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Two proteins central to the pathology of Alzheimer’s disease act as prions — misshapen proteins that spread through tissue like an infection by forcing normal proteins to adopt the same misfolded shape — according to new UC San Francisco research.
Using novel laboratory tests, the researchers were able to detect and measure specific, self-propagating prion forms of the proteins amyloid beta (Aß) and tau in postmortem brain tissue of 75 Alzheimer’s patients. In a striking finding, higher levels of these prions in human brain samples were strongly associated with early-onset forms of the disease and younger age at death.
Alzheimer’s disease is currently defined based on the presence of toxic protein aggregations in the brain known as amyloid plaques and tau tangles, accompanied by cognitive decline and dementia. But attempts to treat the disease by clearing out these inert proteins have been unsuccessful. The new evidence that active Aß and tau prions could be driving the disease – published May 1, 2019 in Science Translational Medicine — could lead researchers to explore new therapies that focus on prions directly.
“I believe this shows beyond a shadow of a doubt that amyloid beta and tau are both prions, and that Alzheimer’s disease is a double-prion disorder in which these two rogue proteins together destroy the brain,” said Stanley Prusiner, MD, the study’s senior author and director of the UCSF Institute for Neurodegenerative Diseases, part of the UCSF Weill Institute for Neurosciences. “The fact that prion levels also appear linked to patient longevity should change how we think about the way forward for developing treatments for the disease. We need a sea change in Alzheimer’s disease research, and that is what this paper does. This paper might catalyze a major change in AD research.”
(Score: 0) by Anonymous Coward on Friday May 03 2019, @06:33PM (2 children)
The point is they put "presence of plaques" in the definition when there is only a weak correlation between presence of plaques and the symptoms. It is all one big fat assumption that has wasted tens of billions of dollars fand 30-40 years of research for no reason.
(Score: 2) by RS3 on Friday May 03 2019, @09:59PM (1 child)
You are really pounding that point into the ground. As far as I know, the discovery / isolation of those plaques was a major breakthrough in Alzheimer's Disease research, and really all they had to go on. You could say everyone was jumping on a bandwagon. Maybe you had to show you were working on plaque research to get grants and other research money? Regardless, if I'm reading the article correctly, the plaques are the result of the prions' effect on the brain, so figuring out what was causing them seems like the path to the prion discovery.
If you want to troll the whole world of research, how about this: we have in some cases hundreds or thousands of researchers and labs working IN PARALLEL, redundantly, competing to solve various diseases. Wouldn't it be much better if everyone could work together, collaboratively?
(Score: 1, Informative) by Anonymous Coward on Friday May 03 2019, @10:45PM
No, before that they hypothesized it was a deficiency in acetylcholine. To this day, drugs based on that hypothesis are the only ones that seem to help. So, they abandoned a better hypothesis for a new hypothesis based on nearly nothing. Then the new hypothesis became dogma, based on nearly nothing.
Then they wasted the next 30 something years on this amyloid BS when it is obvious that amyloids accumulate in every single disease state where anyone has ever looked* (cancer, heart disease, you name it). When a cell gets sick the trash doesn't get taken out so it builds up. The build up of trash could also make the cell sicker of course, but that is another symptom, not a cause.
*Amyloids are the default state (lowest energy configuration) of polypeptides.