Individual socioeconomic status, neighborhood disadvantage, and cognitive aging: A longitudinal analysis of the CLSA DOI Creative Commons
John R. Best

Journal of the American Geriatrics Society, Journal Year: 2024, Volume and Issue: 72(11), P. 3335 - 3345

Published: Aug. 23, 2024

Abstract Background There are likely many contributors to variation in the rate of cognitive decline middle and late adulthood, including individual neighborhood socio‐economic factors. This study examines whether factors, namely income wealth, correlate with decline, part, through neighborhood‐level social material disadvantage. Methods Using three waves data collection from Canadian Longitudinal Study on Aging (CLSA), this included 51,338 participants between age 45 85 years at baseline (51% female). Individual status (SES) was assessed by annual household current value savings investments. Neighborhood disadvantage measured area‐based deprivation indices. Cognition each wave using verbal fluency, mental alternations, delayed word recall. Latent change score models, incorporating direct indirect pathways, were constructed estimate effect SES area‐level Multi‐group models basis age‐group (45–64 years; 65–74 or 75+ years) allow for varying estimates across age. Results Among 45–64‐year‐olds, wealth had effects initial level (standardized = 0.01, p < 0.001), but only an ( 0.019). 65‐74‐year‐olds, 0.01) not > 0.05), among year‐olds, no observed 0.05). Wealth effects, independent disadvantage, cognition all groups Conclusions middle‐aged adults, greater may mitigate allowing individuals live more materially socially advantaged neighborhoods.

Language: Английский

Ageing, Cognitive Decline, and Effects of Physical Exercise: Complexities, and Considerations from Animal Models DOI Open Access

Maria Giovanna Caruso,

Sarah Nicolas, Paul J. Lucassen

et al.

Brain Plasticity, Journal Year: 2024, Volume and Issue: 9(1-2), P. 43 - 73

Published: May 10, 2024

In our ageing global population, the cognitive decline associated with dementia and neurodegenerative diseases represents a major healthcare problem. To date, there are no effective treatments for age-related impairment, thus preventative strategies urgently required. Physical exercise is gaining traction as non-pharmacological approach to promote brain health. Adult hippocampal neurogenesis (AHN), unique form of plasticity which necessary certain functions declines age enhanced in response exercise. Accumulating evidence from research rodents suggests that physical has beneficial effects on cognition through its proneurogenic capabilities. Given ethical technical limitations human studies, preclinical crucial better understanding such exercise-induced behavioural changes. this review, paradigms used compared. We provide an overview different middle-age until older-age. discuss relationship between decrease AHN potential impact mitigating decline. highlight emerging literature gut microbiota during consider role gut-brain axis future possible strategy optimize exercise-enhanced function. Finally, we propose guideline designing optimal protocols rodent would inform clinical contribute developing

Language: Английский

Citations

8
Longitudinal autophagy profiling of the mammalian brain reveals sustained mitophagy throughout healthy aging DOI Creative Commons
Anna Rappe, Helena Vihinen, Fumi Suomi

et al.

The EMBO Journal, Journal Year: 2024, Volume and Issue: unknown

Published: Oct. 4, 2024

Abstract Mitophagy neutralizes mitochondrial damage, thereby preventing cellular dysfunction and apoptosis. Defects in mitophagy have been strongly implicated age-related neurodegenerative disorders such as Parkinson’s Alzheimer’s disease. While decreases throughout the lifespan of short-lived model organisms, it remains unknown whether a decline occurs aging mammalian brain—a question fundamental importance for understanding cell type- region-specific susceptibility to neurodegeneration. Here, we define longitudinal dynamics basal macroautophagy across neuronal non-neuronal types within intact mouse brain vivo. Quantitative profiling reporter cohorts from young geriatric ages reveals cell- tissue-specific alterations between distinct subregions populations, including dopaminergic neurons, cerebellar Purkinje cells, astrocytes, microglia interneurons. We also find that healthy is hallmarked by dynamic accumulation differentially acidified lysosomes several neural subsets. Our findings argue against any widespread mitophagic activity, instead demonstrating fluctuations trajectory, with strong implications ongoing theragnostic development.

