While I didn't think that paper was likely to relate to ME, I noticed another paper on that website that did,
which led to more papers, which led to more papers... That's what the WWW was meant to do.
Items I found interesting:
Microglia can leave the CNS and move into peripheral nerves, and then move back into the brain carrying 'debris', which can cause neurological problems.
There's a drug that can eliminate microglial cells from the brain (not good for long-term health, but useful for research).
They've identified a pair of genes (CD33 and TREM2) that act as on and off switches for neuroinflammation. Certain mutations in TREM2 cause energy deficiency in microglial cells.
Replacement microglial cells come from existing microglial cells. To me that suggests that it's at least possible that ME could involve mutated microglia that reproduce, making ME persistent.
Microglia replace themselves faster than previously expected. A paper stated that we might renew our microglial populations six times in a typical lifetime. However, another paper on that site claims that microglia are longer lived than expected, lasting a lifetime. (Let's see if round two brings a clear winner.)
Allergies deactivate microglia, spurring more neural growth in the hippocampus. Does our memory improve during hayfever season?
Side note: researchers have come up with a peptide (STAT6-IP) that apparently teaches our immune systems to
not develop allergies. Sounds promising.
A new early-stage response to infections has been found: "The newly discovered
immune reaction is activated when the body's mucous membranes are disrupted, as they are when viruses and bacteria attempt to establish an infection. The immune system recognises the virus and produces a substance that neutralises the uninvited guest. The process goes on continuously without us being aware of it. If this first immune reaction is not sufficient to suppress the virus, the infection establishes itself in the body. This in turn triggers the next reaction involving interferon, which not only helps to fight the virus, but also means we become ill."
T-cells, B-cells and NK-cells produce antibodies that are important for getting microglial cells to recognize targets, such as beta-amyloid. We produce fewer T-cells and B-cells as we age, which means that microglial also become less effective. ME does tend to start later in life. Maybe the young ME victims have fewer T-cells and B-cells than normal?
Very interesting site. Thanks antares4141.
