Table 1 Bacterial involvement in AD

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-PS1△E9 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], APP_OSK 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