Lipopolysaccharide exposure during late embryogenesis triggers and drives Alzheimer-like behavioral and neuropathological changes in CD-1 mice.

At the age of 12 months, LPS treatment effects on the levels of Aβ 42 and p‐tau were significant in different hippocampal layers; that is, Aβ 42 in DG‐HL and CA3‐LS [ F (2, 42) = 4.295, 4.147; p = .035, .039] and p‐tau in CA1‐RS and CA1‐PL [ F (2, 42) = 3.919, 3.614; p = .039, .048; Table 2 ], and marginally significant on the level of GFAP in CA3 [ F (2, 42) = 3.244, p = .063; Table 5 ].

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