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Table 1 Bacterial involvement in AD

From: Microbial involvement in Alzheimer disease development and progression

Finding Supported by Model
Amyloid as AMP 19, 20 5XFAD mouse [19], in vitro [19, 20], nematode [19], human brain tissue [20]
Bacteria colocalizes with Aβ plaques 21, 40 Sprague-Dawley rats [21], Human brain tissue [40], specific pathogen-free BALB/c mice [40]
Ab fibrils activate microglia 45 Human THP-1 monocytes and microglia
EP2 induces neuronal damage by toxicity and increased amyloid beta levels 49 APPSWE-PS1E9 mice
Overactive microglia lead to neuroinflammation 53 APP/PS1 mice
LPS is more abundant in AD brain 99, 100 Human brain tissue
LPS stimulation leads to enhanced Aβ accumulation 23, 24 E. coli cultures [23], APP Swe Tg mice [24]
AD induces changes in bacterial communities 25-29 APP/PS1 mouse stool [25], human stool [26,27,28], human brain tissue [29]
Broad-spectrum antibiotic cocktail altered gut bacterial communities and reduced AD hallmark characteristics 89 APPSWE/PS1ΔE9 mice
Rifampicin treatment reduced AD hallmark characteristics 30-33 Cell culture [30,31,32], APPOSK mice [32, 33]
Minocycline treatment reduced AD hallmark characteristics 34, 35 Sprague-Dawley rats [34], APP Tg mice [35]
Periodontal disease risk factor for AD 112 Human patient serum
P. gingivalis can access brain and associate with Aβ plaques 36-38, 40 Human brain tissue [36, 40], ApoE−/− mice [37, 38], specific pathogen-free BALB/c mice [40]
AD patients have increased antibodies to periodontal disease-associated microbes 112, 114 Human patient serum
Probiotic supplementation improves cognitive function and reduces neuroinflammation 102, 103 Human
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