{
  "abstract": "Glucagon-like peptide-1 receptor agonists (GLP-1RAs) have shown promise in preclinical models of neurodegeneration, with emerging evidence suggesting these effects may be driven by modulation of neuroinflammation. However, the cellular mechanisms underlying GLP-1RA effects on neuroinflammation remain poorly understood. Here we show, using a mouse model of lipopolysaccharide-induced neuroinflammation, how semaglutide coordinates cellular responses to resolve neuroinflammation. We find that semaglutide in male mice prevents brain infiltration of neutrophils, excessive cytokine release, and suppresses neuroinflammation-associated transcriptional signatures specifically in microglia, endothelial cells, and a subset of pericytes. Mechanistically, we identify a subset of Glp1r-expressing neurons in the dorsal vagal complex that, upon semaglutide treatment, regulate genes involved in anti-inflammatory signaling. Semaglutide-modulated pathways overlap with inflammatory signatures found in human neurodegenerative diseases, including Alzheimer's disease, suggesting broad relevance for conditions involving neuroinflammation. Together, these findings reveal how GLP-1R signaling in male mice orchestrates resolution of neuroinflammation through coordinated multi-cellular programs.",
  "abstract_shown": true,
  "affiliations": [
    "Novo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, Copenhagen, Denmark",
    "Novo Nordisk Foundation Center for Genomic Mechanisms of Disease, Broad Institute of MIT and Harvard, Cambridge, MA, USA",
    "Research and Development, Novo Nordisk A/S, Måløv, Denmark",
    "Research and Development, Novo Nordisk A/S, Søborg, Denmark",
    "Gubra A/S, Hørsholm, Denmark",
    "Research and Development, Novo Nordisk A/S, Måløv, Denmark. lottebjerreknudsen@icloud.com",
    "Novo Nordisk Foundation Center for Basic Metabolic Research, University of Copenhagen, Copenhagen, Denmark. tune.pers@sund.ku.dk",
    "Novo Nordisk Foundation Center for Genomic Mechanisms of Disease, Broad Institute of MIT and Harvard, Cambridge, MA, USA. tune.pers@sund.ku.dk"
  ],
  "article_type": null,
  "arxiv": null,
  "author_total": 20,
  "authors": [
    {
      "affs": [
        0,
        1,
        2
      ],
      "name": "Dylan M. Rausch",
      "orcid": "0000-0001-6095-4891"
    },
    {
      "affs": [
        0,
        2
      ],
      "name": "Mette Q. Ludwig",
      "orcid": "0000-0002-7814-3859"
    },
    {
      "affs": [
        3
      ],
      "name": "Marie Aare Bentsen",
      "orcid": "0000-0002-2561-2308"
    },
    {
      "affs": [
        2
      ],
      "name": "Stine N. Hansen",
      "orcid": "0000-0003-0270-141X"
    },
    {
      "affs": [
        2
      ],
      "name": "Anna Secher",
      "orcid": "0000-0002-6276-5389"
    },
    {
      "affs": [
        2
      ],
      "name": "Dorte Holst",
      "orcid": "0009-0003-2777-6845"
    },
    {
      "affs": [
        2
      ],
      "name": "Jaime Moreno",
      "orcid": "0009-0006-6173-8879"
    },
    {
      "affs": [
        3
      ],
      "name": "Vivek Das",
      "orcid": "0000-0003-0614-0373"
    },
    {
      "affs": [
        0
      ],
      "name": "Kristoffer Lihme Egerod",
      "orcid": "0000-0003-2781-1594"
    },
    {
      "affs": [
        3
      ],
      "name": "Anne-Mette Bjerregaard",
      "orcid": "0000-0002-1831-6746"
    },
    {
      "affs": [
        2
      ],
      "name": "Kristoffer Niss",
      "orcid": "0000-0001-5910-1525"
    },
    {
      "affs": [
        2
      ],
      "name": "S. Sherona Bau",
      "orcid": "0000-0002-2873-7974"
    },
    {
      "affs": [
        2
      ],
      "name": "Charles Pyke",
      "orcid": "0000-0002-7286-5009"
    },
    {
      "affs": [
        2
      ],
      "name": "Kevin Dalgaard"
    },
    {
      "affs": [
        2
      ],
      "name": "Myrte Merkestein"
    },
    {
      "affs": [
        4
      ],
      "name": "Franziska Wichern"
    },
    {
      "affs": [
        3
      ],
      "name": "Charlotte Thim Hansen"
    },
    {
      "affs": [
        3
      ],
      "name": "Joseph Polex-Wolf",
      "orcid": "0000-0002-0441-8872"
    },
    {
      "affs": [
        5
      ],
      "name": "LOTTE BJERRE KNUDSEN",
      "orcid": "0000-0002-2439-7116"
    },
    {
      "affs": [
        6,
        7
      ],
      "name": "Tune H. Pers",
      "orcid": "0000-0003-0207-4831"
    }
  ],
  "bibtex": "https://research.draconitic.com/paper/0zt7y3g81x9b0.bib",
  "cited_by": 9,
  "doi": "10.1038/s41467-026-74038-4",
  "fulltext_url": null,
  "id": "0zt7y3g81x9b0",
  "issns": [
    "2041-1723"
  ],
  "landing_url": "https://doi.org/10.1038/s41467-026-74038-4",
  "language": "en",
  "licence": "CC-BY-NC-ND",
  "licence_label": "CC BY-NC-ND",
  "licence_source": "journal",
  "licence_url": "https://creativecommons.org/licenses/by-nc-nd/4.0/",
  "metadata_licence": null,
  "native_subjects": [
    [
      "openalex",
      "2808|Neuroinflammation and Neurodegeneration Mechanisms"
    ]
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  "openalex": "W7164043252",
  "pdf_url": null,
  "pmcid": "PMC13402617",
  "pmid": "42265098",
  "published": "2026-06-09",
  "publisher": "Nature Portfolio",
  "ris": "https://research.draconitic.com/paper/0zt7y3g81x9b0.ris",
  "sources": [
    {
      "first_seen": "2026-10-30T13:26:53Z",
      "native_id": "W7164043252",
      "source": "openalex",
      "url": "https://doi.org/10.1038/s41467-026-74038-4"
    }
  ],
  "subjects": [
    {
      "field": "medicine",
      "origin": "openalex:2808|Neuroinflammation and Neurodegeneration Mechanisms",
      "subfield": "neurology"
    }
  ],
  "title": "Semaglutide attenuates neuroinflammation in male mice",
  "title_text": "Semaglutide attenuates neuroinflammation in male mice",
  "type": "peer-reviewed",
  "updated_at": "2026-11-09T13:21:12Z",
  "url": "https://research.draconitic.com/paper/0zt7y3g81x9b0",
  "venue": "Nature Communications",
  "versions": []
}