Evidence map›Paper›PMID 31726991›Full record

ArticleBMC genomics2019

Transcriptional profiling predicts running promotes cerebrovascular remodeling in young but not midlife mice.

Kate E Foley, Hongtian Stanley Yang, Leah C Graham, Gareth R Howell

Abstract read
In one paragraph

Article in BMC genomics, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
–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

5 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. TheFrontiers in aging neuroscience · 2022
    Article
  5. Alzheimer's & dementia (New York, N. Y.) · 2022
    Article
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

4 authors.

Kate E FoleyThe Jackson Laboratory, 600 Main Street, Bar Harbor, ME, 04609, USA.
Hongtian Stanley YangThe Jackson Laboratory, 600 Main Street, Bar Harbor, ME, 04609, USA.
Leah C GrahamThe Jackson Laboratory, 600 Main Street, Bar Harbor, ME, 04609, USA.
Gareth R HowellThe Jackson Laboratory, 600 Main Street, Bar Harbor, ME, 04609, USA. Gareth.Howell@jax.org.ORCID http://orcid.org/0000-0003-0565-6474

Funding

REPRODUCTIVE BIOLOGYT32HD007065 · NICHD · JACKSON LABORATORY · PI BRAUN, ROBERT E · 1985 to 2020
$2.6M
National Institute of Child Health and Human Development T32HD007065NICHD NIH HHS T32 HD007065
6 · The paper itself

Abstract

backgroundThe incidence of dementia and cognitive decline is increasing with no therapy or cure. One of the reasons treatment remains elusive is because there are various pathologies that contribute to age-related cognitive decline. Specifically, with Alzheimer's disease, targeting to reduce amyloid beta plaques and phosphorylated tau aggregates in clinical trials has not yielded results to slow symptomology, suggesting a new approach is needed. Interestingly, exercise has been proposed as a potential therapeutic intervention to improve brain health and reduce the risk for dementia, however the benefits throughout aging are not well understood.

resultsTo better understand the effects of exercise, we preformed transcriptional profiling on young (1-2 months) and midlife (12 months) C57BL/6 J (B6) male mice after 12 weeks of voluntary running. Data was compared to age-matched sedentary controls. Interestingly, the midlife running group naturally broke into two cohorts based on distance ran - either running a lot and more intensely (high runners) or running less and less intensely (low runners). Midlife high runners had lower LDL cholesterol as well as lower adiposity (%fat) compared to sedentary, than midlife low runners compared to sedentary suggesting more intense running lowered systemic markers of risk for age-related diseases including dementias. Differential gene analysis of transcriptional profiles generated from the cortex and hippocampus showed thousands of differentially expressed (DE) genes when comparing young runners to sedentary controls. However, only a few hundred genes were DE comparing either midlife high runners or midlife low runners to midlife sedentary controls. This indicates that, in our study, the effects of running are reduced through aging. Gene set enrichment analyses identified enrichment of genes involved in extracellular matrix (ECM), vascular remodeling and angiogenesis in young runners but not midlife runners. These genes are known to be expressed in multiple vascular-related cell types including astrocytes, endothelial cells, pericytes and smooth muscle cells.

conclusionsTaken together these results suggest running may best serve as a preventative measure to reduce risk for cerebrovascular decline. Ultimately, this work shows that exercise may be more effective to prevent dementia if introduced at younger ages.

Indexed as

Cerebrovascular CirculationGene Expression ProfilingRunningTranscriptomeAge FactorsAnimalsCerebral CortexComputational BiologyExtracellular MatrixGene Expression RegulationGene OntologyMaleMiceModels, BiologicalOrgan SpecificityVascular RemodelingAngiogenesisBasement membraneCerebrovasculatureEndothelial cellsExerciseExtracellular matrixGenomicsMidlifeRunningVascular compromise

Identifiers

PMID31726991
PMCPMC6854620

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LicenceCC BY
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Registered trials

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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.