Curious, dark cells resembling shrunken microglia have been discovered in the brains of Alzheimer's patients  

A research team from Laval University in Québec has stumbled upon small, darkened cells in the brains of mice with Alzheimer's disease. These appear to be a damaged, diminished form of microglia - the brain's 'housekeeping' cells which prune, quarantine and protect against infection. 

“We don’t know yet if they’re a cause or consequence”

The unusual cells were initially difficult to find as they fail to show up using conventional microglia stains. When they were finally observed however, they appeared to be playing a harmful role; wrapping around synapses and heralding synapse degradation. 

Not exclusively in Alzheimer's

While these cells appeared in greatly increased numbers in the brains of mice with Alzheimer's, they can actually be observed in younger mice too. More importantly, they seem to rise in number with ensuing age. 

“There were 10 times as many dark microglia in Alzheimer’s mice as in control mice” 

They have been found in humans too

Credit: Servier Medical Art

The same cells have now been identified in human samples, with an Alzheimer's patient who died at 45 displaying double the number as a healthy individual of the same age.  The most pertinent question now is, 'what do they do and why are they there?'. One theory is that the cells have gone into hyperactive mode and are acting excessively and detrimentally. Further study has also revealed that the smaller and darker the cells appear, the more damaged proteins and DNA they contain, which suggests they have been withered by exposure to stress of some kind. Perhaps they're simply a consequence of other damaging processes going on, but they may be connected to the destructive inflammation tied to Alzheimer's disease progression. 

"Studies in patients show that inflammation arising outside the brain is associated with more rapid decline in Alzheimer’s patients, and it’s important to unravel what role microglia might play in this acceleration of disease”

Read more at The New Scientist

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