scholarly journals Geographic variation in Alzheimer’s disease mortality

PLoS ONE ◽  
2021 ◽  
Vol 16 (7) ◽  
pp. e0254174
Author(s):  
Michael Topping ◽  
Jinho Kim ◽  
Jason Fletcher
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Old Age ◽  
Early Life ◽  
Later Life ◽  
Health Study ◽  
Disease Mortality ◽  
Early Life Conditions ◽  
Large Survey ◽  
Early Life Exposures

Objective Accumulating evidence suggests the possibility that early life exposures may contribute to risk of Alzheimer’s Disease (AD). This paper explores geographic disparities in AD mortality based on both state of residence in older age as well as state of birth measures in order to assess the relative importance of these factors. Methods We use a subset of a large survey, the NIH-AARP Diet and Health Study, of over 150,000 individuals aged 65–70 with 15 years of mortality follow-up, allowing us to study over 1050 cases of AD mortality. We use multi-level logistic regression, where individuals are nested within states of residence and/or states of birth, to assess the contributions of place to AD mortality variation. Results We show that state of birth explains a modest amount of variation in AD mortality, approximately 4%, which is consistent with life course theories that suggest that early life conditions can produce old age health disparities. However, we also show that nearly all of the variation from state of birth is explained by state of residence in old age. Conclusions These results suggest that later life factors are potentially more consequential targets for intervention in reducing AD mortality and provide some evidence against the importance of macro-level environmental exposures at birth as a core determinant of later AD.

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.

Association of Sleep With Risk of Alzheimer’s Disease Mortality: NIH-AARP Diet and Health Study

2021 ◽  
pp. 073346482110192
Author(s):  
Aaron C. Schneider ◽  
Chooza Moon ◽  
Kara Whitaker ◽  
Dong Zhang ◽  
Lucas J. Carr ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Sleep Duration ◽  
Lifestyle Factors ◽  
Health Study ◽  
Current Evidence ◽  
National Death Index ◽  
Older Population ◽  
Disease Mortality ◽  
Long Sleep

Objectives: Alzheimer’s disease (AD) and related dementias contribute to one in three senior deaths. Lifestyle factors, including sleep, may contribute to AD risk and mortality; however, current evidence on sleep and AD mortality is mixed. Methods: We used data from the NIH-AARP Diet and Health Study. Sleep duration and napping were self-reported and AD death were ascertained via linkage to the National Death Index. Results: Long sleep and napping were both associated with increased AD mortality. Specifically, 9+ hr of sleep was associated with 50% increase (hazard ratio = 1.50, 95% CI = [1.17, 1.92]) in AD mortality when compared 7 to 8 hr, while napping for 1+ hr was associated with 29% increase (1.29 [1.08, 1.55]) when compared with no napping. Results appeared to be stronger in men and remained after removing AD deaths within first 5 years after baseline. Discussion: Long sleep and napping may predict higher AD mortality in the older population.

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.

scholarly journals Vulnerability and resilience to Alzheimer’s disease: early life conditions modulate neuropathology and determine cognitive reserve

2018 ◽  
Vol 10 (1) ◽  
Author(s):  
Sylvie L. Lesuis ◽  
Lianne Hoeijmakers ◽  
Aniko Korosi ◽  
Susanne R. de Rooij ◽  
Dick F. Swaab ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Early Life ◽  
Cognitive Reserve ◽  
Life Conditions ◽  
Early Life Conditions

Early-life stress induces the development of Alzheimer's disease pathology via angiopathy

2021 ◽  
Vol 337 ◽  
pp. 113552
Author(s):  
Tomoko Tanaka ◽  
Shinobu Hirai ◽  
Masato Hosokawa ◽  
Takashi Saito ◽  
Hiroshi Sakuma ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Life Stress ◽  
Early Life ◽  
Early Life Stress

scholarly journals The impact of early life factors on cognitive function in old age: The Hordaland Health Study (HUSK)

2013 ◽  
Vol 1 (1) ◽  
Author(s):  
Jens Christoffer Skogen ◽  
Simon Øverland ◽  
A David Smith ◽  
Arnstein Mykletun ◽  
Robert Stewart
Keyword(s):  
Cognitive Function ◽  
Old Age ◽  
Early Life ◽  
Health Study ◽  
Early Life Factors ◽  
The Impact

scholarly journals Early life nutrient restriction impairs blood–brain metabolic profile and neurobehavior predisposing to Alzheimer’s disease with aging

