Evidence map›Paper›PMID 35142700›Full record

ArticleNeural regeneration research2022

Aquaporin 4 deficiency eliminates the beneficial effects of voluntary exercise in a mouse model of Alzheimer's disease.

Yun Liu, Pan-Pan Hu, Shuang Zhai, Wei-Xi Feng, Rui Zhang, Qian Li, Charles Marshall, Ming Xiao, Ting Wu

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

Article in Neural regeneration research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 42 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed, 2 pooled it
5.0field-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

42 citing papers in PubMed, 2 syntheses or guidelines pooled it, 56 citations in OpenAlex.

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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

9 authors at 4 institutions in 2 countries.

Yun LiuDepartment of Neurology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China.
Pan-Pan HuJiangsu Province Key Laboratory of Neurodegeneration, Nanjing Medical University; Brain Institute, the Affiliated Nanjing Brain Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China.
Shuang ZhaiDepartment of Neurology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China.
Wei-Xi FengJiangsu Province Key Laboratory of Neurodegeneration, Nanjing Medical University; Brain Institute, the Affiliated Nanjing Brain Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China.
Rui ZhangDepartment of Neurology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China.
Qian LiDepartment of Neurology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China.
Charles MarshallCollege of Health Sciences, University of Kentucky Center of Excellence in Rural Health, Hazard, KY, USA.
Ming XiaoJiangsu Province Key Laboratory of Neurodegeneration, Nanjing Medical University; Brain Institute, the Affiliated Nanjing Brain Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China.
Ting WuDepartment of Neurology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China.
Nanjing Medical University · CNJiangsu Province Hospital · CNNanjing Brain Hospital · CNUniversity of Kentucky · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Regular exercise has been shown to reduce the risk of Alzheimer's disease (AD). Our previous study showed that the protein aquaporin 4 (AQP4), which is specifically expressed on the paravascular processes of astrocytes, is necessary for glymphatic clearance of extracellular amyloid beta (Aβ) from the brain, which can delay the progression of Alzheimer's disease. However, it is not known whether AQP4-regulated glymphatic clearance of extracellular Aβ is involved in beneficial effects of exercise in AD patients. Our results showed that after 2 months of voluntary wheel exercise, APP/PS1 mice that were 3 months old at the start of the intervention exhibited a decrease in Aβ burden, glial activation, perivascular AQP4 mislocalization, impaired glymphatic transport, synapse protein loss, and learning and memory defects compared with mice not subjected to the exercise intervention. In contrast, APP/PS1 mice that were 7 months old at the start of the intervention exhibited impaired AQP4 polarity and reduced glymphatic clearance of extracellular Aβ, and the above-mentioned impairments were not alleviated after the 2-month exercise intervention. Compared with age-matched APP/PS1 mice, AQP4 knockout APP/PS1 mice had more serious defects in glymphatic function, Aβ plaque deposition, and cognitive impairment, which could not be alleviated after the exercise intervention. These findings suggest that AQP4-dependent glymphatic transport is the neurobiological basis for the beneficial effects of voluntary exercises that protect against the onset of AD.

Indexed as

Alzheimer’s diseaseamyloid-betaaquaporin-4astrocytesglymphatic systemlearning and memorysynaptic proteintransgenic micevoluntary exercise

Identifiers

PMID35142700
PMCPMC8848602
OpenAlexW4210962963

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.