Evidence map›Paper›PMID 31833194›Full record

ReviewAging cell2020

Measuring biological aging in humans: A quest.

Luigi Ferrucci, Marta Gonzalez-Freire, Elisa Fabbri, Eleanor Simonsick, Toshiko Tanaka, Zenobia Moore, Shabnam Salimi, Felipe Sierra, Rafael de Cabo

Open access · goldAbstract readReview
PubMed Full text at PMC Publisher
In one paragraph

Review in Aging cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 466 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
466citing papers in PubMed, 4 pooled it
44.5field-weighted citation impact, top 1% of its field
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

466 citing papers in PubMed, 4 syntheses or guidelines pooled it, 742 citations in OpenAlex.

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406 more citing papers are in PubMed but not listed here.

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

9 authors at 3 institutions in 3 countries.

Luigi FerrucciTranslational Gerontology Branch, Biomedical Research Center, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Marta Gonzalez-FreireTranslational Gerontology Branch, Biomedical Research Center, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Elisa FabbriTranslational Gerontology Branch, Biomedical Research Center, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Eleanor SimonsickTranslational Gerontology Branch, Biomedical Research Center, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Toshiko TanakaTranslational Gerontology Branch, Biomedical Research Center, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Zenobia MooreTranslational Gerontology Branch, Biomedical Research Center, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.
Shabnam SalimiDepartment of Epidemiology and Public Health, University of Maryland School of Medicine, Baltimore, MD, USA.
Felipe SierraDivision of Aging Biology, National Institute on Aging, NIH, Bethesda, MD, USA.
Rafael de CaboTranslational Gerontology Branch, Biomedical Research Center, National Institute on Aging, National Institutes of Health, Baltimore, MD, USA.ORCID 0000-0002-3354-2442
National Institutes of Health · USNational Institute on Aging · USUniversity of Maryland, Baltimore · US

Funding

DNA methylation markers of Multimorbidity in Aging Humans and MiceK01AG059898 · NIA · UNIVERSITY OF WASHINGTON · PI SALIMI, SHABNAM · 2019 to 2023
$613k
NIA NIH HHS K01 AG059898NIH HHS
6 · The paper itself

Abstract

The global population of individuals over the age of 65 is growing at an unprecedented rate and is expected to reach 1.6 billion by 2050. Most older individuals are affected by multiple chronic diseases, leading to complex drug treatments and increased risk of physical and cognitive disability. Improving or preserving the health and quality of life of these individuals is challenging due to a lack of well-established clinical guidelines. Physicians are often forced to engage in cycles of "trial and error" that are centered on palliative treatment of symptoms rather than the root cause, often resulting in dubious outcomes. Recently, geroscience challenged this view, proposing that the underlying biological mechanisms of aging are central to the global increase in susceptibility to disease and disability that occurs with aging. In fact, strong correlations have recently been revealed between health dimensions and phenotypes that are typical of aging, especially with autophagy, mitochondrial function, cellular senescence, and DNA methylation. Current research focuses on measuring the pace of aging to identify individuals who are "aging faster" to test and develop interventions that could prevent or delay the progression of multimorbidity and disability with aging. Understanding how the underlying biological mechanisms of aging connect to and impact longitudinal changes in health trajectories offers a unique opportunity to identify resilience mechanisms, their dynamic changes, and their impact on stress responses. Harnessing how to evoke and control resilience mechanisms in individuals with successful aging could lead to writing a new chapter in human medicine.

Indexed as

AgingAnimalsCellular SenescenceEpigenesis, GeneticGenomic InstabilityGeriatricsHumansInflammationMitochondriaMorbidityProteostasisReactive Oxygen SpeciesStem CellsTelomere HomeostasisReactive Oxygen Speciesagingbiological aginghallmarks of aginginflammationmultimorbidityresiliencesenescence

Identifiers

PMID31833194
PMCPMC6996955
OpenAlexW2995774252

What OpenQuestion holds

Textmetadata
LicenceCC BY
Read underepoch 390

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.