“…Taken together these results suggest that the increased abundance of Bacteroides in patients with AD may result in an increased translocation of LPS from the gut to the systemic circulation, which in turn may exacerbate AD pathology through enhanced pro-inflammatory signaling or related pathogenetic mechanisms [5,10,54,55]. These findings further suggest that LPS and perhaps other bacterial-derived amyloids, sncRNAs, endotoxins and neurotoxins are localized to the same anatomical regions involved in AD-type neuropathology and these may be significant initiators or progressive contributors to inflammatory degeneration, amyloidogenesis and/or an altered innate-immune response in the AD CNS ( Figure 1; [5,34,54,55]). …”