Elevated heat shock proteins actually makes good sense as a reason. We should check ClinicalTrials.gov using the key words: Alzheimer and “heat shock protein”.
I just tried anf found a total of 130 trials using Heat shock proteins 70 or 90 (HSP70 and HSP90) and with very few exceptions they are all cancer trials.
>"I spent 20 years in the Navy, most of it in the hot spots, like the engine rooms of ships—110 degrees is nothing on a ship," he says.
That environment may have caused an increase in heat shock proteins, which were able to limit the spread of tau and prevent the onset of Alzheimer's.
The scientists studying Whitney aren't sure if that's all, or even part, of the explanation. But they are hoping that the paper on Whitney will encourage other researchers to look for answers.
So instead of going to work for the navy, one could just go to the sauna daily.
The link between BMAA (from toxic algae blooms) and neurodegenerative diseases in predisposed people is basically causal and proven at this point, but it's allegedly suppressed by Big Fishing and Aquaculture.
You may be right. There are many other components contributing to the problem in Finland, too.
Presumably, a newer generation of anti-amyloid or anti tau agents. There are current gen ones (targeted monoclonal ab ) which aren’t that incredibly effective but there’s some thought that maybe that’s due to treating the wrong patients at the wrong time, vs starting therapy earlier on
We've been developing Sleep slow-wave enhancement tech for the last few years, and studies are showing promise as a potential prevention and management of AD.
These links were not using our tech, but are based on the same principles of phase-targeted slow-wave enhancement. We have an enhanced protocol aiming to overcome some of the issues these researchers experienced with previous implementations.
We have a lot of correlations and theories and now we can test over more than 10 years and see what happens when with patients where we have successfully kept these markers down from a much earlier start. I just hope they control correctly for brain bleeds and premature death.
As far as I'm aware, we currently have no evidence to suggest whether the appropriate model for this protein accumulation is more "it's like a cancer growing on your organ" or "it's like a scab growing over an open wound".
Are scabs markers of injury? Of course.
Could we reduce injuries by preventing the development of scabs? No, that's a new horrifying medical condition called hemophilia. In the general case, it's rapidly fatal.
This is something that really bothers me about the current craze for suppressing inflammation. In that case, we already know that inflammation is like scabs, a defensive reaction against some other problem. For Alzheimer's, we don't know anything.
There’s been evidence recently that GLP-1 Agonists can delay the onset of Alzheimer's symptoms. Look up the evoke and evoke+ trials. This might be the first “real” treatment for Alzheimer’s, and it’s relatively low risk.
I wonder what interventions they mean here. Drugs, lifestyle changes?