Evidence map›Paper›PMID 32933545›Full record

ArticleJournal of neuroinflammation2020

Astrocyte remodeling in the beneficial effects of long-term voluntary exercise in Alzheimer's disease.

Irina Belaya, Mariia Ivanova, Annika Sorvari, Marina Ilicic, Sanna Loppi, Hennariikka Koivisto, Alessandra Varricchio, Heikki Tikkanen, Frederick R Walker, Mustafa Atalay and 4 more

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

Article in Journal of neuroinflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
50citing papers in PubMed, 3 pooled it
5.1field-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

50 citing papers in PubMed, 3 syntheses or guidelines pooled it, 86 citations in OpenAlex.

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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

14 authors at 3 institutions in 2 countries.

Irina BelayaA.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, FI-70211, Kuopio, Finland.
Mariia IvanovaA.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, FI-70211, Kuopio, Finland.
Annika SorvariA.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, FI-70211, Kuopio, Finland.
Marina IlicicSchool of Biomedical Sciences and Pharmacy and the Priority Research Centre for Stroke and Brain Injury, The University of Newcastle, University Dr, Callaghan, NSW, 2308, Australia.
Sanna LoppiA.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, FI-70211, Kuopio, Finland.
Hennariikka KoivistoA.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, FI-70211, Kuopio, Finland.
Alessandra VarricchioA.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, FI-70211, Kuopio, Finland.
Heikki TikkanenInstitute of Biomedicine, University of Eastern Finland, FI-70211, Kuopio, Finland.
Frederick R WalkerSchool of Biomedical Sciences and Pharmacy and the Priority Research Centre for Stroke and Brain Injury, The University of Newcastle, University Dr, Callaghan, NSW, 2308, Australia.
Mustafa AtalayInstitute of Biomedicine, University of Eastern Finland, FI-70211, Kuopio, Finland.
Tarja MalmA.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, FI-70211, Kuopio, Finland.
Alexandra GrubmanDepartment of Anatomy and Developmental Biology, Monash University, Melbourne, Australia.
Heikki TanilaA.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, FI-70211, Kuopio, Finland.
Katja M KanninenA.I. Virtanen Institute for Molecular Sciences, University of Eastern Finland, FI-70211, Kuopio, Finland. katja.kanninen@uef.fi.ORCID http://orcid.org/0000-0002-6717-8589
University of Eastern Finland · FIUniversity of Newcastle Australia · AUAustralian Regenerative Medicine Institute · AU

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundIncreased physical exercise improves cognitive function and reduces pathology associated with Alzheimer's disease (AD). However, the mechanisms underlying the beneficial effects of exercise in AD on the level of specific brain cell types remain poorly investigated. The involvement of astrocytes in AD pathology is widely described, but their exact role in exercise-mediated neuroprotection warrant further investigation. Here, we investigated the effect of long-term voluntary physical exercise on the modulation of the astrocyte state.

methodsMale 5xFAD mice and their wild-type littermates had free access to a running wheel from 1.5 to 7 months of age. A battery of behavioral tests was used to assess the effects of voluntary exercise on cognition and learning. Neuronal loss, impairment in neurogenesis, beta-amyloid (Aβ) deposition, and inflammation were evaluated using a variety of histological and biochemical measurements. Sophisticated morphological analyses were performed to delineate the specific involvement of astrocytes in exercise-induced neuroprotection in the 5xFAD mice.

resultsLong-term voluntary physical exercise reversed cognitive impairment in 7-month-old 5xFAD mice without affecting neurogenesis, neuronal loss, Aβ plaque deposition, or microglia activation. Exercise increased glial fibrillary acid protein (GFAP) immunoreactivity and the number of GFAP-positive astrocytes in 5xFAD hippocampi. GFAP-positive astrocytes in hippocampi of the exercised 5xFAD mice displayed increases in the numbers of primary branches and in the soma area. In general, astrocytes distant from Aβ plaques were smaller in size and possessed simplified processes in comparison to plaque-associated GFAP-positive astrocytes. Morphological alterations of GFAP-positive astrocytes occurred concomitantly with increased astrocytic brain-derived neurotrophic factor (BDNF) and restoration of postsynaptic protein PSD-95.

conclusionsVoluntary physical exercise modulates the reactive astrocyte state, which could be linked via astrocytic BDNF and PSD-95 to improved cognition in 5xFAD hippocampi. The molecular pathways involved in this modulation could potentially be targeted for benefit against AD.

Indexed as

Alzheimer DiseaseAnimalsAstrocytesExercise TestHippocampusInflammation MediatorsMaleMaze LearningMiceMice, TransgenicPhysical Conditioning, AnimalTreatment OutcomeInflammation Mediators5xFAD mouseAlzheimer’s diseaseAstrocyteBDNFBehaviorGFAPMorphologyVoluntary exercise

Identifiers

PMID32933545
PMCPMC7493971
OpenAlexW3086184545

What Socratic 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 Socratic graph.