The Temblors Continue, Ctd

One aspect not receiving a lot of attention in the concussion issue and the NFL is the technical aspects – how do concussions trigger chronic traumatic encephalopathy (CTE)? Researchers working on expanding understanding of the blood-brain barrier have discovered it’s not the unbreachable wall so long assumed – and what happens when it suffers physical shocks? NewScientist‘s James Mitchell Crow (18 March 2017, paywall) has some information from bleeding edge research:

So how can a series of minor blows to the head have such catastrophic consequences? Earlier this year, Matthew Campbell at Trinity College Dublin in Ireland came up with an answer: disruptions in the blood-brain barrier, a protective cellular seal around blood vessels in the brain (see main story). Campbell’s team showed that sub-concussive blows can temporarily rupture this barrier, letting in all sorts of potentially damaging cells and molecules.

The main story discusses how researchers are changing the general understanding of the blood-brain barrier, and the insights, hopefully to be confirmed and enlarged upon, this has to do with various degenerative neurological diseases:

In 2013, [Michal Schwartz, a neuroscientist at the Weizmann Institute for Science] and her colleagues found that the normal blood-brain barrier rules don’t apply at a structure called the choroid plexus. Here, a different kind of cellular seal separates blood from brain – one which macrophages can cross, a process controlled in part by a cytokine called interferon gamma. Schwartz found that cytokine signalling here tends to weaken as we age, reducing the number of macrophages that get into the brain. She later found that the communication across this border was shut down completely in mice bred to have a condition equivalent to Alzheimer’s – “just when you need the macrophages most”, Schwartz says.

Intrigued, Schwartz decided to see what happens to these mice when you block the signals that suppress interferon gamma production and gum up the barrier. The result was a surge of macrophages crossing into the brain and a reduction in the number of amyloid plaques. What’s more, the mice showed improvements in their symptoms. Schwartz’s team is now working towards human clinical trials of the technique.

Macrophages are responsible for mopping up cellular debris, foreign bodies, and other undesirables. This is what I’d call cutting-edge research, to be treated like rumors until confirmed. The article ends with speculation concerning autism and even general sociability being dependent on the proper presence, or perhaps more accurately the improper absence, of macrophages in the brain.

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About Hue White

Former BBS operator; software engineer; cat lackey.

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