Evidence map›Paper›PMID 40457749›Full record

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

Acute experimental colitis in 5xFAD Alzheimer's disease mice leads to enhanced monocyte infiltration into the brain accompanied by reduced β-amyloid deposition.

Nanda K Navalpur Shanmugam, Frank Zamudio, Deepak K Vijaya Kumar, Kianna A Barrett, Ryan VanDoren, Meng Chen, Olivia M Barr, Sara Watson, Chih-Chung Jerry Lin, William A Eimer and 4 more

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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 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
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  6. Review
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.

Nanda K Navalpur ShanmugamGenetics and Aging Research Unit, Henry and Allison McCance Center for Brain Health, Department of Neurology, Massachusetts General Hospital, and Harvard Medical School, Charlestown, Massachusetts, USA.
Frank ZamudioGenetics and Aging Research Unit, Henry and Allison McCance Center for Brain Health, Department of Neurology, Massachusetts General Hospital, and Harvard Medical School, Charlestown, Massachusetts, USA.
Deepak K Vijaya KumarGenetics and Aging Research Unit, Henry and Allison McCance Center for Brain Health, Department of Neurology, Massachusetts General Hospital, and Harvard Medical School, Charlestown, Massachusetts, USA.
Kianna A BarrettGenetics and Aging Research Unit, Henry and Allison McCance Center for Brain Health, Department of Neurology, Massachusetts General Hospital, and Harvard Medical School, Charlestown, Massachusetts, USA.
Ryan VanDorenGenetics and Aging Research Unit, Henry and Allison McCance Center for Brain Health, Department of Neurology, Massachusetts General Hospital, and Harvard Medical School, Charlestown, Massachusetts, USA.
Meng ChenGenetics and Aging Research Unit, Henry and Allison McCance Center for Brain Health, Department of Neurology, Massachusetts General Hospital, and Harvard Medical School, Charlestown, Massachusetts, USA.
Olivia M BarrGenetics and Aging Research Unit, Henry and Allison McCance Center for Brain Health, Department of Neurology, Massachusetts General Hospital, and Harvard Medical School, Charlestown, Massachusetts, USA.
Sara WatsonGenetics and Aging Research Unit, Henry and Allison McCance Center for Brain Health, Department of Neurology, Massachusetts General Hospital, and Harvard Medical School, Charlestown, Massachusetts, USA.
Chih-Chung Jerry LinGenetics and Aging Research Unit, Henry and Allison McCance Center for Brain Health, Department of Neurology, Massachusetts General Hospital, and Harvard Medical School, Charlestown, Massachusetts, USA.
William A EimerGenetics and Aging Research Unit, Henry and Allison McCance Center for Brain Health, Department of Neurology, Massachusetts General Hospital, and Harvard Medical School, Charlestown, Massachusetts, USA.
Mehdi JorfiGenetics and Aging Research Unit, Henry and Allison McCance Center for Brain Health, Department of Neurology, Massachusetts General Hospital, and Harvard Medical School, Charlestown, Massachusetts, USA.
Se Hoon ChoiGenetics and Aging Research Unit, Henry and Allison McCance Center for Brain Health, Department of Neurology, Massachusetts General Hospital, and Harvard Medical School, Charlestown, Massachusetts, USA.
Robert D MoirGenetics and Aging Research Unit, Henry and Allison McCance Center for Brain Health, Department of Neurology, Massachusetts General Hospital, and Harvard Medical School, Charlestown, Massachusetts, USA.
Rudolph E TanziGenetics and Aging Research Unit, Henry and Allison McCance Center for Brain Health, Department of Neurology, Massachusetts General Hospital, and Harvard Medical School, Charlestown, Massachusetts, USA.

Funding

Cure Alzheimer's Fund
6 · The paper itself

Abstract

introductionEmerging evidence has connected Alzheimer's disease (AD) to systemic inflammation, intestinal abnormalities, and altered gut microbiota, highlighting the significance of the gut-brain axis. Here, we investigated the impact of acute experimental colitis (acute colitis) on AD pathology.

methodsAcute colitis was induced in 2-month-old 5xFAD mice using dextran sodium sulfate (DSS) to assess the effects of intestinal inflammation on the microbiome, systemic inflammation, neuroinflammation, and beta-amyloid deposition.

resultsInduction of acute colitis in 5xFAD mice led to microbial dysbiosis and systemic inflammation. As a result, monocyte infiltration was observed in the brain accompanied by reduced cerebral beta-amyloid deposition and increased beta-amyloid efflux into the bloodstream. DISCUSSION: Increased infiltration of monocytes and elevated beta-amyloid release into the bloodstream could both be responsible for the reduced beta-amyloid deposition in 5xFAD mice following acute colitis. These results further highlight an important connection between gut-induced peripheral inflammation and the progression of AD. HIGHLIGHTS: Microbial dysbiosis occurs as a result of acute colitis in 5xFAD mice. Acute colitis in 5xFAD mice affects beta-amyloid deposition. Increased IL-2 and IL-6 cytokine levels in the hippocampus of 5xFAD colitis mice. Colitis in 5xFAD mice increases serum proinflammatory cytokine levels and endotoxins. Acute colitis in 5xFAD mice increases monocyte infiltration and serum beta-amyloid.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesBrainColitisMonocytesAnimalsDextran SulfateDisease Models, AnimalDysbiosisGastrointestinal MicrobiomeMiceMice, TransgenicAmyloid beta-PeptidesDextran Sulfatecolitisintestinal inflammationneuroinflammationβ‐amyloid

Identifiers

PMID40457749
PMCPMC12130571

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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.