Journal of Alzheimer's Disease
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Home > Postmortem Adult Human Microglia Proliferate in Culture to High Passage and Maintain Their Response to Amyloid-β.

TitlePostmortem Adult Human Microglia Proliferate in Culture to High Passage and Maintain Their Response to Amyloid-β.
Publication TypeJournal Article
Year of Publication2016
AuthorsGuo, L, Rezvanian, A, Kukreja, L, Hoveydai, R, Bigio, EH, Mesulam, M-M, Khoury, JEl, Geula, C
JournalJ Alzheimers Dis
Volume54
Issue3
Pagination1157-1167
Date Published2016 Oct 04
ISSN1875-8908
Abstract

Microglia are immune cells of the brain that display a range of functions. Most of our knowledge about microglia biology and function is based on cells from the rodent brain. Species variation in the complexity of the brain and differences in microglia response in the primate when compared with the rodent, require use of adult human microglia in studies of microglia biology. While methods exist for isolation of microglia from postmortem human brains, none allow culturing cells to high passage. Thus cells from the same case could not be used in parallel studies and multiple conditions. Here we report a method, which includes use of growth factors such as granulocyte macrophage colony stimulating factor, for successful culturing of adult human microglia from postmortem human brains up to 28 passages without significant loss of proliferation. Such cultures maintained their phenotype, including uptake of the scavenger receptor ligand acetylated low density lipoprotein and response to the amyloid-β peptide, and were used to extend in vivo studies in the primate brain demonstrating that inhibition of microglia activation protects neurons from amyloid-β toxicity. Significantly, microglia cultured from brains with pathologically confirmed Alzheimer's disease displayed the same characteristics as microglia cultured from normal aged brains. The method described here provides the scientific community with a new and reliable tool for mechanistic studies of human microglia function in health from childhood to old age, and in disease, enhancing the relevance of the findings to the human brain and neurodegenerative conditions.

DOI10.3233/JAD-160394
Alternate JournalJ. Alzheimers Dis.
PubMed ID27567845
PubMed Central IDPMC5075451
Grant ListP30 AG013854 / AG / NIA NIH HHS / United States
R21 NS084210 / NS / NINDS NIH HHS / United States
RF1 AG051506 / AG / NIA NIH HHS / United States
UL1 TR001422 / TR / NCATS NIH HHS / United States
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