scholarly journals Life Course Socioeconomic Status and Later Life Alzheimer’s Disease-Related Neuropathological Lesions

2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 164-164
Author(s):  
Sarah Tom ◽  
Amol Mehta ◽  
Stepanie Izard ◽  
Paul Crane ◽  
David Bennett ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Socioeconomic Status ◽  
Life Course ◽  
Early Life ◽  
Parental Education ◽  
Brain Aging ◽  
Late Life ◽  
Later Life ◽  
Braak Stage

Abstract While higher life course socioeconomic status (SES) is associated with lower Alzheimer’s Disease (AD) risk, relationships with AD-related neuropathological lesions are unclear. We hypothesize that high SES in early, mid and late life will be associated with lower frequency of AD-related pathological lesions. The Rush Memory and Aging Project is a cohort of 2025 people age ≥ 65 years from Northeastern Illinois recruited 1997 – 2018; 972 participants died. We created binary variables for Braak stage (0-II versus III-VI), NIA-Reagan score (low likelihood/no AD pathology versus high/intermediate likelihood), presence of microinfarcts and, separately, macroinfarcts, and life course SES based on median for late life (baseline income), midlife (income at age 40 years), and early life (composite of parental education and number of siblings). Logistic regression models adjusted for ages at baseline and death, sex, presence of APOE-Ɛ4 alleles, and separately, vascular factors and education. Of 761 participants with relevant data, 69% were women, and mean ages at baseline and death were 83 + 6 years and 90 + 6 years, respectively. High early life SES was related to lower frequency of AD pathology (OR= 0.69, 95% CI 0.50, 0.96) and macroinfarcts (OR= 0.69, 95% CI 0.51, 0.94). Results were similar when adjusting for vascular factors; adjustment for education modestly attenuated these associations. Mid-life and late life SES were not associated with AD-related neuropathological lesions. High early life SES was related to lower frequency of AD pathology and macroinfarct presence. Environment during early development may influence later life brain aging.

Early Life Socioeconomic Status and Late Life Risk of Alzheimer’s Disease

2005 ◽  
Vol 25 (1) ◽  
pp. 8-14 ◽  
Author(s):  
Robert S. Wilson ◽  
Paul A. Scherr ◽  
George Hoganson ◽  
Julia L. Bienias ◽  
Denis A. Evans ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Socioeconomic Status ◽  
Early Life ◽  
Late Life

scholarly journals Life Course Socioeconomic Status and Late-Life Cognition and Cognitive Decline in the Rush Memory and Aging Project

2020 ◽  
Vol 4 (Supplement_1) ◽  
pp. 259-259
Author(s):  
Anna Krasnova ◽  
Sarah Tom ◽  
Linda Valeri ◽  
Maria Glymour ◽  
Paul Crane ◽  
...  
Keyword(s):  
Socioeconomic Status ◽  
Cognitive Function ◽  
Life Course ◽  
Cognitive Decline ◽  
Parental Education ◽  
Late Life ◽  
Later Life ◽  
Cognitive Capacity ◽  
Global Cognitive Function ◽  
Financial Need

Abstract The relationships among life course socioeconomic status (SES) measures with later life cognition and cognitive decline are unclear. We test the hypothesis that life-course SES is associated with late life level of cognition and rate of cognitive decline. The Rush Memory and Aging Project enrolled 1,864 dementia-free people aged ≥65 years between 1994 – 2018. Participants reported early life (parental education, number of siblings, and childhood financial need), mid-life (income at 40 years), and late life (baseline income) SES. Global cognitive function is a composite of 19 neuropsychological tests, administered annually. We utilized marginal structural models to assess the effect of SES (dichotomized at the median) at three life-course stages on late life global cognitive function and decline. We calculated inverse probability weights to adjust for socio-demographic confounders at each life-course stage. A total 1,063 participants had all relevant variables. Average follow-up was 4.4 years, and mean baseline age was 80.4 years. Most respondents were non-Hispanic white (89.7%) and female (74.1%). In the fully adjusted model, high childhood SES (coefficient 0.10; 95% CI 0.01, 0.20) and high late-life SES were associated with higher cognition intercept (coefficient 0.21; 95% CI 0.09, 0.32). High mid-life SES was associated with slower rate of cognitive decline (coefficient 0.02; 95% CI 0.001, 0.05). Childhood and late-life SES measures were not related to cognitive decline. Childhood and adult SES may reflect processes in building cognitive capacity, while midlife SES may reflect cognition maintenance. Interventions relating to SES across the life-course may benefit later life cognition.

scholarly journals Body size throughout the life-course and incident benign prostatic hyperplasia-related outcomes and nocturia

BMC Urology ◽  
2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Saira Khan ◽  
K. Y. Wolin ◽  
R. Pakpahan ◽  
R. L. Grubb ◽  
G. A. Colditz ◽  
...  
Keyword(s):  
Body Size ◽  
Benign Prostatic Hyperplasia ◽  
Life Course ◽  
Early Life ◽  
Prostate Volume ◽  
Late Life ◽  
Later Life ◽  
Normal Weight ◽  
Prostatic Hyperplasia ◽  
The Life Course

