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. Author manuscript; available in PMC: 2023 Sep 12.
Published in final edited form as: Curr Alzheimer Res. 2022;19(5):335–350. doi: 10.2174/1567205019666220617121255

Table 1.

Gastrointestinal-associated inflammatory changes that may contribute to AD.

GI Tract
Regions		 Inflammatory Changes References
Oral Cavity Invasion of periodontal pathogens or their harmful products directly into the brain via systemic circulation or peripheral nerves correlates with inflammation and neurodegeneration in humans. (45-53)
Periodontitis induces systemic inflammation, potentially resulting in neuronal injury via a compromised blood-brain barrier (BBB) in rodent models. (57-59)
Stomach Stomach infection of mice with H. pylori alters eating behavior, brain cytokine levels and increases gliosis. (83, 85)
88% of AD patients and 46.7% of controls are H. pylori-positive. H. pylori eradication significantly improves cognitive performance. (89)
Small Intestine Human AD intestines have increased Aβ and CD68 immunoreactivity compared to controls. (190)
APP/PS1 mouse model has increased ileum Aβ and CD68 immunoreactivity and elevated luminal IgA compared to wild-type mice. (190)
Large Intestine IBD-like disease induced by 2,4,6-trinitrobenzene sulfonic acid (TNBS) results in microglial activation and elevation of TNF-α levels in the hippocampus of adult male rats. (114)
Colonic inflammation induced by 2 bouts of 2% DSS administration led to Aβ plaque load increase in the hippocampus and temporal cortices and decreased microglial CD68 immunoreactivity in AppNL-G-F mice. (115)
Induction of colonic inflammation is associated with alteration in hippocampal neurogenesis and memory dysfunction in IBD mouse models. (116-118)
Human IBD patients are at higher risk of dementia with an average onset of 7 years younger compared to controls. (122)
Bacteroides colonization increased intestinal inflammation and exacerbated Aβ deposition in the Tg2576 mouse model of AD. (153)
A diet containing wheat amylase trypsin inhibitor in an AD mouse mice induced dysbiosis, increased intestinal myeloid immune cell subsets, and potentiated pathological hallmarks of AD. (136)
Gut dysbiosis elevated bloodstream/brain LPS in human AD brains. (52, 53, 161, 162)
Antibiotic treatment-induced dysbiosis altered circulating levels of cytokines/chemokines and reduced Aβ plaques in the APPSWE/PS1ΔE9 mouse model of AD. (157)
The altered ratio of Firmicutes/Bacteroidetes correlated with intestinal proinflammatory cytokine changes and increased intestinal permeability in the AppNLG-F mouse AD model. (137)