Language: Английский

Citations

7
Cognitive impairments in chronic pain: a brain aging framework DOI Creative Commons
Lei Zhao, Libo Zhang,

Yilan Tang

et al.

Trends in Cognitive Sciences, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 1, 2025

Language: Английский

Citations

0
Effect of serum uric acid to creatinine ratio on cognitive function decline in middle-aged adults: Longitudinal evidence from CHARLS DOI Creative Commons
Xiangjun Zhou, Zhe Wang, Yi Zhun Zhu

et al.

Journal of Alzheimer s Disease, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 10, 2025

Background Serum uric acid (SUA) was a predictor of cognitive function. The association SUA/serum creatinine ratio (Scr), which represents renal function-normalized SUA and function is unknown. Objective This study investigated the SUA/Scr with potential mediation effect inflammation in above relationship. Methods used 1–5 waves data from China Health Retirement Longitudinal Study. 3302 participants aged 45–60 years at baseline were included. Among them, 1129 who attended subsequent 2–3 further included for cumulative exposure calculation to ratio. Cox models evaluate impact its on decline. Results During median follow-up 8.6 years, there 1512 (45.8%) declined. After adjustment, highest quartile SUA/SCr associated risk decline (Hazard ratio, 1.175; 95% confidence interval, 1.015–1.360). Restricted cubic spline showed linear between (p non−linear = 0.514). There stronger burden [the versus lowest quartile: 1.635 (1.006–2.656), high low group: 1.729 (1.212–2.466), respectively]. No significant mediating through white blood cell count or C-reactive protein ratio-cognitive found. Conclusions higher decline, whereas mechanism mediated by indicators not

Language: Английский

Citations

0
Aggregation of HAPLN2, a component of the perinodal extracellular matrix, is a hallmark of physiological brain aging in mice DOI Creative Commons

Ayaka Watanabe,

Shoshiro Hirayama,

Itsuki Kominato

et al.

bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 10, 2025

Abstract Protein aggregation is a hallmark of neurodegenerative diseases and also observed in the brains elderly individuals without such conditions, suggesting that aging drives accumulation protein aggregates. However, comprehensive understanding age-dependent aggregates involved brain remains unclear. Here, we investigated proteins become sarkosyl-insoluble with age identified hyaluronan proteoglycan link 2 (HAPLN2), hyaluronic acid-binding extracellular matrix at nodes Ranvier, as an aggregating mouse brains. Elevated acid levels impaired microglial function reduced clearance HAPLN2, leading to its accumulation. HAPLN2 oligomers induced inflammatory responses both vitro vivo . Furthermore, age-associated was human cerebellum. These findings suggest results from age-related decline homeostasis may exacerbate environment by activating microglia. This study provides new insights into mechanisms underlying cerebellar highlights role changes brain. Author Summary To identify unrelated disease, analyzed proteome young aged We discovered existing nodal matrix, accumulated age. Age-dependently formed large cannot be solubilized anionic detergent sarkosyl or hyaluronidase digestion. In addition, irregularly shaped puncta were mislocalized Ranvier white matter not only mice but Oligomers full-length specifically activation Our possible factor contributing inflammation.

Language: Английский

Citations

0
Public perceptions of brain health in young and middle-aged adults in Cuba: Opportunities for intervention DOI
Yunier Broche‐Pérez, Zoylen Fernández-Fleites, Diego D. Díaz‐Guerra

et al.

Neuroscience, Journal Year: 2025, Volume and Issue: unknown

Published: Jan. 1, 2025

Language: Английский

Citations

0
Age-Related Changes to Gabaergic Synapses Across the Central Inferior Colliculus DOI
Jeffrey G. Mellott,

Alexa Wawrzyniak,

Justine Busby

et al.

Published: Jan. 1, 2025

Language: Английский

Citations

0
Editorial: Midlife brain health: understanding brain aging in middle-age and effects of interventions to prevent neurodegeneration in late life DOI Creative Commons
Junyeon Won, Marissa A. Gogniat,

Takuya Kurazumi

et al.

