| layout | title | byline | doi | tags | summary | |||||||
|---|---|---|---|---|---|---|---|---|---|---|---|---|
post |
Microglia and macrophages in brain homeostasis and disease |
Li & Barres |
10.1038/nri.2017.125 |
|
Microglia and other CNS macrophages are responsible for much more than just simple structural or immune mediation in the brain, and further research into glial cells is likely to shed light on poorly-understood disorders like ALS, Alzheimer's, Parkinson's, and many more. |
Ben Barres's death earlier this week was an enormous loss both to the field of neuroscience and to the world. I wanted to be sure to include at least one of his publications in this week's reading.
This review covers much of the community's work enabled by Barres's research: Namely, it interrogates the role of microglia and macrophages in brain inflammation and recovery.
Microglia — a macrophage class of non-neuron brain cells that are derived from — are known to interact in realtime with, and constantly monitor, brain activity. These cells actively introduce and retract their processes to modulate the functional relationships between neurons; these cells' ubiquity in the CNS also means that they are among the first-responders when injury or inflammation occurs.
Because the CNS is protected behind the blood-brain-barrier, CNS macrophages are difficult to study — which is something that I remember from the entire course I took on neuroimmunology even though a distressingly large number of these terms are just barely ringing a bell for me anymore.
Dysfunctions of these cells, along with diseases of other CNS macrophages, is the likely culprit in many poorly understood human diseases including gliomas and disorders like Rett syndrome, or neurodegenerative disorders like ALS, Alzheimer's, or Parkinson's. Studying these cells further — along with other glial cells — is the next logical step in understanding neuroinflammatory diseases and many types of neurodegenerative diseases.