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• W2896616749 abstract "Identifying microglia phenotypes in pathological tissue is an important step in understanding their function. Activated microglia are a feature of Alzheimer's disease (AD), and inflammatory mechanisms could contribute to AD neurodegeneration, but the antigenic markers used in microglial pathology studies have been limited. To extend findings, we compared expression by microglia of progranulin, an anti-inflammatory growth factor with purinergic receptor P2RY12, a microglial specific receptor for ADP/ATP that identifies non-activated microglia. In vitro studies with human microglia have shown that progranulin and P2RY12 are upregulated by interleukin-4 identifying them as alternative activation markers. This study employed fixed human brain tissue sections of middle temporal gyrus (MTG) from low plaque (LP)(n=12), high plaque (HP)(n=14) non-demented (ND), and AD (n=14) cases. Cellular localization of progranulin and P2RY12 was identified with validated antibodies by light and confocal immunohistochemistry. Studies were carried out to identify how microglia identified with antibodies to progranulin (R&D Systems, AF2420) and P2RY12 (Novus, NBP2-33870) colocalized with amyloid beta (Aβ), phosphorylated tau (pTAU), and microglial markers IBA-1, HLA-DR, and CD45. This study showed that most progranulin-positive microglia were immunoreactive for P2RY12. There were significant differences in patterns of expression of progranulin and P2RY12. Progranulin strongly stained microglia accumulated on Aβ plaques, while P2RY12 mostly identified microglia adjacent to plaques. CD45 and HLA-DR-positive microglia clustered on plaques were mostly P2RY12 negative, while all progranulin positive microglia were positive for CD45. Progranulin and P2RY12 positive microglia had a range of morphologies. LP cases mostly had progranulin and P2RY12 microglia with ramified morphologies, but with increasing plaque and tangle pathology, those with activated morphology were more strongly immunoreactive. Using quantitative measures, there were no significant differences between disease-groups for P2YR12 indicating that many microglia in AD brains are non-activated. Confocal microscopy showed P2RY12 and HLA-DR co-localized in only few microglia, while progranulin and HLA-DR colocalization was widely observed. Microglial immunoreactivity for progranulin and P2RY12 was widespread in AD brains. As these factors can describe microglia with anti-inflammatory properties, the concept that inflammatory damage by microglia in AD brains needs to be refined to consider these findings when designing anti-inflammatory therapies for AD." @default.
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• W2896616749 date "2018-07-01" @default.
• W2896616749 modified "2023-10-16" @default.
• W2896616749 title "P4‐255: IMMUNOPHENOTYPING OF MICROGLIA IN ALZHEIMER'S DISEASE BRAINS: COMPARISON OF EXPRESSION OF PROGRANULIN AND PURINERGIC RECEPTOR P2RY12" @default.
• W2896616749 doi "https://doi.org/10.1016/j.jalz.2018.07.077" @default.
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