Frontiers in Aging Neuroscience, Journal Year: 2025, Volume and Issue: 17

Published: Feb. 19, 2025

With the rapid increase in aging population, prevalence of age-related neurodegenerative diseases such as Alzheimer's disease (AD) has risen significantly, affecting over 55 million people worldwide 2023, with projections suggesting this number will exceed 78 by 2030 (Better, 2023). While much research been focused on understanding and treating AD older adults, there is growing emphasis early interventions to prevent its onset (Crous-Bou et al., 2017;Dohm-Hansen 2024). In regard, middle-age gained recognition a critical period for development prevention (Ritchie 2017). For example, midlife vascular risk factors including diabetes, obesity, hypertension increased developing late life (Livingston 2020). This topic includes eight human rodent studies, three review papers, exploring strategies reduce cognitive decline mechanisms memory middle-aged individuals, adults normal cognition, those mild impairment (MCI), AD.Exercise InterventionIn their personality traits molecular signaling well health playing roles 107 adaptation (Gogniat 2020;Won, Gogniat, 2025;Won, Tomoto, 108 2025). Moving forward, future should focus elucidating underlying 109 that link late-life outcomes 110 J.W. drafted paper J.W., M.G., T.K., K.N. edited paper. All authors reviewed, revised, 115 approved final manuscript. 116Funding 117This study was supported American Heart Association (25POST1366119). 118

Language: Английский

Citations

0
Fitness and Exercise Effects on Brain Age: A Randomized Clinical Trial DOI Creative Commons
Lu Wan, Cristina Molina‐Hidalgo, Mary E. Crisafio

et al.

medRxiv (Cold Spring Harbor Laboratory), Journal Year: 2025, Volume and Issue: unknown

Published: Feb. 26, 2025

Examine the effect of aerobic exercise on structural brain age and explore potential mediators. In a single-blind, 12-month randomized clinical trial, 130 healthy participants aged 26-58 years were into moderator-to-vigorous intensity group or usual-care control group. The attended 2 supervised 60-minute sessions per week in laboratory setting plus home-based to achieve 150 minutes week. Brain-predicted difference (brain-PAD) cardiorespiratory fitness (CRF) assessed at baseline 12 months. Intention-to-treat (ITT) completers analyses performed. (67.7% female) had mean (SD) 41.28 (9.93) years. At baseline, higher CRF (VO 2peak ) was associated with smaller brain-PAD (β=-0.309, p=0.012). After intervention, showed decrease (estimated (EMD) =-0.60; 95% CI: -1.15 -0.04; p=0.034) compared (EMD=0.35; -0.21 0.92; p=0.22); time×group interaction (between-group (BGD)= -0.95; -1.72 -0.17; p=0.019). VO improved (EMD=1.60; 0.29 2.90; p=0.017) (EMD=-0.78; -2.17 0.60; p=0.26); (BGD=2.38; 0.52 4.25; p=0.015). Body composition, blood pressure, brain-derived neurotrophic factor levels unaffected. None proposed pathways statistically mediated brain-PAD. results from similar. Engaging months moderate-to-vigorous reduced early-to-midlife adults. by which these effects occur remain unknown. What is already known this topic: Midlife risk factors influence aging, physical activity conferring protective benefits, yet evidence for midlife underlying mechanisms remains limited.What study adds: Participation intervention significantly neuroimaging marker age. Higher also younger age.How might affect research, practice policy: Findings complement scarce literature examining health confirm neuroprotective against accelerated aging

Language: Английский

Citations

0
Signatures of Nonlinear Aging: Molecular Stages of Life DOI Open Access
Maja Olecka, Helen Morrison, Steve Hoffmann

et al.

BioEssays, Journal Year: 2025, Volume and Issue: unknown

Published: March 16, 2025

ABSTRACT The traditional view of aging as a gradual, progressive process is increasingly being challenged. A growing body evidence suggests the existence abrupt transitions in process, marked by sudden molecular shifts. Interestingly, data indicates that such occur not only late life but also throughout entire lifespan. Further research on nature events could enhance our understanding and pave way for novel therapeutic strategies, including personalized medicine. We propose these shifts serve biomarkers, dividing lifespan into distinct stages providing foundation much‐needed staging system aging. Furthermore, we argue changes may be hallmarks tipping points, is, points time where processes are quickly amplified after surpassing critical biological thresholds.

Language: Английский

Citations

0