Publications by authors named "H G Davtyan"

Alzheimer's disease (AD) is the most prevalent neurodegenerative disorder characterized by extracellular amyloid plaques and neuronal Tau tangles. A recent study found that the APOE3 Christchurch (APOECh) variant could delay AD progression. However, the underlying mechanisms remain unclear.

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Article Synopsis
  • - Microglia are the central nervous system's immune cells, playing essential roles in brain development and maintaining neuron activity, but their involvement at the blood-brain barrier (BBB) in healthy brains is less understood.
  • - A study using the CSF1R inhibitor PLX5622 to deplete microglia showed that they are not crucial for maintaining the structure or function of the healthy BBB, despite their close contact with endothelial cells.
  • - However, treatment with PLX5622 was found to affect cholesterol metabolism in brain endothelial cells independently of microglial presence, indicating that the drug has unintended effects on brain blood vessels.
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The central nervous system (CNS) is constantly surveilled by microglia, highly motile and dynamic cells deputed to act as the first line of immune defense in the brain and spinal cord. Alterations in the homeostasis of the CNS are detected by microglia that respond by extending their processes or - following major injuries - by migrating toward the affected area. Understanding the mechanisms controlling directed cell migration of microglia is crucial to dissect their responses to neuroinflammation and injury.

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APOE4 is the strongest genetic risk factor for Alzheimer's disease (AD), with increased odds ratios in female carriers. Targeting amyloid plaques shows modest improvement in male non-APOE4 carriers. Leveraging single-cell transcriptomics across APOE variants in both sexes, multiplex flow cytometry and validation in two independent cohorts of APOE4 female carriers with AD, we identify a new subset of neutrophils interacting with microglia associated with cognitive impairment.

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