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Abstract

Aim: Prenatal exposure to a disadvantageous circumstance may produce accelerated brain aging. Previously, our middle-aged model of CD-1 mice with maternal exposure to low-dose lipopolysaccharide (LPS) showed accelerated memory aging at a behavioral level. Here we investigated whether there was a corresponding pathophysiological alteration in the brain.Materials and Methods: The mothers in the LPS group were administered a low dose (i.p. 50μg/kg) of LPS daily for 3 days during late gestation to simulate an inflammatory condition in maternal infection.Results: The treatment accelerated the age-related decline of spatial learning and memory in the Morris water maze in the middle-aged offspring. Compared to control mice (n = 12), these mice (n = 12) exhibited elevated malondialdehyde contents (P = 0.042), decreased activities of superoxide dismutase (P < 0.001) and glutathione peroxidase (P = 0.010) in the brain, and elevated levels of amyloid beta (Ps < 0.005) and synaptotagmin-1 (Ps < 0.037) in several hippocampal layers. These age-related indicators correlated with a decline in spatial learning and memory (Ps < 0.05).Conclusions: During gestation, maternal illness in mice might be an initiator of accelerated brain aging in offspring, as indicated by behavioral-cognitive and neurochemical measures.