“…Only a few of the many supporting facts for the above hypothesis are as follows: - Changes in the gut microbiome, correlating with the pathophysiology of AD, observed in both AD patients and mouse models of AD [ 24 , 25 , 27 , 28 , 29 ];
- Studies, using antibiotic treatment [ 30 , 31 , 32 , 33 ] or mice bred in germ-free conditions and devoid of gut microbiota [ 34 , 35 , 36 ], showing a strong reduction in Aβ pathology and in microglial activation in AD mice models;
- Evidence that gut dysbiosis may lead to raised levels of circulating gut microbiota metabolites, including β-N-methylamino-L-alanine and microbial amyloids, the former, a gut cyanobacteria-produced neurotoxin, shown to cause hippocampal cell death and learning and memory deficits [ 37 , 38 , 39 ];
- Studies on probiotic supplementation based on lactobacilli and bifidobacteria showing beneficial effects on cognitive function and other disease parameters in AD patients and animal models of AD and dementia [ 40 , 41 , 42 , 43 ].
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