Abstract Background Existing evidence suggests that there is an association between body size and prevalent Benign Prostatic Hyperplasia (BPH)-related outcomes and nocturia. However, there is limited evidence on the association between body size throughout the life-course and incident BPH-related outcomes. Methods Our study population consisted of men without histories of prostate cancer, BPH-related outcomes, or nocturia in the intervention arm of the Prostate, Lung, Colorectal, and Ovarian Cancer Screening Trial (PLCO) (n = 4710). Associations for body size in early- (age 20), mid- (age 50) and late-life (age ≥ 55, mean age 60.7 years) and weight change with incident BPH-related outcomes (including self-reported nocturia and physician diagnosis of BPH, digital rectal examination-estimated prostate volume ≥ 30 cc, and prostate-specific antigen [PSA] concentration > 1.4 ng/mL) were examined using Poisson regression with robust variance estimation. Results Men who were obese in late-life were 25% more likely to report nocturia (Relative Risk (RR): 1.25, 95% Confidence Interval (CI): 1.11–1.40; p-trendfor continuous BMI < 0.0001) and men who were either overweight or obese in late-life were more likely to report a prostate volume ≥ 30 cc (RRoverweight: 1.13, 95% CI 1.07–1.21; RRobese: 1.10, 95% CI 1.02–1.19; p-trendfor continuous BMI = 0.017) as compared to normal weight men. Obesity at ages 20 and 50 was similarly associated with both nocturia and prostate volume ≥ 30 cc. Considering trajectories of body size, men who were normal weight at age 20 and became overweight or obese by later-life had increased risks of nocturia (RRnormal to overweight: 1.09, 95% CI 0.98–1.22; RRnormal to obese: 1.28, 95% CI 1.10–1.47) and a prostate volume ≥ 30 cc (RRnormal to overweight: 1.12, 95% CI 1.05–1.20). Too few men were obese early in life to examine the independent effect of early-life body size. Later-life body size modified the association between physical activity and nocturia. Conclusions We found that later-life body size, independent of early-life body size, was associated with adverse BPH outcomes, suggesting that interventions to reduce body size even late in life can potentially reduce the burden of BPH-related outcomes and nocturia.

scholarly journals CHILDHOOD SOCIOECONOMIC STATUS AND SENSE OF CONTROL OVER COGNITIVE AGING: DO GENES MODERATE?

2019 ◽  
Vol 3 (Supplement_1) ◽  
pp. S881-S881
Author(s):  
Addam S Reynolds ◽  
Emily Greenfield
Keyword(s):  
Socioeconomic Status ◽  
Cognitive Aging ◽  
Early Life ◽  
Parental Education ◽  
Protective Factor ◽  
Brain Aging ◽  
The United States ◽  
Environment Interaction ◽  
Sense Of Control ◽  
Age Related

Abstract Individuals who lack a sense of control over cognitive aging (SOC-CA) believe little can be done to optimize their cognitive functioning. While prior research indicates that higher SOC-CA is a protective factor against age-related cognitive decline, few studies have examined predictors of change in SOC-CA. To address this gap, we used data from the Midlife in the United States (MIDUS) study. Guided by prior research on linkages between socioeconomic status (SES) and control beliefs, we examined childhood SES as an early life course influence on changes in SOC-CA. The analytic sample consisted of 663 White participants, ages 34 to 81, who were interviewed in 2004 and approximately nine years later. SOC-CA was measured by using three items from the Personality in Aging Context scale, and childhood SES encompassed retrospective reports of parental education and occupational status. A hierarchical linear model was estimated, which modeled SOC-CA at baseline, as well as change over the study period, controlling for gender, age, ancestry, and adult SES. While childhood SES was not associated with SOC-CA at baseline nor over time, a statistically significant gene-environment interaction was found over the 9-year study period. Specifically, participants who scored high on a polygenetic measure for cognitive ability and reported high childhood SES demonstrated a faster rate of decline in SOC-CA. These findings indicate that inter-individual differences stemming from early life influence people’s SOC-CA as they age. Overall, results suggest the importance of subgroup differences within efforts to engage individuals in preventive measures to optimize healthy brain aging.

