I do believe this theory really has legs folks!

A study performed in 2015 with green monkey subjects found that animals orally administered BMAA developed hallmark histopathology features of Alzheimer's Disease including amyloid beta plaques and neurofibrillary tangle accumulation. Animal subjects in the trial fed smaller doses of BMAA were found to have correlative decreases in these pathology features. Additionally, animals that were co-administered BMAA with serine were found to have 70% less beta-amyloid plaques and neurofibrillary tangles than those administered BMAA alone, suggesting that serine may be protective against the neurotoxic effects of BMAA. This experiment represents the first in-vivo model of Alzheimer's Disease that features both beta-amyloid plaques and hyperphosphorylated tau protein. This study also demonstrates that BMAA, an environmental toxin, can trigger neurodegenerative disease.[16]

BMAA may also misincorporate into nascent proteins in place of L-serine, possibly causing protein misfolding and aggregation, both hallmarks of tangle diseases, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis (ALS), progressive supranuclear palsy (PSP), and Lewy body disease. In vitro research has shown that protein association of BMAA can be inhibited in presence of excess L-serine.

BMAA bacteria can be found in water, lakes, seafood etc.

https://en.wikipedia.org/wiki/Beta-M...mino-L-alanine