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Single Cell RNA-Seq Sheds Light on the Role of Microglia in Alzheimer’s Disease


The genetic absence of microglia in Alzheimer’s disease mice causes a shift from parenchymal amyloid plaques to cerebral amyloid angiopathy, brain calcification, hemorrhages, and premature death (Shabestari et al.). A single injection of adult microglia prevents each of these pathological changes – demonstrating that microglia protect the brain against detrimental Alzheimer’s disease co-pathologies. These results indicate the protective functions of microglia in reducing cerebral amyloid angiopathy (CAA), blood-brain barrier dysfunction, and brain calcification.

Data was generated using the Parse WT kit on nuclei from brain tissue. 8 mice (4 female/4 male) were used in 6 experimental conditions listed below. Many different neuronal, glial, and vascular cell types, including region-specific excitatory neurons, inhibitory neurons, multiple subtypes of astrocytes and oligodendrocytes, and an immune cell population containing signatures of microglia and other immune cells were resolved. Cell types were well mixed across genotype and sex.

Data Table

GroupsTest Condition
(A) 5x-FIREAD-mouse – no microglia
(B) 5x-FADAD-mouse
(C) WT-FIREWT mouse – no microglia
(D) WT-WTWT mouse
(E) 5x-FIRE-PBSAD-mouse – no microglia
(F) 5x-FIRE-MGAD-mouse – transplanted microglia
Products: WT
Tissue Type: Brain

"48 samples, across 6 conditions, in 1 experiment with important implications."

-Vivek Swarup, Associate Professor, University of California, Irvine

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