Blue-green algae or cyanobacteria in the intestinal micro-flora may produce neurotoxins such as Beta-N-Methylamino-l-Alanine (BMAA) which may be related to development of amyotrophic lateral sclerosis, Alzheimer’s disease and Parkinson-Dementia-Complex in humans and Equine Motor Neuron Disease in Horses

Alzheimer’s disease and gut microbiota

“…Then the cecal plus colonic microbiota were harvested from the high fat or regular chow fed mice, and transplanted to mice with normal weight and microbiota depletion by antibiotics. Results showed that the mice transplanted with high fat fed microbiota reflected selective disruptions in exploratory, cognitive and stereotypical behavior and accompanied with increase intestinal permeability, systemic inflammation and brain inflammation (Bruce-Keller et al, 2015). These data suggested that high fat diet related behavior changes were likely to be caused by diet induce changes of gut microbiota.…”

“…Cyanobacteria or blue-green algae in the gut microbiota may produce neurotoxin -N-methylamino-L-alanine (BMAA) which is considered to be related to development of AD (Banack et al, 2010;Brenner, 2013). Stress, anxiety, chronic intestinal inflammatory disease or malnutrition may further induce BMAA production and eventually lead to dysfunction of nervous system.…”

“…Recent research found that chronic dietary exposure to cyanobacterial toxin BMAA triggered NFT and A deposits in the brain and increased the risk of AD (Cox et al, 2016). Other cyanobacteria produced neurotoxins including saxitoxin and anatoxin- may further lead to neurological diseases, especially in the process of aging (Brenner, 2013). Therefore, an increase in the number of cyanobacteria in the gut may increase the risk of AD.…”

Gastrointestinal (GI) Tract Microbes and Microbial Neurotoxins in the Human Central Nervous System (CNS) in Alzheimer’s Disease (AD)

“…Evidence for the possible existence of a brain microbiome comes from the study at the point of death that the thanatomicrobiome (after the Greek 'thanatos'=death; the microbiome that appears and subsequently proliferates at the time of death) plays a primary role in the rapid decomposition and decay of host tissues [34,[56][57][58][59][60][61]. In the Western world death is defined as the complete loss and irreversible absence of brain activity including involuntary activities (such as heartbeat and breathing) necessary to sustain life [56][57][58].…”

“…Kinetic considerations and limitations involving the thanatomicrobiome support the idea of a brain microbiome due to the rapidity in which microbial populations appear and proliferate within the brain and CNS suggest that there would not be enough time for GI tract bacteria to cross both the GI tract and BBB to enter these CNS compartments to proliferate, so they may be already be resident within the confines of the BBB and/or compartments of the CNS [6]. Further support originates from the observation that blood-borne microbes are not appreciably elevated at early time-points of the PMI ( [60,61]; unpublished observations; manuscript in preparation).…”