Evidence map›Paper›PMID 29203796›Full record

ArticleScientific reports2017

Aerobic exercise and a BDNF-mimetic therapy rescue learning and memory in a mouse model of Down syndrome.

Martina Parrini, Diego Ghezzi, Gabriele Deidda, Lucian Medrihan, Enrico Castroflorio, Micol Alberti, Pietro Baldelli, Laura Cancedda, Andrea Contestabile

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers, 3 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed, 3 pooled it
6.2field-weighted citation impact, top 3% 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

46 citing papers in PubMed, 3 syntheses or guidelines pooled it, 75 citations in OpenAlex.

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  15. Molecular origin and biological effects of exercise mimetics.Journal of exercise science and fitness · 2024
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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

9 authors at 2 institutions in 4 countries.

Martina ParriniDepartment of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, Genova, Italy.
Diego GhezziDepartment of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, Genova, Italy.ORCID 0000-0002-0554-7510
Gabriele DeiddaDepartment of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, Genova, Italy.
Lucian MedrihanDepartment of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, Genova, Italy.
Enrico CastroflorioCenter for Synaptic Neuroscience, Istituto Italiano di Tecnologia, Genova, Italy.
Micol AlbertiDepartment of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, Genova, Italy.
Pietro BaldelliCenter for Synaptic Neuroscience, Istituto Italiano di Tecnologia, Genova, Italy.ORCID 0000-0001-9599-3436
Laura CanceddaDepartment of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, Genova, Italy.ORCID 0000-0003-0566-057X
Andrea ContestabileDepartment of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, Genova, Italy. andrea.contestabile@iit.it.ORCID 0000-0002-5417-4722
Italian Institute of Technology · ITUniversity of Malta · MT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Down syndrome (DS) is caused by the triplication of human chromosome 21 and represents the most frequent genetic cause of intellectual disability. The trisomic Ts65Dn mouse model of DS shows synaptic deficits and reproduces the essential cognitive disabilities of the human syndrome. Aerobic exercise improved various neurophysiological dysfunctions in Ts65Dn mice, including hippocampal synaptic deficits, by promoting synaptogenesis and neurotransmission at glutamatergic terminals. Most importantly, the same intervention also prompted the recovery of hippocampal adult neurogenesis and synaptic plasticity and restored cognitive performance in trisomic mice. Additionally, the expression of brain-derived neurotrophic factor (BDNF) was markedly decreased in the hippocampus of patients with DS. Since the positive effect of exercise was paralleled by increased BDNF expression in trisomic mice, we investigated the effectiveness of a BDNF-mimetic treatment with 7,8-dihydroxyflavone at alleviating intellectual disabilities in the DS model. Pharmacological stimulation of BDNF signaling rescued synaptic plasticity and memory deficits in Ts65Dn mice. Based on our findings, Ts65Dn mice benefit from interventions aimed at promoting brain plasticity, and we provide evidence that BDNF signaling represents a potentially new pharmacological target for treatments aimed at rescuing cognitive disabilities in patients with DS.

Indexed as

AnimalsBrain-Derived Neurotrophic FactorDisease Models, AnimalDown SyndromeExcitatory Postsynaptic PotentialsFemaleFlavonesHippocampusHumansLearningMaleMemoryMiceMice, Inbred C57BLMice, TransgenicNeurogenesis6,7-dihydroxyflavoneBrain-Derived Neurotrophic FactorFlavones

Identifiers

PMID29203796
PMCPMC5715062
OpenAlexW2769573610

What OpenQuestion holds

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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.