An Inflammatory Theory of Brain Disease

Tina

Well-Known Member
This article is about brain inflammation, not ME/CFS. If you believe that brain inflammation could be the cause of ME/CFS then it might be a good read. Although the article is longish, I found it to be written in a nice, easy style.

And if brain inflammation is a great unifier of many diseases then let’s hope that one of these many diseases that gets so much more funding than ME/CFS can be a catalyst to find a cure that can help us.

The article discusses items that we have heard before….
… there are times when inflammation doesn’t know when to quit, and many doctors and researchers believe it plays a role in many chronic diseases. The growing list goes beyond autoimmune diseases, such as arthritis, diabetes, or multiple sclerosis, to include cardiovascular disease and possibly even brain diseases such as Alzheimer’s, Parkinson’s, epilepsy, or depression.

… But inflammation also causes collateral damage, a sort of friendly fire. The same processes that get rid of foreign agents can damage good cells as well. The death of those cells can in turn trigger further inflammation. For reasons that remain unclear, sometimes this creates a vicious cycle that becomes self-sustaining. Steven Meier, a neuroscientist at the University of Colorado who researches how the brain regulates immune responses points out that, “like many, many other adaptive mechanisms that are adaptive when they’re activated briefly, they may not be so adaptive when they’re activated chronically.”

However, when they’re activated by injury or infection, microglia multiply, shape-shift into blobby, amoeba-like structures, release inflammatory chemicals, and engulf damaged cells, tissue debris, or microbes.
And something that researchers are beginning to understand; that those who have been sick short-term are not the same as those of us who have been sick long-term:

“Once you have this fully established chronic inflammation, it’s much, much more difficult to deliver effective treatments to those areas,” Bielekova says. “In multiple sclerosis, it is very clear that whichever drug you take that is efficacious, the efficacy decreases as you delay the treatment. So if you use the treatment very, very early on, every drug looks like a winner. But you wait just a couple of years and you take patients that are now three four years longer in the disease duration you may lose 50% efficacy of your drug.”
Maybe an easier target?

Damir Janigro, a blood brain barrier researcher at Cleveland Clinic who studies traumatic brain injury and epilepsy, has a very different take on how to approach brain diseases linked with inflammation. He considers both of these diseases to be “blood brain barrier” diseases because repeated seizures and traumatic brain injury can damage the blood brain barrier, making it leakier. That means that not only can substances that don’t belong inside the brain slip through, materials from inside the brain can travel to the rest of the body…. Janigro is part of what he calls a “vocal minority” of researchers who look at inflammation outside the brain as being another cause of inflammation inside the brain—and potentially even a better target for treatment.
Here is the article:
http://www.pbs.org/wgbh/nova/next/body/brain-inflammation/
 

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