Evidence map›Paper›PMID 31606888›Full record

ArticleTranslational stroke research2020

Treadmill Exercise Suppresses Cognitive Decline and Increases White Matter Oligodendrocyte Precursor Cells in a Mouse Model of Prolonged Cerebral Hypoperfusion.

Ryo Ohtomo, Keita Kinoshita, Gaku Ohtomo, Hajime Takase, Gen Hamanaka, Kazuo Washida, Mohammad Rashedul Islam, Christiane D Wrann, Hiroshi Katsuki, Atsushi Iwata and 3 more

Open access · greenAbstract read
In one paragraph

Article in Translational stroke research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

22 citing papers in PubMed, 33 citations in OpenAlex.

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  10. A brief overview of a mouse model of cerebral hypoperfusion by bilateral carotid artery stenosis.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2023
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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

13 authors at 3 institutions in 2 countries.

Ryo OhtomoNeuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, MGH East 149-2401, Charlestown, MA, 02129, USA.
Keita KinoshitaDepartment of Chemico-Pharmacological Sciences, Graduate School of Pharmaceutical Sciences, Kumamoto University, Kumamoto, 862-0973, Japan.
Gaku OhtomoDepartment of Neurology, The University of Tokyo Graduate School of Medicine, Tokyo, Japan.
Hajime TakaseNeuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, MGH East 149-2401, Charlestown, MA, 02129, USA.
Gen HamanakaNeuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, MGH East 149-2401, Charlestown, MA, 02129, USA.
Kazuo WashidaNeuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, MGH East 149-2401, Charlestown, MA, 02129, USA.
Mohammad Rashedul IslamCardiovascular Research Center, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, 02129, USA.
Christiane D WrannCardiovascular Research Center, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, 02129, USA.
Hiroshi KatsukiDepartment of Chemico-Pharmacological Sciences, Graduate School of Pharmaceutical Sciences, Kumamoto University, Kumamoto, 862-0973, Japan.
Atsushi IwataDepartment of Neurology, The University of Tokyo Graduate School of Medicine, Tokyo, Japan.
Josephine LokNeuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, MGH East 149-2401, Charlestown, MA, 02129, USA.
Eng H LoNeuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, MGH East 149-2401, Charlestown, MA, 02129, USA.
Ken AraiNeuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, MGH East 149-2401, Charlestown, MA, 02129, USA. karai@partners.org.ORCID 0000-0003-1615-3258
Harvard University · USKumamoto University · JPThe University of Tokyo · JP

Funding

Targeting ROCK for Neurogliovascular Plasticity & Remodeling After StrokeP01NS055104 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI LO, ENG H. · 2007 to 2018
$13.3M
Oligo-Vascular Signaling in StrokeR01NS065089 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI ARAI, KEN · 2010 to 2019
$3.8M
Role of Tau Conformations in Vascular Contribution to Cognitive Impairment and DementiaR01AG055559 · NIA · BETH ISRAEL DEACONESS MEDICAL CENTER · PI LO, ENG H., SHEHADAH, AMJAD · 2017 to 2021
$3.4M
Effects of Hypertension and Hypoperfusion on the Brain VasculomeR01NS110818 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI ARAI, KEN, LO, ENG H. · 2019 to 2019
$2.4M
Oligodendrocyte Precursor Cells Regulate White Matter Remodeling in Vascular Cognitive Impairment and DementiaR01NS113556 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI ARAI, KEN · 2019 to 2023
$2.4M
Comparative transcriptome of brain blood vessels: age, hypertension and diabetesRC2NS069335 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI LO, ENG H. · 2009 to 2010
$1.3M
Aging dampens compensatory angiogenesis via downregulation of VEGF signaling in subcortical ischemic vascular dementiaR21AG066478 · NIA · MASSACHUSETTS GENERAL HOSPITAL · PI ARAI, KEN · 2020 to 2020
$453k
Japan Society for the Promotion of Science 16H05319NIA NIH HHS R01 AG055559NIA NIH HHS R21 AG066478NIH HHS P01 NS055104NIH HHS R01 AG055559NINDS NIH HHS P01 NS055104NINDS NIH HHS R01 NS065089NINDS NIH HHS R01 NS110818NINDS NIH HHS R01 NS113556NINDS NIH HHS RC2 NS069335
6 · The paper itself

Abstract

Clinical evidence suggests that patients with subcortical ischemic vascular dementia (SIVD) perform better at cognitive tests after exercise. However, the underlying mechanism for this effect is largely unknown. Here, we examined how treadmill exercise changes the cognitive function and white matter cellular pathology in a mouse model of SIVD. Prolonged cerebral hypoperfusion was induced in 2-month-old male C57BL/6J mice by bilateral common carotid artery stenosis. A week later, the mice were randomly divided into a group that received 6-week treadmill exercise and a sedentary group for observation. In multiple behavioral tests (Y-maze, novel object recognition, and Morris water maze tests), the treadmill exercise training was shown to ameliorate cognitive decline in the hypoperfused SIVD mice. In addition, immunohistological analyses confirmed that there was a larger population of oligodendrocyte precursor cells in the subventricular zone of exercised versus sedentary mice. Although further investigations are needed to confirm a causal link between these findings, our study establishes a model and cellular foundation for investigating the mechanisms through which exercise preserves cognitive function in SIVD.

Indexed as

AnimalsCognitive DysfunctionDementia, VascularDisease Models, AnimalMaleMice, Inbred C57BLOligodendrocyte Precursor CellsPhysical Conditioning, AnimalWhite MatterOligodendrocyte precursor cellSubcortical ischemic vascular dementiaSubventricular zoneTreadmill exerciseWhite matter

Identifiers

PMID31606888
PMCPMC7298669
OpenAlexW2979507254

What OpenQuestion holds

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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.