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nidan7500

02/18/18 1:08 PM

#141577 RE: Amatuer17 #141576

"Even though we really concentrate on these plaques and tangles in Alzheimer's disease, it looks like it's the brain's immune system — the very primitive immune system of the brain — that's gone awry," Tanzi says, "and the plaques and tangles are a part of that system."
The question now is: What's causing the glitch in the ancient immune system?
One possibility is that it's overreacting to viruses and bacteria that get into the brain. Or, the system could be getting confused and attacking healthy cells — a lot like what happens in diseases like lupus or multiple sclerosis.
If either idea holds up, it may be possible to interrupt the process before it causes Alzheimer's, Moir says. "That's a pretty good outcome from a couple of Coronas 10 years ago."



https://www.npr.org/sections/health-shots/2018/02/18/580475245/scientists-explore-ties-between-alzheimers-and-brains-ancient-immune-system

At least it helps to explain why the plaques and tangles causal theory could not be proven. Billions and years down the chute.
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F1ash

02/18/18 1:19 PM

#141579 RE: Amatuer17 #141576

Interesting - seems Amyloid Beta maybe protective layer - generating in excess leads to issues



Another article by Moir and Tanzi.



“When the researchers looked even closer, Moir said, at the center of each plaque was a single microbe."


http://news.harvard.edu/gazette/story/2017/05/devastating-chain-of-events-found-in-alzheimers-path/

"Moir adds, "Our findings raise the intriguing possibility that Alzheimer's pathology may arise when the brain perceives itself to be under attack from invading pathogens, although further study will be required to determine whether or not a bona fide infection is involved. It does appear likely that the inflammatory pathways of the innate immune system could be potential treatment targets. If validated, our data also warrant the need for caution with therapies aimed at totally removing beta-amyloid plaques. Amyloid-based therapies aimed at dialing down but not wiping out beta-amyloid in the brain might be a better strategy."

Says Tanzi, "While our data all involve experimental models, the important next step is to search for microbes in the brains of Alzheimer's patients that may have triggered amyloid deposition as a protective response, later leading to nerve cell death and dementia. If we can identify the culprits -- be they bacteria, viruses, or yeast -- we may be able to therapeutically target them for primary prevention of the disease."



A video that does a good job of explaining Alzheimer’s that I posted before, but seemed worth repeating: