Evidence map›Paper›PMID 28843509›Full record

ArticleExperimental gerontology2017

Walking speed decline in older adults is associated with elevated pro-BDNF in plasma extracellular vesicles.

Caitlin N Suire, Erez Eitan, Nancy Chiles Shaffer, Qu Tian, Stephanie Studenski, Mark P Mattson, Dimitrios Kapogiannis

Abstract read
In one paragraph

Article in Experimental gerontology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
4.9field-weighted citation impact, top 4% 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

36 citing papers in PubMed, 49 citations in OpenAlex.

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  10. Hitting the target: cell signaling pathways modulation by extracellular vesicles.Extracellular vesicles and circulating nucleic acids · 2024
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  18. Extracellular Vesicles in CNS Developmental Disorders.International journal of molecular sciences · 2020
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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

7 authors at 1 institution in 1 country.

Caitlin N SuireLaboratory of Neurosciences, National Institute on Aging on Intramural Research Program, Baltimore, MD 21224, United States.
Erez EitanLaboratory of Neurosciences, National Institute on Aging on Intramural Research Program, Baltimore, MD 21224, United States.
Nancy Chiles ShafferTranslational Gerontology Branch, National Institute on Aging on Intramural Research Program, Baltimore, MD 21224, United States.
Qu TianTranslational Gerontology Branch, National Institute on Aging on Intramural Research Program, Baltimore, MD 21224, United States.
Stephanie StudenskiTranslational Gerontology Branch, National Institute on Aging on Intramural Research Program, Baltimore, MD 21224, United States.
Mark P MattsonLaboratory of Neurosciences, National Institute on Aging on Intramural Research Program, Baltimore, MD 21224, United States.
Dimitrios KapogiannisLaboratory of Neurosciences, National Institute on Aging on Intramural Research Program, Baltimore, MD 21224, United States. Electronic address: kapogiannisd@mail.nih.gov.
National Institute on Aging · US

Funding

Studies in Dementia and Neurodegenerative DiseasesZIAAG000975 · NIA · NATIONAL INSTITUTE ON AGING · PI KAPOGIANNIS, DIMITRIOS · 2009 to 2025
$31.5M
Intramural NIH HHS Z99 AG999999Intramural NIH HHS ZIA AG000975
6 · The paper itself

Abstract

backgroundBrain-derived neurotrophic factor (BDNF) is produced by cleavage of proBDNF, and BDNF and proBDNF may play antagonistic roles in nervous system development, learning, memory and neuronal stress resistance. BDNF and proBDNF are present in blood, but the origin and relative contributions of soluble and extracellular vesicle (EV)-associated levels are unknown.

methodsIn this study we used validated immunoassays to measure proBDNF and BDNF levels in plasma, total plasma EVs and a subpopulation of EVs enriched for neuronal origin (expressing the neuronal marker L1CAM) in 150 Baltimore Longitudinal Study of Aging participants with and without decline in walking speed (reflecting aging-associated motor decline).

resultsLevels of BDNF and proBDNF were highest in L1CAM+ EVs. Participants with walking speed decline had higher levels of proBDNF in L1CAM+ EVs compared to non-decliners, but no differences in proBDNF levels in plasma and total EV.

conclusionsOur findings suggest that levels of proBDNF and BDNF in circulating L1CAM+ EVs might be used as biomarkers for conditions involving altered BDNF signaling.

Indexed as

Walking SpeedAgedAged, 80 and overAge FactorsAgingBiomarkersBrain-Derived Neurotrophic FactorEnzyme-Linked Immunosorbent AssayExercise TestExtracellular VesiclesFemaleHumansMaleNeural Cell Adhesion Molecule L1Protein PrecursorsTime FactorsBDNF protein, humanBiomarkersBrain-Derived Neurotrophic Factorbrain-derived neurotrophic factor precursorNeural Cell Adhesion Molecule L1Protein PrecursorsAgingBDNFBLSAExosomesExtracellular vesiclesMotor functionproBDNFWalking speed

Identifiers

PMID28843509
PMCPMC5642035
OpenAlexW2745342799

What OpenQuestion holds

Textmetadata
LicenceTDM
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.