"It tells us there are some factors that are protecting their brains and memories against the Alzheimer’s pathology of plaques and tangles. Now we have to find out what those are.”

There are just a few researchers that believe that the plaques are protective. I found some that think that they are there to isolate the toxoplasmosis parasites that can get thru the blood/brain barrier. The apicomplexians can "tunnel" thru cell walls with a special organ in their cytoplasms, and some other microbes get in by tunneling along the myelin sheaths where nerves pathways enter/exit. edit: Also has been found that one of the basic sugars can open the BB for up to 20 min. IIRC correctly, it was maltose.

Also young blood , possibly stem cells from youngsters is again shown to reduce effects of aging.

"Minami says she has identified some factors in young blood that might be responsible for these benefits, but that she won’t reveal what they are yet. Some of them seem to be crossing into the brain, while others may be acting remotely, elsewhere in the body, she says."

https://www.newscientist.com/article/2112829-blood-from-human-teens-rejuvenates-body-and-brains-of-old-mice/

"New role in cells suggested for ATP Known as an energy carrier, molecule can also solubilize proteins"

"investigated the effects of ATP on the aggregation of several proteins. They found that ATP could prevent the aggregation of two proteins known to form amyloid clumps. For a third protein, ATP was further able to dissolve fibers of already aggregated protein. And ATP kept proteins in boiled egg white from aggregating.

“Most healthy cell functions require that proteins remain soluble at enormous intracellular concentrations, without aggregating into pathogenic deposits,” write Allyson M. Rice and Michael K. Rosen of the University of Texas Southwestern Medical Center in a perspective accompanying the paper. “The cell may exploit a natural hydrotrope to keep itself in a functioning, dynamic state.”

http://cen.acs.org/articles/95/i21/New-role-cells-suggested-ATP.html

I wonder if they were taking drugs for depression, because

http://www.bbc.com/news/health-39641123

"Two were shown to prevent both a form of dementia and prion disease by stopping brain cells dying"

"Both were very highly protective and prevented memory deficits, paralysis and dysfunction of brain cells." (in mice)

The best known drug of the pair is trazodone, which is already taken by patients with depression.

The other, DBM, is being tested in cancer patients.

https://academic.oup.com/brain/article/doi/10.1093/brain/awx074/3737867/Repurposed-drugs-targeting-eIF2-P-mediated

Altering pH bumps proteins from clumping

"While prion's transmission method is quite unusual, the process of protein clumping is quite common in a number of diseases, such as Alzheimer's and Parkinson's disease,"

"the team found that prion-related protein chains reconfigure slowly at neutral pH, thus avoiding the sticky middle speeds.

"If rearrangement is fast, when two chains come into contact, they can rearrange rapidly enough to avoid making interactions that lead to clumping," Lapidus said. "When moving slow, neither chains will have sticky patches exposed. But when the rearrangements are happening at the same speed as the random collisions between two proteins, then clumping can occur more quickly."

Lapidus proved that astemizole is effective in speeding up protein self-interactions even further and preventing prion clumping.

Astemizole was once used to treat allergies, but it was pulled from the market due to rare but sometimes fatal side effects. The antihistamine, however, also has shown promise in some Alzheimer's research."

http://msutoday.msu.edu/news/2017/altering-ph-bumps-prions-out-of-danger-zone/

I seem to recall similar discoveries during the Nun Study, that what had been thought to be biological correlates of the disease were mostly unrelated to noticeable progression of the disease. I don't know enough to tell you the difference between what they're noticing here and there.

It's good news and bad news in a way. It casts a lot of doubt on the efficacy of beta-amyloid (plaque) targeting drugs that are in the pipeline right now.