Evidence map›Paper›PMID 36653878›Full record

ArticleActa neuropathologica communications2023

Sleep fragmentation affects glymphatic system through the different expression of AQP4 in wild type and 5xFAD mouse models.

Valeria Vasciaveo, Antonella Iadarola, Antonino Casile, Davide Dante, Giulia Morello, Lorenzo Minotta, Elena Tamagno, Alessandro Cicolin, Michela Guglielmotto

Abstract read
In one paragraph

Article in Acta neuropathologica communications, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing 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

43 citing papers in PubMed.

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  13. Wake-promoting neuromodulators in Alzheimer's disease: Implications for sleep and brain clearance.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026
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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.

Valeria VasciaveoDepartment of Neuroscience Rita Levi Montalcini, University of Torino, Via Cherasco 15, 10126, Turin, Italy.
Antonella IadarolaDepartment of Neuroscience and Mental Health, AOU Città della Salute e della Scienza, Corso Bramante 88, 10126, Turin, Italy.
Antonino CasileSchool of Pharmacy, Pharmacology Unit, University of Camerino, Via Madonna delle Carceri, 9, 62032, Camerino, MC, Italy.
Davide DanteNeuroscience Institute of Cavalieri Ottolenghi Foundation (NICO), University of Torino, Regione Gonzole 10, 10043, Orbassano, Turin, Italy.
Giulia MorelloDepartment of Neuroscience Rita Levi Montalcini, University of Torino, Via Cherasco 15, 10126, Turin, Italy.
Lorenzo MinottaNeuroscience Institute of Cavalieri Ottolenghi Foundation (NICO), University of Torino, Regione Gonzole 10, 10043, Orbassano, Turin, Italy.
Elena TamagnoDepartment of Neuroscience Rita Levi Montalcini, University of Torino, Via Cherasco 15, 10126, Turin, Italy.
Alessandro CicolinDepartment of Neuroscience Rita Levi Montalcini, University of Torino, Via Cherasco 15, 10126, Turin, Italy.
Michela GuglielmottoDepartment of Neuroscience Rita Levi Montalcini, University of Torino, Via Cherasco 15, 10126, Turin, Italy. michela.guglielmotto@unito.it.ORCID 0000-0002-3900-9876

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is characterized by genetic and multifactorial risk factors. Many studies correlate AD to sleep disorders. In this study, we performed and validated a mouse model of AD and sleep fragmentation, which properly mimics a real condition of intermittent awakening. We noticed that sleep fragmentation induces a general acceleration of AD progression in 5xFAD mice, while in wild type mice it affects cognitive behaviors in particular learning and memory. Both these events may be correlated to aquaporin-4 (AQP4) modulation, a crucial player of the glymphatic system activity. In particular, sleep fragmentation differentially affects aquaporin-4 channel (AQP4) expression according to the stage of the disease, with an up-regulation in younger animals, while such change cannot be detected in older ones. Moreover, in wild type mice sleep fragmentation affects cognitive behaviors, in particular learning and memory, by compromising the glymphatic system through the decrease of AQP4. Nevertheless, an in-depth study is needed to better understand the mechanism by which AQP4 is modulated and whether it could be considered a risk factor for the disease development in wild type mice. If our hypotheses are going to be confirmed, AQP4 modulation may represent the convergence point between AD and sleep disorder pathogenic mechanisms.

Indexed as

Alzheimer DiseaseAquaporin 4Glymphatic SystemSleep Wake DisordersAmyloid beta-PeptidesAnimalsBrainDisease Models, AnimalMiceMice, TransgenicSleep DeprivationAmyloid beta-PeptidesAqp4 protein, mouseAquaporin 4Alzheimer’s diseaseAmyloid-βAquaporin-4 channelNeuroinflammationp-tauSleep fragmentation

Identifiers

PMID36653878
PMCPMC9850555

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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.