The Journal of Alzheimer’s Disease has published an editorial, signed by thirty-one researchers from institutions across several continents, calling on a re-evaluation of the disease’s origins:
We are researchers and clinicians working on Alzheimer’s disease (AD) or related topics, and we write to express our concern that one particular aspect of the disease has been neglected, even though treatment based on it might slow or arrest AD progression. We refer to the many studies, mainly on humans, implicating specific microbes in the elderly brain. . .
They’re referring specifically to HSV1, chlamydia, and some spirochete bacteria species, all of which have been found (in one study or another) to be elevated in the brain tissue of AD patients. They reference the (not very strong) studies suggesting fungal infection, but those aren’t really part of their argument, most of which concerns evidence for HSV1. They propose that these infectious agents are latent in brain tissue until reactivation by aging or stress, and that the pathology of Alzheimer’s is due to their actions and to the inflammatory response to them.
This is not a crazy idea (nor is it a new one, for that matter). It’s certainly not in the mainstream of Alzheimer’s research, as many in the field have said when called on for comment over the last few days, but it’s not the work of a bunch of cranks, either. The editorial ends up by saying “We propose that further research on the role of infectious agents in AD causation, including prospective trials of antimicrobial therapy, is now justified”. And that’s both the good part and the bad one about this area. The good part, which is indeed very good, is that this is a testable hypothesis. There are therapies for all the infectious agents mentioned, and if they really are the cause of Alzheimer’s, then you’d think that giving them to an elderly cohort would lead to a notable decrease in AD compared to the general population.
The bad part is that clinicians have been reluctant to dose these patients with years of antibiotics or antivirals for what may be no good reason. You’d want to be sure that whatever drugs you’re giving can achieve sufficient levels in the brain as well, which could be a challenge – if you have to go to the more direct methods of dosing for the CNS, that’s going to make getting a clinical trial off the ground nearly impossible. This editorial, in the end, is saying that it’s time to go ahead and try this, though, that the existing AD therapies have by now had enough trouble delivering meaningful results that other hypotheses are looking more valuable than they might have twenty-five years ago.
It’ll still be a tough sell. Ideally, you’re going to want to find older patients who (as far as can be told) have nothing wrong with them, and sign them up for what could well be years of anti-infectious drug dosing. You’re going to have to find someone who’s willing to pay for this, someone who’s willing to sign off on it as an acceptable clinical trial, and round up enough patients who are willing, after informed consent, to give it a try. None of those are going to be trivial. But overall, I tend to think that these authors are right – not that Alzheimer’s is caused by infectious organisms (I have no idea if it is or not). But I think that they’re right that it’s time to find out.