CD11a expression distinguishes infiltrating myeloid cells from plaque‐associated microglia in Alzheimer's disease

• DOI: 10.1002/glia.23575
• Publication Date: 2018-12-27T04:00:22Z
• Authors: Ankita K. Shukla; Laura L. McIntyre; Samuel E. Marsh; Christine A. Schn...; Evelyn M. Hoover; Craig M. Walsh; Melissa B. Lodoen; Mathew Blurton‐Jones; Matthew A. Inlay
• Keywords: TREM2; Monocyte; Amyloid beta

Abstract Alzheimer's disease (AD) is the leading cause of age‐related neurodegeneration and characterized neuropathologically by accumulation insoluble beta‐amyloid (Aβ) peptides. In AD brains, plaque‐associated myeloid (PAM) cells cluster around Aβ plaques but fail to effectively clear phagocytosis. PAM were originally thought be brain‐resident microglia. However, several studies have also suggested that Aβ‐induced inflammation causes peripheral monocytes enter otherwise immune‐privileged brain. The relationship between progression in brain remains ambiguous because microglia monocyte‐derived macrophages are extremely difficult distinguish from one another an inflamed Whether microglia, macrophages, or a mixture both unclear. CD11a component β2 integrin LFA1. We determined highly expressed on immune cells, including not mouse These expression patterns remain consistent LPS‐treated mice, as well two models AD. Thus, can used marker murine infiltrating cells. Using CD11a, we show transgenic brains comprised entirely demonstrate novel fluorescence‐assisted quantification technique (FAQT), which reveals significant increase T lymphocytes, especially female mice. Our findings support notion lead players rejuvenating their phagocytic potential may important therapeutic strategy.