Religious Orders Study and Rush Memory and Aging Project

Bennett, David A.; Buchman, Aron S.; Boyle, Patricia A.; Barnes, Lisa L.; Wilson, Robert S.; Schneider, Julie A.

doi:10.3233/jad-179939

Cited by 919 publications

(1,168 citation statements)

References 447 publications

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“…Studies’ methods have been described in detail elsewhere [10]. ROS began enrolling participants in 1994, and recruits older Catholic nuns, priests, and brothers from sites across the United States.…”

Section: Methodsmentioning

confidence: 99%

Sex differences in Alzheimer’s disease and common neuropathologies of aging

et al. 2018

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Alzheimer’s dementia is significantly more common in women than in men. However, few pathological studies have addressed sex difference in Alzheimer’s disease (AD) and other brain pathologies. We leveraged post mortem data from 1453 persons who participated in one of two longitudinal community-based studies of older adults, the Religious Orders Study and the Rush Memory and Aging Project. Postmortem examination identified AD pathologies, neocortical Lewy bodies, DNA-binding protein 43 (TDP-43), hippocampal sclerosis, gross and micro infarcts, atherosclerosis, arteriolosclerosis, and cerebral amyloid angiopathy. Linear and logistic regressions examined the association of sex with each of the pathologic measures. Two thirds of subjects were women (n=971; 67%), with a mean age-at-death of 89.8 (SD=6.6) years in women and 87.3 (SD=6.6) in men. Adjusted for age and education, women had higher levels on a global measure of AD pathology (estimate=0.102, SE=0.022, p<0.001), and tau tangle density in particular (estimate=0.334, SE=0.074, p<0.001), and there was a borderline difference between women and men in amyloid-β load (estimate=0.124, SE=0.065, p=0.056). In addition, compared to men, women were more likely to have more severe arteriolosclerosis (OR=1.28, 95% CI:1.04–1.58, p=0.018), and less likely to have gross infarcts (OR=0.78, 95% CI:0.61–0.98, p=0.037), although the association with gross infarct was attenuated after controlling for vascular risk factors. These data help elucidate the neuropathologic footprint of sex difference in AD and other common brain pathologies of ageing.

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Section: Methodsmentioning

confidence: 99%

Sex differences in Alzheimer’s disease and common neuropathologies of aging

et al. 2018

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“…The subjects in this study are participants of the Religious Orders Study (ROS) and the Memory and Aging Project (MAP). ROS and MAP are longitudinal cohort studies of Alzheimer's disease and aging maintained by investigators at the Rush Alzheimer's Disease Center in Chicago, IL (11)(12)(13). Both studies recruit participants without known dementia at baseline and follow them annually using detailed clinical evaluation.…”

Section: Study Subjectsmentioning

confidence: 99%

Genetic control of the human brain proteome

Robins

Wingo

Fan

et al. 2019

Preprint

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Alteration of protein abundance and conformation are widely believed to be the hallmark of neurodegenerative diseases. Yet relatively little is known about the genetic variation that controls protein abundance in the healthy human brain. The genetic control of protein abundance is generally thought to parallel that of RNA expression, but there is little direct evidence to support this view. Here, we performed a large-scale protein quantitative trait locus (pQTL) analysis using single nucleotide variants (SNVs) from whole-genome sequencing and tandem mass spectrometry-based proteomic quantification of 12,691 unique proteins (7,901 after quality control) from the dorsolateral prefrontal cortex (dPFC) in 144 cognitively normal individuals. We identified 28,211 pQTLs that were significantly associated with the abundance of 864 proteins. These pQTLs were compared to dPFC expression quantitative trait loci (eQTL) in cognitive normal individuals (n=169; 81 had protein data) and a meta-analysis of dPFC eQTLs (n=1,433). We found that strong pQTLs are generally only weak eQTLs, and that the majority of strong eQTLs are not detectable pQTLs. These results suggest that the genetic control of mRNA and protein abundance may be substantially distinct and suggests inference concerning protein abundance made from mRNA in human brain should be treated with caution.

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“…Analyses are based on participants in the Rush memory and aging project (MAP), an ongoing longitudinal clinical-pathologic cohort study that began in 1997. 12 Eligibility required agreement to annual clinical evaluations and brain autopsy at death. Individuals were recruited from retirement communities, social service agencies, subsidized housing facilities, and churches.…”

Section: Participantsmentioning

confidence: 99%

Hospitalization, Alzheimer's Disease and Related Neuropathologies, and Cognitive Decline

James

Wilson

Capuano

et al. 2019

Annals of Neurology

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Objective To test the hypothesis that Alzheimer's disease and related neuropathologies contribute to the association between hospitalization and cognitive decline in old age. Methods As part of a longitudinal clinical–pathologic cohort study, 526 older persons (mean age at death = 90.9 years, 71% female) without dementia at baseline completed annual cognitive testing and were autopsied at death. Hospitalization information was obtained from linked Medicare claims records. Neuropathologic examination assessed β‐amyloid burden, tau tangle density, neocortical Lewy bodies, hippocampal sclerosis, chronic gross and microscopic cerebral infarcts, and transactive response DNA binding protein 43 kDa. Results Over a mean of 5.1 years, a total of 1,383 hospitalizations occurred, and the mean annual rate of hospitalization was 0.5 (standard deviation = 0.6, median = 0.4). Higher rate of hospitalization was not directly related to higher burden for any of the neuropathologic markers. Higher rate of hospitalization was associated with more rapid cognitive decline (estimate = −0.042, standard error [SE] = 0.012, p < 0.001), and after controlling for all 7 neuropathologic markers, the association was essentially the same (estimate = −0.040, SE = 0.013, p = 0.002). In a multivariable model with 3‐way interactions of neuropathologic markers with hospitalization rate and time, the association between hospitalization rate and faster cognitive decline was greater in persons with more tangle pathology (estimate for interaction = −0.007, SE = 0.002, p = 0.002) and in persons with neocortical Lewy bodies (estimate for interaction = −0.117, SE = 0.042, p = 0.005). Interpretation Older persons with more hospitalizations experienced faster rates of cognitive decline, and this association was more pronounced in persons with more tau tangle density and with neocortical Lewy body pathologies. ANN NEUROL 2019;86:844–852

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Religious Orders Study and Rush Memory and Aging Project

Abstract: Complexity at multiple levels needs to be understood and overcome to develop effective treatments and preventions for cognitive decline and AD dementia.

Cited by 919 publications

References 447 publications

Sex differences in Alzheimer’s disease and common neuropathologies of aging

Sex differences in Alzheimer’s disease and common neuropathologies of aging

Genetic control of the human brain proteome

Hospitalization, Alzheimer's Disease and Related Neuropathologies, and Cognitive Decline

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