Maybe zinc works like serine?
https://www.clinicaltrials.gov/ct2/show/NCT01259050 . But I don't understand the applicability to AD, as Cox's research points to a motor neuron disease, ALS, or Lytico-bodig disease, and the description from Guam of connection to BMAA is a lytico paralysis ending in a bodig dementia "like AD". The vervet study of BMAA showed neurdegeneration like AD but not ALS. I think there is room for more controversy and Cox and allies need better research before applying to AD treatment or prevention.
Thus I am especially alarmed at the paper today "Cyanobacterial neurotoxin BMAA and brain pathology in stranded dolphins" at
https://doi.org/10.1371/journal.pone.0213346 that found BMAA and beta amyloid in stranded dolphin brains. BMAA are mostly produced by cyanobacteria, and dolphins like humans are at the top of the food chain, but all the links from the bottom to top of that chain haven't been filled in for BMAA and its isomers. And BMAA measurements haven't been sufficiently standardized. It seems most likely to me that there are many factors including heredity behind both AD and BMAA susceptibility. And now enviromental politics.
https://www.sciencealert.com/beached-do ... -to-us-all comments
"these creatures [dolphins] may very well be our first indication of poor environmental conditions, and while it's still not clear if these blooms directly lead to Alzheimer's in dolphins or in humans, the researchers say it's a risk we shouldn't be willing to take. "The $64,000 question is whether these marine mammals experienced cognitive deficits and disorientation that led to their beaching," says co-author Paul Alan Cox, an ethnobotanist at the Brain Chemistry Labs in Jackson Hole. Until further research clarifies this question, people should take simple steps to avoid cyanobacterial exposure."
