Table 2.

Recent data on the role of microbiota in AD pathogenesis from animal and human studies.

AD model	Main findings	References
1. CONVR-APPPS1 and GF mice	Change in the gut microbiota composition: A significant reduction in cerebral Aβ pathology in GF mice compared to control mice; colonization of GF mice with microbiota from conventionally-raised mice increased cerebral Aβ pathology, whereas colonization with microbiota from WT mice was less effective in increasing cerebral Aβ levels	(40)
2.5X FAD mice	Changes in the composition of the feces microbiota with increasing age; human APP expressed not only in the brain but also in the gut tissue and lowered trypsin level in fecal proteins	(8)
3. APOE−/− mice	Porphyromonas gingivalis active invasion and infection-induced complement activation in APOE−/− mice brains	(37)
4. AD rat model	Lactobacillus plantarum improved cognitive function by restoring acetylcholine levels, reducing Aβ plaque formation	(82)
5. Transgenic Drosophila	Enterobacteria infection promotes immunological haemocyte recruitment to the brain, which exacerbates the development of AD; elimination of haemocytes reduces neuroinflammation and prevents neurodegeneration	(79)
6. Living AD subjects	Increased pro-inflammatory and decreased anti-inflammatory bacteria. LPS levels were significantly greater in AD plasma specimens, and there was a positive association between level of blood monocyte/macrophage activation in the disease groups	(38).
7. Post mortem brain samples	Poole et al. (37) reported the presence of LPS from Porphyromonas gingivalis in sections of AD brains. 16S rRNA sequencing revealed increased bacterial populations in AD brain tissue (39). DNA specific to Borrelia burgdorferi was found in senile plaques by Miklossy	(83)