So, what probiotics do we take? Do they know yet?
Soluble fiber, fewer simple sugars/carbs, and more taurine (meat), seem to be indicated, which would shift the existing populations and increase a key amino acid.
The results of the present study confirm that Alzheimer's disease is characterized by systemic and gut inflammation.29,93 Moreover, the decrease in abundance of the phyla Firmicutes and the increase in Bacteroidetes observed in Alzheimer's patients compared with age-matched cognitively healthy subjects is in line with several findings in US35 and Chinese populations.34,36 At genera level and in agreement with our findings, reduced abundance of Clostridium sensu stricto 1 is associated with adverse outcomes in Alzheimer's disease.33,35 The parabiont Desulfovibrio has also been found to be enriched in other Alzheimer's cohorts33,94 and is associated with reduced caecal levels of SCFAs and with inflammation in mice.95 As previously reported, we found a lower proportion of bacteria with the potential to synthetize butyrate,33,94 a microbial metabolite negatively associated with cortical amyloid accumulation.96 Furthermore, we confirmed reduced abundance of the genus Coprococcus in Alzheimer's disease,33 which is associated with amyloid accumulation.97 When interpreting microbiota data however, it is important to keep in mind that results may be influenced by geography,98 the inclusion criteria of study participants and methodological difference (i.e. sample collection and processing, freeze-thaw, storage methods, different bioinformatics pipelines).99,100 Not surprisingly, human faeces from different donors engrafted in rats at different rates. Notwithstanding, transfer of faecal microbiota from cognitively healthy subjects to rats resulted in the taxa diversity remaining relatively stable over time, whereas after transfer from Alzheimer's donors, there was a greater alteration in taxa between 10 and 59 days post-FMT. Notably, one of the genera that was increased at Day 59 post Alzheimer's-FMT compared to Day 10 was Desulfovibrio, a genus that was also significantly enriched in Alzheimer's participants.
Notably, however, the free amino acid taurine was decreased in the hippocampus of Alzheimer's-FMT rats. Taurine administration has repeatedly been shown to increase hippocampal neural stem and progenitor cell proliferation, survival and neurogenesis both in vivo and in vitro.88 Given its blood–brain barrier permeability,126 it is conceivable that some of the observed effects of Alzheimer's-FMT on AHN could partly be mediated via taurine.