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The researchers subsequently transplanted GALC expressing monocytes, a type ofwhitebloodcell involved in theresponse to injury and infection, directly into the CNS of themice. This approach replacedmore than 80% of microglia withhealthy monocytes, virtually eliminating the GCs, protecting againstdamage, and extending survival.
Additionally, the researchers noted that a companionpaper, "Monocytes can efficiently replaceall brain macrophages and fetal liver monocytes can generate bona fide Sall1+ microglia,"ledby the Mohavedi Lab in Brussels,Belgium and publishedtoday in Immunity, complements their work and highlightskeynext steps toward developing new therapies. Frederick Christian Bennett,MD, an Assistant Professor of Psychiatry in the Perelman School of Medicineand a co-senior and corresponding author, also contributed to the companionpaper.
"We are eager tospotlightthe power of microglia replacement," said Bennett. "Our findings supportbuildingon our research to better understand microglia's formation andorigin,allowing us to unlock their role in disease and developmore precision therapies."
The researchwas supportedby the Penn MetabolomicsCore (RRID:SCR_022381), the Penn Cardiovascular Institute and, in part,by NCI (P30 CA016520) andNIH (P30DK050306),NIH (5T32MH019112) and (5T32MH014654). Additional fundingwas providedby Partners for Krabbe Research (P4KR), the University of Pittsburgh Brain Institute internal funding,NIH (DP5OD036159),NIH (R01-NS-120960), Klingenstein-Simons Fellowship in Neuroscience, thePaulAllen FrontiersGroup and Children's Hospital ofPhiladelphia K readiness award. The researchwas also supportedby the Alzheimer's ResearchUK Senior Fellowship (ARUK-SRF2022A-006), theNIHR Newcastle Biomedical Research Centre (BRC), a partnershipbetween Newcastle Hospitals NHS Foundation Trust, Newcastle University, and Cumbria, Northumberland and Tyne andWear NHS Foundation Trust and theNational Institute for Health and Care Research (NIHR).
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