Developmental toxicant exposure in a mouse model of Alzheimer’s disease induces differential sex-associated microglial activation and increased susceptibility to amyloid accumulation

2017 ◽  
Vol 8 (4) ◽  
pp. 493-501 ◽  
Author(s):  
A. N. vonderEmbse ◽  
Q. Hu ◽  
J. C. DeWitt
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Early Life ◽  
Microglial Activation ◽  
Later Life ◽  
Amyloid Burden ◽  
Toxicant Exposure ◽  
Female Mice ◽  
Model Of Alzheimer’S Disease ◽  
Amyloid Accumulation

As the resident macrophage of the central nervous system, microglia are thought to contribute to Alzheimer’s disease (AD) pathology through lack of neuroprotection. The role of immune dysfunction in AD may be due to disruption of regulatory signals for the activation of microglia that may occur early in development. We hypothesized that early toxicant exposure would systematically activate microglia, possibly reversing the pathological severity of AD. Offspring of a triple transgenic murine model for AD (3×TgAD) were exposed to a model neurotoxicant, lead acetate, from postnatal days (PND) 5–10. Our results indicated that female mice exposed to Pb had a greater and earlier incidence of amyloid burden within the hippocampus, coinciding with decreased markers of microglial activation at PND 50. Pb-exposed males had increased microglial activation at PND 50, as evidence by CD11b expression and microglial abundance, with no significant increase in amyloid burden at that time. There was greater amyloid burden at PND 90 and 180 in both male and female mice exposed to Pb compared with control. Together, these data suggest that activated microglia are neuroprotective against amyloid accumulation early in AD pathology, and that early exposure to Pb could increase susceptibility to later-life neurodegeneration. Likewise, females may be more susceptible to early-life microglial damage, and, subsequently, AD. Further investigation into the sex biased mechanisms by which microglial activation is altered by an early-life immune insult will provide critical insight into the temporal susceptibility of the developing neuroimmune system and its potential role in AD etiopathology.

scholarly journals Associations between Brain Reserve Proxies and Clinical Progression in Alzheimer’s Disease Dementia

2021 ◽  
Vol 18 (22) ◽  
pp. 12159
Author(s):  
Hyung-Jun Yoon ◽  
Seung-Gon Kim ◽  
Sang Hoon Kim ◽  
Jong Inn Woo ◽  
Eun Hyun Seo ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Glucose Metabolism ◽  
Early Life ◽  
Late Life ◽  
Cox Proportional Hazards Model ◽  
Cerebral Glucose Metabolism ◽  
Intracranial Volume ◽  
Clinical Progression ◽  
Brain Reserve

The purpose of this study was to investigate whether brain and cognitive reserves were associated with the clinical progression of AD dementia. We included participants with AD dementia from the Alzheimer’s Disease Neuroimaging Initiative, provided they were followed up at least once, and candidate proxies for cognitive (education for early-life reserve and Adult Reading Test for late-life reserve) or brain reserve (intracranial volume [ICV] for early-life reserve and the composite value of [18F] fluorodeoxyglucose positron emission tomography regions of interest (FDG-ROIs) for late-life reserve) were available. The final analysis included 120 participants. Cox proportional hazards model revealed that FDG-ROIs were the only significant predictor of clinical progression. Subgroup analysis revealed a significant association between FDG-ROIs and clinical progression only in the larger ICV group (HR = 0.388, p = 0.028, 95% CI 0.167–0.902). Our preliminary findings suggest that relatively preserved cerebral glucose metabolism might delay further clinical progression in AD dementia, particularly in the greater ICV group. In addition to ICV, cerebral glucose metabolism could play an important role as a late-life brain reserve in the process of neurodegeneration. Distinguishing between early- and late-life reserves, and considering both proxies simultaneously, would provide a wider range of factors associated with the prognosis of AD dementia.

scholarly journals Early-life Health as a Lifelong Precursor of Self-Related Views of Aging in Later Life

2020 ◽  
Author(s):  
Jacqui Smith ◽  
Marina Larkina
Keyword(s):  
Socioeconomic Status ◽  
Chronic Illness ◽  
Early Life ◽  
Late Life ◽  
Later Life ◽  
Chronic Illnesses ◽  
Subjective Age ◽  
Childhood Health ◽  
Using Data ◽  
Demographic Covariates

Abstract Objectives Age stereotypes and expectations about one’s own aging commence in childhood but most research focuses on predictive associations with midlife health behaviors, later-life chronic conditions, biomarkers, and longevity. Surprisingly little is known about the role of poor childhood health in these associations. This study aims to fill this gap. Methods Using data from the Health and Retirement Study (HRS: N = 5,773, aged 50–98), we investigated whether diagnosed chronic illness before age 16 and self-rated childhood health predict late-life self-perceptions of aging (SPA) and proportional subjective age discrepancy (PSAD). We conducted multivariate multiple regression analysis (MMRA) to determine the joint and partial effects of the two indicators of childhood health. Models included controls for childhood family financial status as well as late-life self-rated health, chronic illnesses, memory status, and demographic covariates (age, gender, race/ethnicity, marital status, socioeconomic status) in 2016. Results Over and above all covariates and the covariation of the two views of one’s own aging, the MMRA models revealed that the number of childhood chronic illnesses predicted SPA but not for PSAD. Self-rated childhood health predicted both SPA and PSAD in the unadjusted models, but not in the adjusted models. Discussion This study provides new insight into potential early-life precursors of self-evaluations of aging. In particular, childhood diagnoses of chronic illness enhance negative SPA up to 50 years later. Non-normative experiences related to poor health in childhood are lifelong foundations for socioeconomic status, health, and for self-related beliefs about age and aging.

Sign in / Sign up

Export Citation Format

Share Document