1 min read

ID: 26

Short Link: https://gregory-ms.com/articles/26/

Discovery Date: 23 February 2021, 11:11:00 UTC

Published Date: 2021-01-08 00:00:00

Source: PubMed

Link: https://pubmed.ncbi.nlm.nih.gov/33608912/?utm_source=Other&utm_medium=rss&utm_campaign=pubmed-2&utm_content=10guX6I3SqrbUeeLKSTD6FCRM44ewnrN2MKKTQLLPMHB4xNsZU&fc=20210216052009&ff=20210221121510&v=2.1

Manual Selection: none

Machine Learning Gaussian Naive Bayes Model: false


J Neurochem. 2021 Feb 20. doi: 10.1111/jnc.15327. Online ahead of print.


There is growing evidence that excessive microglial phagocytosis of neurons and synapses contributes to multiple brain pathologies. RNA-seq and genome wide association (GWAS) studies have linked multiple phagocytic genes to neurodegenerative diseases, and knock-out of phagocytic genes has been found to protect against neurodegeneration in animal models, suggesting that excessive microglial phagocytosis contributes to neurodegeneration. Here, we review recent evidence that microglial phagocytosis of live neurons and synapses causes neurodegeneration in animal models of Alzheimer's disease and other tauopathies, Parkinson's disease, frontotemporal dementias, multiple sclerosis, retinal degeneration, and neurodegeneration induced by ischaemia, infection or ageing. We also review factors regulating microglial phagocytosis of neurons, including: nucleotides, frackalkine, phosphatidylserine, calreticulin, UDP, CD47, sialylation, complement, galectin-3, Apolipoprotein E, phagocytic receptors, Siglec receptors, cytokines, microglial epigenetics and expression profile. Some of these factors may be potential treatment targets to prevent neurodegeneration mediated by excessive microglial phagocytosis of live neurons and synapses.

PMID:33608912 | DOI:10.1111/jnc.15327

Noun Phrases in Title

  • Microglial phagocytosis
  • neurons
  • neurodegeneration
  • its regulation
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