Cited by 1,260Dementia and Cognitive Impairment ResearchAlzheimer's disease research and treatmentsNeuroinflammation and Neurodegeneration Mechanisms

Religious Orders Study and Rush Memory and Aging Project

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Bennett, David A., Buchman, Aron S., Boyle, Patricia A., Barnes, Lisa L., Wilson, Robert S., Schneider, Julie A.·2018·Journal of Alzheimer's Disease

Abstract

BACKGROUND: The Religious Orders Study and Rush Memory and Aging Project are both ongoing longitudinal clinical-pathologic cohort studies of aging and Alzheimer's disease (AD). OBJECTIVES: To summarize progress over the past five years and its implications for understanding neurodegenerative diseases. METHODS: Participants in both studies are older adults who enroll without dementia and agree to detailed longitudinal clinical evaluations and organ donation. The last review summarized findings through the end of 2011. Here we summarize progress and study findings over the past five years and discuss new directions for how these studies can inform on aging and AD in the future. RESULTS: We summarize 1) findings on the relation of neurobiology to clinical AD; 2) neurobiologic pathways linking risk factors to clinical AD; 3) non-cognitive AD phenotypes including motor function and decision making; 4) the development of a novel drug discovery platform. CONCLUSION: Complexity at multiple levels needs to be understood and overcome to develop effective treatments and preventions for cognitive decline and AD dementia.

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  • Genes associated with Alzheimer's disease progression are enriched in dopaminergic and inhibitory neuron subtypes, validated across two independent datasets.

    “This key finding, validated across two independent datasets [41, 100], points specifically to the enrichment of these progression genes in dopaminergic and inhibitory neuron subtypes.”

    From Genetic drivers of progression in Alzheimer’s disease are distinct from disease risk (2026) · cites this paper as [100]

    The Introduction (page unavailable) identifies the Religious Orders Study and Rush Memory and Aging Project as cohort studies and describes their datasets, supporting this paper as a citation for a data resource. The paper does not report that Alzheimer’s progression genes are enriched in dopaminergic or inhibitory neuron subtypes, or that this finding was validated across two datasets. (LLM, conf=0.82)

    Experimental — accuracy not yet measured
  • All ROSMAP participants enrolled without known dementia and agreed to detailed clinical evaluation and brain donation at death.

    “All ROSMAP partici- pants enrolled without known dementia and agreed to detailed clinical evaluation and brain donation at death.”
  • Aged individuals can harbor a high burden of AD brain lesions at autopsy while remaining cognitively intact, indicating resilience to AD pathology.

    “several studies have revealed the existence of aged individuals harboring a high burden of brain lesions at autopsy while remaining cognitively intact, indicating resilience to AD pathology [3, 7, 21, 22, 56, 57, 68, 76, 78, 96].”
  • Some studies have identified selected overlaps in expression changes between AD mouse models and human brains.

    “Although some studies have identified selected overlaps in expression changes between AD mouse models and human brains (Bennett et al., 2018; Castillo et al., 2017; Mostafavi et al., 2018; Neuner et al., 2019; Rojo et al., 2017), other studies have questioned the overall degree of conservation (Burns et al., 2015; Galatro et al., 2017; Hargis and Blalock, 2017).”

    From Meta-Analysis of the Alzheimer’s Disease Human Brain Transcriptome and Functional Dissection in Mouse Models (2020) · cites this paper as Bennett et al., 2018

    The Results section on the novel drug and biomarker discovery pipeline discusses human-brain omics and an ex vivo model, but does not compare expression changes in AD mouse models with human brains. Searches for mouse models, cross-species comparisons, and overlapping expression changes found no passage in our copy reporting the claimed overlap; pages were not provided. (LLM, conf=0.72)

    Experimental — accuracy not yet measured
  • miR-1908-5p is relevant to bipolar disorder despite its relatively low abundance.

    “Notable among those, miR-1908–5p was previously observed to be differentially expressed in blood in the acute bipolar state compared to remission state62, which suggests that miR-1908–5p is relevant to bipolar disorder despite its relatively low abundance.”

    From Mapping the microRNA landscape in the older adult brain and its genetic contribution to neuropsychiatric conditions (2024) · cites this paper as [62]

    The Materials section discusses miRNA data from the Religious Orders Study and Rush Memory and Aging Project, but does not identify miR-1908-5p or address bipolar disorder. Searches for miR-1908-5p, acute bipolar state versus remission, and low abundance found no passage supporting the observation attributed to this source. (LLM, conf=0.77)

    Experimental — accuracy not yet measured

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Authors
Bennett, D. A., Buchman, A. S., Boyle, P. A., Barnes, L. L., Wilson, R. S., & Schneider, J. A.
Affiliations
Rush University Medical Center (US)
Corresponding author
Bennett, David A.
Venue
Journal of Alzheimer's Disease
Published
2018-06-12
Volume
64
Issue
s1
Pages
S161-S189
ISSN
  • 1387-2877 (ISSN-L)
  • 1875-8908
OpenAlex
W2809330972
Cited by
1,260
References
50
Citations by year
2026: 160 · 2025: 249 · 2024: 194 · 2023: 181 · 2022: 169 · 2021: 127 · 2020: 88 · 2019: 75 · 2018: 12 · 2017: 1 · 2013: 1
FWCI
11.67
Type
journal article
Language
en
Open access
Locations
  • Journal of Alzheimer s Disease (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institute on Aging (R01AG043379, R01AG017917, R01AG056352, R01AG042210, RF1AG022018, U01AG046152, R01AG036042, R01AG015819, P30AG010161, R01AG040039, R01AG047976, RF1AG054057, RF1AG015819, RF1AG036042, R01AG033678, R01AG034374, R01AG022018)
  • National Institute of Neurological Disorders and Stroke (UH3NS100599, UH2NS100599, R01NS078009, UF1NS100599)
Topics
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
Alzheimer's disease, aging
MeSH terms
Aging, Alzheimer Disease, Humans, Memory, United States, Religious Personnel

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

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