Evidence map›Paper›PMID 41065132›Full record

ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2025

Intestinal inflammation induces glymphatic remodeling, priming early neurodegenerative signals in male mice.

Clara Ciampi, Francesca Fagiani, Valentina Murtaj, Federica Comella, Veronica Torre, Marta Filibian, Annapaola Andolfo, Clarissa Braccia, Nicola Opallo, Maria Grazia Bottone and 11 more

Abstract read
In one paragraph

Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing 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

7 citing papers in PubMed.

  1. Article
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  7. Intestinal inflammation induces glymphatic remodeling, priming early neurodegenerative signals in male mice.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025
    Article
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

21 authors.

Clara CiampiDepartment of Neuroscience, Psychology, Drug Research and Child Health-NEUROFARBA, Pharmacology and Toxicology Section, University of Florence, Florence, Italy.
Francesca FagianiDepartment of Drug Sciences, University of Pavia, Pavia, Italy.
Valentina MurtajDivision of Neuroscience, Vita-Salute San Raffaele University, Milan, Italy.
Federica ComellaDepartment of Pharmacy, School of Medicine, University of Naples "Federico II,", Naples, Italy.
Veronica TorreDepartment of Pharmacy, University of Genoa, Genoa, Italy.
Marta FilibianCentro Grandi Strumenti, University of Pavia, Pavia, Italy.
Annapaola AndolfoProMeFa, Proteomics and Metabolomics Facility, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Clarissa BracciaProMeFa, Proteomics and Metabolomics Facility, IRCCS San Raffaele Scientific Institute, Milan, Italy.
Nicola OpalloDepartment of Drug Sciences, University of Pavia, Pavia, Italy.
Maria Grazia BottoneDepartment of Biology and Biotechnology, Laboratory of Cellular Biology and Neurobiology, University of Pavia, Pavia, Italy.
Edoardo PedriniCenter for Omic Sciences, Vita-Salute San Raffaele University, Milan, Italy.
Elena LucariniDepartment of Neuroscience, Psychology, Drug Research and Child Health-NEUROFARBA, Pharmacology and Toxicology Section, University of Florence, Florence, Italy.
Maria BoveDepartment of Clinical and Experimental Medicine, University of Foggia, Foggia, Italy.
Stefano GovoniDepartment of Drug Sciences, University of Pavia, Pavia, Italy.
Carla GhelardiniDepartment of Neuroscience, Psychology, Drug Research and Child Health-NEUROFARBA, Pharmacology and Toxicology Section, University of Florence, Florence, Italy.
Rosaria MeliDepartment of Pharmacy, School of Medicine, University of Naples "Federico II,", Naples, Italy.
Luigia TrabaceDepartment of Clinical and Experimental Medicine, University of Foggia, Foggia, Italy.
Anna PittalugaDepartment of Pharmacy, University of Genoa, Genoa, Italy.
Giuseppina Mattace RasoDepartment of Pharmacy, School of Medicine, University of Naples "Federico II,", Naples, Italy.
Lorenzo Di Cesare MannelliDepartment of Neuroscience, Psychology, Drug Research and Child Health-NEUROFARBA, Pharmacology and Toxicology Section, University of Florence, Florence, Italy.
Cristina LanniDepartment of Drug Sciences, University of Pavia, Pavia, Italy.

Funding

Italian Ministry of University and Research PRIN 2020SCBBN2Italian Ministry of University and Research PRIN P2022Y9W3RItalian Society of PharmacologyNational Recovery and Resilience Plan - MNESYS PE0000006Università degli Studi di Pavia AARG-23-1140660
6 · The paper itself

Abstract

introductionInflammatory bowel disease triggers extraintestinal manifestations, including in the central nervous system (CNS). However, the direct impact of peripheral inflammation on the CNS is largely unknown.

methodsUsing a mouse model of colitis with pain and anxiety-like behavior, we investigated the intricate pathogenic link between colonic inflammation, disruptions in circadian rhythmicity and impaired glymphatic circulation.

resultsBy in vivo magnetic resonance imaging, we observed a derangement of brain fluid dynamics, with a significant enlargement of the cerebral lateral ventricles and waste deposition within the brain parenchyma. Proteomics revealed changes in cerebrospinal fluid (CSF) composition, enriched in proteins related to inflammation, immune response, complement, neuronal, and lipid metabolic pathways. Alterations in brain metabolite concentrations and in inhibitory control mechanisms and excitatory transmission were detected. DISCUSSION: Colonic inflammation induces remodeling in CSF volume distribution, clearance, and metabolism, with derangement of the crosstalk between neurons and astrocytes, priming synaptopathy. HIGHLIGHTS: An acute peripheral inflammatory trigger affects the central level by remodeling central nervous system (CNS) fluid distribution and priming early signals of synaptopathy. A single dextran sulfate sodium (DSS) challenge disrupts the circadian clock machinery and alters CNS fluid distribution, a so far neglected system, thereby impairing glymphatic clearance of waste products and indirectly altering neurotransmitter release dynamics. These combined effects ultimately impact brain function, extending to the regulation of behavior. Understanding how an intestinal inflammatory insult may derange the daily rhythm of the mechanisms controlling brain waste disposal may help identify specific groups of subjects at high risk of developing neurological disorders.

Indexed as

BrainColitisGlymphatic SystemInflammationInflammatory Bowel DiseasesNeurodegenerative DiseasesAnimalsCircadian RhythmDisease Models, AnimalMagnetic Resonance ImagingMaleMiceMice, Inbred C57BLaquaporin‐4brain waste clearancecircadian regulationdextran sulfate sodium–driven painful colitisinflammationneurotransmitter release

Identifiers

PMID41065132
PMCPMC12509038

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.