Evidence map›Paper›PMID 32685657›Full record

ArticleAlzheimer's & dementia (New York, N. Y.)2020

Shared mechanisms for cognitive impairment and physical frailty: A model for complex systems.

Lana Sargent, Mike Nalls, Elaine J Amella, Patricia W Slattum, Martina Mueller, Stefania Bandinelli, Qu Tian, Theresa Swift-Scanlan, Sarah K Lageman, Andrew Singleton

Abstract read
In one paragraph

Article in Alzheimer's & dementia (New York, N. Y.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed, 2 pooled it
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

32 citing papers in PubMed, 2 syntheses or guidelines pooled it.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Lana SargentLaboratory of Neurogenetics National Institute on Aging National Institutes of Health Bethesda Maryland USA.
Mike NallsLaboratory of Neurogenetics National Institute on Aging National Institutes of Health Bethesda Maryland USA.
Elaine J AmellaMedical University of South Carolina School of Nursing Charleston North Carolina USA.
Patricia W SlattumDepartment of Pharmacotherapy & Outcomes Science Geriatric Pharmacotherapy Program, School of Pharmacy Virginia Commonwealth University Richmond VA USA.
Martina MuellerMedical University of South Carolina School of Nursing Charleston North Carolina USA.
Stefania BandinelliLaboratory of Clinical Epidemiology InCHIANTI Study Group Local Health Unit Tuscany Center Florence Italy.
Qu TianLongitudinal Studies Section Translational Gerontology Branch National Institute on Aging Baltimore Maryland USA.
Theresa Swift-ScanlanVirginia Commonwealth University School of Nursing Richmond Virginia USA.
Sarah K LagemanDepartment of Neurology Virginia Commonwealth School of Medicine Richmond Virginia USA.
Andrew SingletonLaboratory of Neurogenetics National Institute on Aging National Institutes of Health Bethesda Maryland USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionWe describe findings from a large study that provide empirical support for the emerging construct of cognitive frailty and put forth a theoretical framework that may advance the future study of complex aging conditions. While cognitive impairment and physical frailty have long been studied as separate constructs, recent studies suggest they share common etiologies. We aimed to create a population predictive model to gain an understanding of the underlying biological mechanisms for the relationship between physical frailty and cognitive impairment.

methodsData were obtained from the longitudinal "

resultsWe developed two highly accurate predictive models, with a Model I area under the curve (AUC) of 0.88 (95% confidence interval [CI] 0.83-0.90) and a Model II AUC of 0.86 (95% CI 0.80-0.90). These models indicate cognitive frailty is driven by dysregulation across multiple cellular processes including genetic alterations, nutrient and lipid metabolism, and elevated levels of circulating pro-inflammatory proteins. DISCUSSION: While our results establish a foundation for understanding the underlying biological mechanisms for the relationship between cognitive decline and physical frailty, further examination of the molecular pathways associated with our predictive biomarkers is warranted. Our framework is in alignment with other proposed biological underpinnings of Alzheimer's disease such as genetic alterations, immune system dysfunction, and neuroinflammation.

Indexed as

bioinformaticscognitive frailtycognitive impairmentfrailtymachine learning

Identifiers

PMID32685657
PMCPMC7362211

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.