{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,27]],"date-time":"2026-08-27T14:23:33Z","timestamp":1787840613000,"version":"build-2784847793"},"reference-count":54,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"6","license":[{"start":{"date-parts":[[2025,6,19]],"date-time":"2025-06-19T00:00:00Z","timestamp":1750291200000},"content-version":"unspecified","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0 http:\/\/creativecommons.org\/licenses\/by\/4.0"}],"content-domain":{"domain":["lww.com","ovid.com"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2026,6]]},"abstract":"<jats:p>JOURNAL\/nrgr\/04.03\/01300535-202606000-00057\/figure1\/v\/2026-04-16T195327Z\/r\/image-tiff<\/jats:p>\n                  <jats:p>\n                    In Alzheimer\u2019s disease, microglial phagocytosis is engaged in the pathogenesis as it clears abnormal protein accumulations, debris, and apoptotic cells in the early stages of Alzheimer\u2019s disease, but fuels neuroinflammation and accelerates disease progression in later stages.\n                    <jats:italic toggle=\"yes\">In vivo<\/jats:italic>\n                    parabiosis experiments in aged animals have demonstrated that blood-born factors modulate synaptic plasticity, neurogenesis, and microglial responses. We hypothesize that peripheral factors can modulate microglial function and thereby possibly influence Alzheimer\u2019s disease pathology. The objective of this study is to investigate the effects of Alzheimer\u2019s disease serum on microglial phagocytosis. Here, we use an immortalized human microglial cell line in an\n                    <jats:italic toggle=\"yes\">in vitro<\/jats:italic>\n                    parabiosis assay to investigate the impact of the serum from individuals diagnosed with Alzheimer\u2019s disease (\n                    <jats:italic toggle=\"yes\">n<\/jats:italic>\n                    = 30) and age-matched controls (\n                    <jats:italic toggle=\"yes\">n<\/jats:italic>\n                    = 30) (PRODEM study) on microglial phagocytosis. Exposure to Alzheimer\u2019s disease serum increased microglial phagocytic uptake of pH-sensitive fluorescent particles and downregulated expression of the lysosomal master regulator transcription factor EB (\n                    <jats:italic toggle=\"yes\">TFEB<\/jats:italic>\n                    ) and of ATPase H\n                    <jats:sup>+<\/jats:sup>\n                    transporting lysosomal V1 subunit B2 (\n                    <jats:italic toggle=\"yes\">ATP6V1B2<\/jats:italic>\n                    ), a component of the vacuolar ATPase. To identify serum components that may relate to changes in phagocytosis, serum samples of the Three-City Study (3C Study) were used. In the 3C Study, blood samples were collected up to 12 years before the onset of cognitive decline or dementia and their serum metabolome is well-defined. Microglia exposed to the serum of future Alzheimer\u2019s disease patients from the 3C Study displayed an increased phagocytic uptake compared with the serum of matched controls, depending on the presence of the apolipoprotein E \u03b54 allele in the Alzheimer\u2019s disease patients. Furthermore, microglial phagocytosis correlated inversely with serum levels of the omega-3 fatty acid eicosapentaenoic acid. We confirmed this inverse correlation between eicosapentaenoic acid and phagocytosis in the serum samples of the PRODEM cohort. In addition,\n                    <jats:italic toggle=\"yes\">in vitro<\/jats:italic>\n                    testing of eicosapentaenoic acid on microglial phagocytosis showed a concentration-dependent decrease in phagocytic uptake. In conclusion, following incubation with Alzheimer\u2019s disease blood serum, we observed increased microglial phagocytic uptake and the downregulation of\n                    <jats:italic toggle=\"yes\">TFEB<\/jats:italic>\n                    and\n                    <jats:italic toggle=\"yes\">ATP6V1B2<\/jats:italic>\n                    , possibly indicating lysosomal dysfunction. Furthermore, microglial phagocytosis was inversely correlated with serum eicosapentaenoic acid levels, suggesting an important role for dietary eicosapentaenoic acid in microglial function.\n                  <\/jats:p>","DOI":"10.4103\/nrr.nrr-d-24-01287","type":"journal-article","created":{"date-parts":[[2025,6,19]],"date-time":"2025-06-19T15:00:15Z","timestamp":1750345215000},"page":"2433-2439","update-policy":"https:\/\/doi.org\/10.1097\/lww.0000000000001000","source":"Crossref","is-referenced-by-count":1,"title":["Blood serum from individuals with Alzheimer\u2019s disease alters microglial phagocytosis in vitro"],"prefix":"10.4103","volume":"21","author":[{"given":"Barbara","family":"Altendorfer","sequence":"first","affiliation":[{"name":"Institute of Molecular Regenerative Medicine, Paracelsus Medical University, Salzburg, Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rodolphe","family":"Poupardin","sequence":"additional","affiliation":[{"name":"Experimental and Clinical Cell Therapy Institute, Paracelsus Medical University, Salzburg, Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sophie","family":"Lef\u00e8vre-Arbogast","sequence":"additional","affiliation":[{"name":"University of Bordeaux, Inserm, Bordeaux Population Health Research Center, Bordeaux, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Claudine","family":"Manach","sequence":"additional","affiliation":[{"name":"Universit\u00e9 Clermont Auvergne, INRAE, UMR1019, Human Nutrition Unit, Clermont