2013 ◽  
Vol 1495 ◽  
pp. 61-75 ◽  
Author(s):  
Masatoshi Tomi ◽  
Yuanzi Zhao ◽  
Shanthie Thamotharan ◽  
Bo-Chul Shin ◽  
Sherin U. Devaskar
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Early Life ◽  
Metabolic Profile ◽  
Nutrient Restriction ◽  
Blood Brain

Early life factors as predictors of age-associated deficit accumulation across 17 years from midlife into old age

2022 ◽  
Author(s):  
Markus J Haapanen ◽  
Juulia Jylhävä ◽  
Lauri Kortelainen ◽  
Tuija M Mikkola ◽  
Minna Salonen ◽  
...  
Keyword(s):  
Old Age ◽  
Early Life ◽  
Mixed Model ◽  
Linear Mixed Model ◽  
Frailty Index ◽  
Rate Of Change ◽  
Birth Cohort Study ◽  
Maternal Body Mass Index ◽  
Early Life Factors ◽  
Early Life Exposures

Abstract Background Early life exposures have been associated with the risk of frailty in old age. We investigated whether early life exposures predict the level and rate of change in a frailty index (FI) from midlife into old age. Methods A linear mixed model analysis was performed using data from three measurement occasions over 17 years in participants from the Helsinki Birth Cohort Study (n=2000) aged 57-84 years. A 41-item FI was calculated on each occasion. Information on birth size, maternal body mass index (BMI), growth in infancy and childhood, childhood socioeconomic status (SES), and early life stress (wartime separation from both parents), was obtained from registers and healthcare records. Results At age 57 years the mean FI level was 0.186 and the FI levels increased by 0.34 percent/year from midlife into old age. Larger body size at birth associated with a slower increase in FI levels from midlife into old age. Per 1kg greater birth weight the increase in FI levels per year was -0.087 percentage points slower (95% CI=-0.163, -0.011; p=0.026). Higher maternal BMI was associated with a higher offspring FI level in midlife and a slower increase in FI levels into old age. Larger size, faster growth from infancy to childhood, and low SES in childhood were all associated with a lower FI level in midlife but not with its rate of change. Conclusions Early life factors seem to contribute to disparities in frailty from midlife into old age. Early life factors may identify groups that could benefit from frailty prevention, optimally initiated early in life.

scholarly journals Epigenetics and DOHaD: from basics to birth and beyond

2017 ◽  
Vol 8 (5) ◽  
pp. 513-519 ◽  
Author(s):  
T. Bianco-Miotto ◽  
J. M. Craig ◽  
Y. P. Gasser ◽  
S. J. van Dijk ◽  
S. E. Ozanne
Keyword(s):  
Dna Methylation ◽  
Chronic Disease ◽  
Chronic Diseases ◽  
Early Life ◽  
Later Life ◽  
Metabolic Health ◽  
Number Of Children ◽  
Early Life Environment ◽  
Increased Risk ◽  
Early Life Exposures

Developmental origins of health and disease (DOHaD) is the study of how the early life environment can impact the risk of chronic diseases from childhood to adulthood and the mechanisms involved. Epigenetic modifications such as DNA methylation, histone modifications and non-coding RNAs are involved in mediating how early life environment impacts later health. This review is a summary of the Epigenetics and DOHaD workshop held at the 2016 DOHaD Society of Australia and New Zealand Conference. Our extensive knowledge of how the early life environment impacts later risk for chronic disease would not have been possible without animal models. In this review we highlight some animal model examples that demonstrate how an adverse early life exposure results in epigenetic and gene expression changes that may contribute to increased risk of chronic disease later in life. Type 2 diabetes and cardiovascular disease are chronic diseases with an increasing incidence due to the increased number of children and adults that are obese. Epigenetic changes such as DNA methylation have been shown to be associated with metabolic health measures and potentially predict future metabolic health status. Although more difficult to elucidate in humans, recent studies suggest that DNA methylation may be one of the epigenetic mechanisms that mediates the effects of early life exposures on later life risk of obesity and obesity related diseases. Finally, we discuss the role of the microbiome and how it is a new player in developmental programming and mediating early life exposures on later risk of chronic disease.

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