Non-genetic environmental hazards are thought to be associated with genetic susceptibility factors that increase Alzheimer's disease (AD) pathogenesis. Aging and chronic noise exposure have been considered important factors in the AD. Here， we investigated the impact of chronic noise exposure on the AD-like neuropathology in the senescence-accelerated prone mouse (SAMP8) and the underlying mechanisms of such effects. We examined the consequences of AD-like neuropathology in 3-month-old SAMP8 mice using low- and high-intensity noise exposure and 8-month-old SAMP8 mice as aging positive controls. Immunoblotting and immunohistochemistry were conducted to examine AD-like pathological changes and potential mechani... More
Non-genetic environmental hazards are thought to be associated with genetic susceptibility factors that increase Alzheimer's disease (AD) pathogenesis. Aging and chronic noise exposure have been considered important factors in the AD. Here， we investigated the impact of chronic noise exposure on the AD-like neuropathology in the senescence-accelerated prone mouse (SAMP8) and the underlying mechanisms of such effects. We examined the consequences of AD-like neuropathology in 3-month-old SAMP8 mice using low- and high-intensity noise exposure and 8-month-old SAMP8 mice as aging positive controls. Immunoblotting and immunohistochemistry were conducted to examine AD-like pathological changes and potential mechanisms. Chronic noise exposure led to progressive overproduction of Aβ and increased the hyperphosphorylation of tau at Ser396， Thr205， and Thr231 sites in the hippocampus and the prefrontal cortex (PFC) in young SAMP8 mice， similar to that observed in aging SAMP8 mice. Both noise exposure and aging could cause a significant downregulation in Wnt signaling expression. These findings demonstrate that chronic noise stress exacerbated AD-like neuropathology， possibly by disrupting Wnt signaling and triggering aberrant tau hyperphosphorylation and Aβ in the PFC and hippocampus.
