreases across body composition (Beta = -1.55, 95% CI: -2.94 to -0.16), energetics (Beta = -2.36, 95% CI: -4.30 to -0.42), and homeostatic mechanisms (Beta = -3.83, 95% CI: -6.71 to -0.96).

Conclusions: These findings suggest potential protective effects of certain medications on phenotypic aging. Further research is needed to validate these results, particularly with data from other populations.

Background: To evaluate the associations of sleep health with carotid intima-media thickness (CIMT) and arterial stiffness.

Methods: A total of 41 465 UK Biobank participants were included. Sleep traits were assessed at baseline via self-reported questionnaires, and a composite sleep score was constructed based on six factors: sleep duration, snoring, insomnia, chronotype, daytime napping, and daytime sleepiness, with higher scores indicating poorer sleep health. CIMT and arterial stiffness were measured at follow-up. Multivariable logistic regression was used to estimate odds ratios (ORs) and 95% confidence intervals (CIs) for the association between sleep score and study outcomes, adjusting for baseline demographics, socioeconomic status, physical measurements, and medication use.

Results: The mean age of the study population was 55.08 years (SD = 7.57), with 52.91% females and 96.99% Whites. Compared with those for participants with a sleep score of 0, the multivariate-adjusted ORs (95% CI) for those with sleep scores of 1, 2, 3, 4, and 5-6 were 1.04 (0.93, 1.16), 1.09 (0.98, 1.21), 1.17 (1.05, 1.30), 1.15 (1.02, 1.29), and 1.18 (1.03, 1.35) for CIMT thickening, respectively, and 1.04 (0.92, 1.18), 1.13 (1.00, 1.27), 1.25 (1.08, 1.40), 1.23 (1.08, 1.40), and 1.31 (1.12, 1.53) for arterial stiffness, respectively. Poor sleep health was associated with an increased risk of CIMT thickening within all genetic risk categories, and no interaction between the sleep and genetic risk scores was found.

Conclusion: This study highlighted the importance of healthy sleep behaviors in slowing the progression of subclinical cardiovascular disease, regardless of individual's genetic risk status.

Prolonged exposure to air pollution and systemic inflammation has both been associated with deteriorating self-reported health (SRH), however, the underlying mechanisms remained poorly understood. This study included 8,292 middle-aged and older adults (≥45 years) from the China Health and Retirement Longitudinal Study (CHARLS). High spatial-temporal gridded air pollution datasets were utilized to estimate individual air pollution exposure at county level. Systemic inflammation was measured using C-reactive protein (CRP) and white blood cell (WBC) numbers from CHARLS blood samples. Generalized linear modeling (GLM) was employed to examine the relationships between air pollution exposure, systemic inflammation, and SRH. After adjusting for confounders, this study found that a 3-year average PM2.5 concentration was associated with a higher risk of poor SRH (OR = 1.005, 95% CI: 1.002-1.009). Elevated CRP and WBC levels were also linked to an increased risk of poor SRH (OR = 1.019, 95% CI: 1.011-1.027; OR = 1.035, 95% CI: 1.010-1.061, respectively). Interaction analysis revealed that elevated CRP levels exacerbated the adverse effect of chronic air pollution exposure on SRH. In addition, residential location and educational attainment influenced how systemic inflammation moderated the relationship between PM2.5 exposure and SRH. Long-term exposure to air pollution was associated with an increased likelihood of poor SRH among middle-aged and older adults, with inflammatory markers potentially amplifying this association. Therefore, it is essential to implement multidisciplinary strategies to reduce air pollution and alleviate systemic inflammation in this population.

Background: There has been growing interest in the interrelationship between age-related reductions in cognitive and motor function. To advance the understanding of this interrelationship, we sought to determine whether a mentally fatiguing task differentially effects hand grip motor function in older versus younger adults.

Methods: Young (n = 10, 33 ± 3 years) and older adults (n = 15, 69 ± 3 years) free of overt neurological disease and who did not report chronic fatigue symptoms participated in two testing sessions. During both sessions, participants had their composite grip strength (GS) and their multifinger force deficit (MFFD) measured. The MFFD assays the degree of neural inactivation observed during a composite GS test. During one session participants completed a series of psychomotor vigilance tasks (PVT) to induce mental fatigue. The other session served as a control condition.

Results: Older adults exhibited an ∼18% reduction in composite GS associated with mental effort, which was significantly greater than that observed in young adults. Indirect neural activation, assessed via the MFFD, was reduced by approximately 22% in older adults during mental effort, which was significantly greater than the reduction observed in young adults.

Conclusions: These findings indicate that mental exertion/fatigue results in decreased composite GS and increasing impairments in neural activation in older adults. No effect on indices of neuromuscular performance were observed in young adults. These findings suggest that neural mechanisms are heavily involved in the regulation of composite GS, and that the relative contribution of neural and muscular mechanisms of handgrip strength are state dependent in older adults.

Background: Cognitive impairment and sarcopenia each negatively impact functional recovery after hip fracture, yet their combined effects remain underexplored. This study investigated the influence of these conditions on 1-year independent walking recovery in older adults undergoing post-fracture rehabilitation.

Methods: This secondary analysis used data from the Fragility Fracture Integrated Rehabilitation Management clinical trial, a parallel-group, single-blind, multicenter superiority randomized controlled trial, and its preliminary feasibility study. A total of 114 patients aged ≥65 years from three tertiary hospitals in South Korea were included. Patients were classified into four groups based on the presence of cognitive impairment and/or sarcopenia. Walking ability was assessed over a 12-month period. Kaplan-Meier analysis and multivariate Cox regression were used to evaluate independent ambulation rates and associated factors.

Results: Patients with sarcopenia had lower independent ambulation rates than those without (71.9% vs. 84.4%; P = .025), as did those with cognitive impairment (65.2% vs. 89.1%; P = .010). The lowest rate was inpatients with both conditions (60.8%, P = .022) and the highest in those without either (90.2%). Post hoc pairwise comparisons confirmed significant differences (P = .011). Cox regression showed cognitive impairment reduced independent ambulation likelihood by 45.8% (HR: 0.542, 95% CI: 0.340-0.865, P = .010), while both conditions together lowered it by 57% (HR: 0.431, 95% CI: 0.233-0.798, P = .007).

Conclusions: Cognitive impairment, especially with sarcopenia, significantly hinders walking recovery after hip fracture. Targeted rehabilitation strategies are crucial to addressing their combined impact in older adults.