In one paragraphArticle in Cell death & disease, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
–field-weighted citation impact
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 registryThe 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 literatureWho cites it
0 citing papers in PubMed.
No citing paper in PubMed yet.
4 · The recordCorrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
5 · Who and what moneyAuthors and funding
13 authors.
Victoria Pozzi-RuizLaboratory of Functional Epi-Genomics of Aging and Alzheimer's disease, Instituto de Neurociencias, Universidad Miguel Hernández-Consejo Superior de Investigaciones Científicas (UMH-CSIC), Alicante, Spain.ORCID http://orcid.org/0000-0001-7672-357X Aida Giner de GraciaLaboratory of Functional Epi-Genomics of Aging and Alzheimer's disease, Instituto de Neurociencias, Universidad Miguel Hernández-Consejo Superior de Investigaciones Científicas (UMH-CSIC), Alicante, Spain.
Liliane GlauserLaboratory of Neuroepigenetics, School of Life Sciences, Brain Mind Institute, École Polytechnique Fédérale de Lausanne, Lausanne, Switzerland.
Alejandro González-RamónLaboratory of Functional Epi-Genomics of Aging and Alzheimer's disease, Instituto de Neurociencias, Universidad Miguel Hernández-Consejo Superior de Investigaciones Científicas (UMH-CSIC), Alicante, Spain.ORCID http://orcid.org/0000-0003-2472-8533 Mahmood Haj-YahyaLaboratory of Molecular and Chemical Biology of Neurodegeneration, School of Life Sciences, Brain Mind Institute, École Polytechnique Fédérale de Lausanne, Lausanne, Switzerland.
Rajasekhar KollaLaboratory of Molecular and Chemical Biology of Neurodegeneration, School of Life Sciences, Brain Mind Institute, École Polytechnique Fédérale de Lausanne, Lausanne, Switzerland.
Hilal A LashuelLaboratory of Molecular and Chemical Biology of Neurodegeneration, School of Life Sciences, Brain Mind Institute, École Polytechnique Fédérale de Lausanne, Lausanne, Switzerland.
Johan AuwerxLaboratory of Integrative Systems Physiology, Institute of Bioengineering, École Polytechnique Fédérale de Lausanne, Lausanne, Switzerland.
Johannes GräffLaboratory of Neuroepigenetics, School of Life Sciences, Brain Mind Institute, École Polytechnique Fédérale de Lausanne, Lausanne, Switzerland. johannes.graeff@epfl.ch.ORCID http://orcid.org/0000-0002-3219-3578 Jose V Sanchez-MutLaboratory of Functional Epi-Genomics of Aging and Alzheimer's disease, Instituto de Neurociencias, Universidad Miguel Hernández-Consejo Superior de Investigaciones Científicas (UMH-CSIC), Alicante, Spain. j.sanchezm@umh.es.ORCID http://orcid.org/0000-0002-9292-8521 Funding
EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 European Research Council (H2020 Excellent Science - European Research Council) ERC-AdG-787702Ministry of Economy and Competitiveness | Agencia Estatal de Investigación (Spanish Agencia Estatal de Investigación) PID2022-143263OB-I00Ministry of Economy and Competitiveness | Agencia Estatal de Investigación (Spanish Agencia Estatal de Investigación) PRE2020-093389Ministry of Economy and Competitiveness | Agencia Estatal de Investigación (Spanish Agencia Estatal de Investigación) PRE2020-093825Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung (Swiss National Science Foundation) SNSF 31003A_179435
6 · The paper itselfAbstract
There is increasing evidence of microglia participation in Alzheimer's disease (AD), which incentives their modulation to intercept the disease. Here, we describe a new mechanism by which the recently AD-associated Peptidase M20 Domain Containing 1 (PM20D1) instructs microglia to tackle AD. We show that the PM20D1-derived N-oleoyl-Leucine (OLE) improves AD pathologies in two animal models of AD. OLE induces microglia association with amyloid beta (Aβ) plaques, reduce their size, number and toxicity, and leads to enhanced neuroprotection and cognition. Furthermore, OLE also increases Aβ chemotaxis and clearance in microglia cultures and enhances cell viability in neurons subjected to AD-related stressors. Finally, we also find evidence for a PM20D1- and OLE-mediated microglia association with amyloid plaques and neuroprotection in human AD brains. In sum, our results provide further insight into the protective role of PM20D1 in AD and support the use of OLE as a microglia-modifying treatment for AD.
Indexed as
Alzheimer DiseaseAmidohydrolasesLeucineMicrogliaSignal TransductionAmyloid beta-Protein PrecursorAnimalsBrainCaenorhabditis elegansCell Line, TumorChemotaxisDisease Models, AnimalFemaleGene Expression RegulationHumansMaleAmidohydrolasesAmyloid beta-Protein PrecursorLeucinePM20D1 protein, mouse
Identifiers
PMID42045164
PMCPMC13254073
What OpenQuestion holds
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LicenceCC BY
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