The brain's very own immune cells, called microglia, are both cops and trash collectors. They continuously police the brain, making sure everything is running smoothly. When they sense a pathogen, they engulf it, incarcerate it in their innards and work it over until there's nothing left but some stuff you wouldn't want to see. If they spot a dead cell or a pile of debris, they don their overalls and hasten to remove it, likewise by engulfing it, internalizing it and pounding it to a pulp.
Breaking research by neuroscientist Tony Wyss-Coray, PhD, just published in a study in Neuron, strongly hints that when these trash collectors go on disability, the resulting garbage stack-up spells serious injury to nearby nerve cells in the brain.
This connection appears to hold up not only in laboratory mice but in humans, too, as I wrote in a fairly detailed news release describing the study's findings:
"We were fortunate in being able to compare microglia... from five patients who died of Alzheimer's disease with five who died of other causes," said... Wyss-Coray... "And we discovered that in Alzheimer's disease, the microglia are defective. One of these cells' main functions, removing garbage, is impaired."
Wyss-Coray's team also demonstrated one likely culprit behind the loss of microglia's scavenging skills: ironically, a failure in these cells' internal recycling program. Receptors positioned on microglia's outer membranes recognize a variety of bad actors including a substance called A-beta, aggregations of which have been implicated in Alzheimer's disease. When microglia resort to their standard modus operandi (slurping up the offending material or microorganism), those surface-based receptors go along for the ride. But unlike the ingested junk or germ, which get thoroughly broken down, these receptors are carefully shuttled back to the cell surface for another shift.
In a series of sophisticated experiments, Wyss-Coray and his associates found that a particular protein called beclin plays a starring role in microglia's receptor-recycling scheme and that deficits in beclin's production or activity seriously mess up microglia's snoop-swoop-and-scoop troupe capabilities.
The finding opens the possibility that drugs directed at restoring beclin's activity - and, by extension, microglial rubbish chomping - may delay, stop or reverse neurodegenerative disease.
Previously: Protein known for initiating immune response may set up our brains for neurodegenerative disorders, Neuroinflammation, microglia, and brain health in the balance and Old blood+ young brain = old brain
Photo by SrLigYnnek
