Now we have two promising candidates for the cause of Alzheimer's -- gingivalis, and herpes-family viruses.
That doesn't mean one is right and the other wrong. Maybe herpes gets in first and lets gingivalis in, or vice versa, or some other, more interesting interaction.
What's tragic is that effectively none of the present researchers are virologists or bacteriologists. As consequences, (1) progress studying and generating a useful clinical response will be radically slowed by resistance from the old guard to the threat to their livelihood, and (2) they will all need to find something else to do, because you can't pick up those specializations overnight.
The herpes connection was noted twenty years ago, but is only now getting traction. If it's right, then almost everybody who died of AS since then was killed by the structural resistance to the idea.
The best way to accelerate progress, now, would be to find another urgent health problem that seems to need the skillset that had previously been brought to bear on AS, so they jump ship and get the hell out of the way.
What blocks someone who has expertise from trying it? There's no secret cabal of scientists who stops people from studying other ideas. This is quite a bit different than a new physicist studying a perpetual motion machine.
Nothing blocks them from trying it, except (1) grants are controlled by existing researchers and (2) publication is controlled by existing researchers.
Progress will happen eventually, but many, many people will die first.
Ask them? Biochemistry. Genetics. Proteinomics. Maybe they can design drugs?
They have the disadvantage that everybody will know they have been staring the solution to their central problem in the face for decades without seeing it. ("What, infection? Too conventional.")
In what way its dishonest? I'm not in the field so I can comment on technical points but looking at abstract, article seems to have good representation of the conclusion.
Two caveats - first, like most things, antibiotic resistance becomes a problem rapidly; second, it turns out crossing the blood-brain barrier reliably is tricky, and not incidentally triggering a severe immune response in destroying whatever you came there to attack is nasty too.
You know, you say that should be a rapid discovery, but "whoops this medication has even stronger effects in a very different domain" is a thing that periodically happens, and because treatment facilities aren't necessarily looking for or even asking the right questions to notice extremely different side effects, you might not see it.
- We realized ketamine had psychiatric benefits from after-the-fact research trying to figure out why some people had better PTSD outcomes than others
- Rogaine was being tested as an ulcer treatment when they noticed its now synonymous effects
- a number of classes of antibiotics have been seeing research publications of "hey I think this might help {depression,bipolar,anxiety,schizoaffective} symptoms" (cycloserine is one I know of offhand) and have all had known possible psychiatric side effects (albeit undesirable ones) on their boxes for decades
- Listerine was originally targeted as a general antiseptic and gonorrhea cure
- dextromethorphan was originally discovered during research for codeine alternatives
- Prozac was discovered from people attempting to improve on observed antidepressant properties in an existing antihistamine (and thus, in turn, turning attention to the entire chain of SSRI and related drug classes)
- MAOIs (the oldest class of antidepressant drugs) were discovered from noticing a tuberculosis drug relieved some depressive patients.
- TCAs (the "less harsh" family of antidepressants compared to MAOIs) were discovered around the same time as MAOIs by spontaneously noticing a synthetic antihistamine relieved depressive symptoms during testing
- One of my favorite serendipitous discoveries is a woman who realized she could smell Parkinson's when her partner developed a weird smell beginning almost a decade before he got a diagnosis, and then noticed all the patients at the support group they attended had the smell too...so she went to some researchers, and now we know there's a dozen or so molecules that are ~uniquely extremely heavily concentrated on the skins and sweat of Parkinson's patients.
The linked paper says besides the bacteria developing resistance to antibiotics, they found Kgp inhibitors seemed to continue to work.
"We have demonstrated that P. gingivalis develops rapid resistance to a broad-spectrum antibiotic, moxifloxacin, but not to the Kgp inhibitor COR388. Therefore, with the growing concern about widespread antibiotic resistance (103), ..., an antivirulence factor inhibition approach to treatment of P. gingivalis is the most promising path while reducing pressures for resistance."
That doesn't mean one is right and the other wrong. Maybe herpes gets in first and lets gingivalis in, or vice versa, or some other, more interesting interaction.
What's tragic is that effectively none of the present researchers are virologists or bacteriologists. As consequences, (1) progress studying and generating a useful clinical response will be radically slowed by resistance from the old guard to the threat to their livelihood, and (2) they will all need to find something else to do, because you can't pick up those specializations overnight.
The herpes connection was noted twenty years ago, but is only now getting traction. If it's right, then almost everybody who died of AS since then was killed by the structural resistance to the idea.
The best way to accelerate progress, now, would be to find another urgent health problem that seems to need the skillset that had previously been brought to bear on AS, so they jump ship and get the hell out of the way.