Ferrand, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Dorrain Y.","family":"Low","sequence":"additional","affiliation":[{"name":"Universit\u00e9 Clermont Auvergne, INRAE, UMR1019, Human Nutrition Unit, Clermont Ferrand, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mireia","family":"Urpi-Sarda","sequence":"additional","affiliation":[{"name":"Nutrition, Food Science and Gastronomy Department, Faculty of Pharmacy and Food Science, Nutrition and Food Safety Research Institute (INSA), CIBER Fragilidad y Envejecimiento Saludable (CIBERFES), Instituto de Salud Carlos III, University of Barcelona, Barcelona, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cristina","family":"Andres-Lacueva","sequence":"additional","affiliation":[{"name":"Nutrition, Food Science and Gastronomy Department, Faculty of Pharmacy and Food Science, Nutrition and Food Safety Research Institute (INSA), CIBER Fragilidad y Envejecimiento Saludable (CIBERFES), Instituto de Salud Carlos III, University of Barcelona, Barcelona, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ra\u00fal","family":"Gonz\u00e1lez-Dom\u00ednguez","sequence":"additional","affiliation":[{"name":"Nutrition, Food Science and Gastronomy Department, Faculty of Pharmacy and Food Science, Nutrition and Food Safety Research Institute (INSA), CIBER Fragilidad y Envejecimiento Saludable (CIBERFES), Instituto de Salud Carlos III, University of Barcelona, Barcelona, Spain"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas K.","family":"Felder","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine, Paracelsus Medical University, Salzburg, Austria"},{"name":"Institute of Pharmacy, Paracelsus Medical University, Salzburg, Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julia","family":"Tevini","sequence":"additional","affiliation":[{"name":"Department of Laboratory Medicine, Paracelsus Medical University, Salzburg, 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Neuroscience, University of Amsterdam, Amsterdam, Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Silvie R.","family":"Ruigrok","sequence":"additional","affiliation":[{"name":"Brain Plasticity Group, Swammerdam Institute for Life Sciences, Center for Neuroscience, University of Amsterdam, Amsterdam, Netherlands"},{"name":"\u00c9cole Polytechnique F\u00e9d\u00e9rale de Lausanne - Brain Mind Institute - Laboratory of Behavioral Genetics, Lausanne, Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Chiara","family":"de Lucia","sequence":"additional","affiliation":[{"name":"Department of Basic and Clinical Neuroscience, Maurice Wohl Clinical Neuroscience Institute, Institute of Psychiatry, Psychology and Neuroscience, King\u2019s College London, London, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Andrea","family":"Du Preez","sequence":"additional","affiliation":[{"name":"Department of Basic and Clinical Neuroscience, Maurice Wohl Clinical Neuroscience Institute, Institute of Psychiatry, Psychology and Neuroscience, King\u2019s College London, London, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Catherine","family":"Helmer","sequence":"additional","affiliation":[{"name":"University of Bordeaux, Inserm, Bordeaux Population Health Research Center, Bordeaux, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeanne","family":"Neuffer","sequence":"additional","affiliation":[{"name":"University of Bordeaux, Inserm, Bordeaux Population Health Research Center, Bordeaux, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C\u00e9cile","family":"Proust-Lima","sequence":"additional","affiliation":[{"name":"University of Bordeaux, Inserm, Bordeaux Population Health Research Center, Bordeaux, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Aniko","family":"Korosi","sequence":"additional","affiliation":[{"name":"Brain Plasticity Group, Swammerdam Institute for Life Sciences, Center for Neuroscience, University of Amsterdam, Amsterdam, Netherlands"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"C\u00e9cilia","family":"Samieri","sequence":"additional","affiliation":[{"name":"University of Bordeaux, Inserm, Bordeaux Population Health Research Center, Bordeaux, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sandrine","family":"Thuret","sequence":"additional","affiliation":[{"name":"Department of Basic and Clinical Neuroscience, Maurice Wohl Clinical Neuroscience Institute, Institute of Psychiatry, Psychology and Neuroscience, King\u2019s College London, London, UK"},{"name":"Department of Neurology, University Hospital Carl Gustav Carus, Technische Universit\u00e4t Dresden, Dresden, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-1653-8046","authenticated-orcid":false,"given":"Ludwig","family":"Aigner","sequence":"additional","affiliation":[{"name":"Institute of Molecular Regenerative Medicine, Paracelsus Medical University, Salzburg, Austria"},{"name":"Austrian Cluster of Tissue Regeneration, Vienna, Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","published-online":{"date-parts":[[2025,6,19]]},"reference":[{"key":"R1-20260416","doi-asserted-by":"crossref","first-page":"26043","DOI":"10.1074\/jbc.M115.679043","article-title":"Apolipoprotein E is a ligand for triggering receptor expressed on myeloid cells 2 (TREM2)","volume":"290","author":"Atagi","year":"2015","journal-title":"J Biol Chem"},{"key":"R2-20260416","doi-asserted-by":"crossref","first-page":"954","DOI":"10.3390\/cells12060954","article-title":"Impact of translocator protein 18 kDa (TSPO) deficiency on mitochondrial 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