Abstract
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.
Highlights
Alzheimer’s disease (AD) is a neurodegenerative disease in which the significant pathological changes are an overproduction of amyloid beta (Aβ) and increased hyperphosphorylation of tau[1]
AD-like neuropathology and play important roles in the development of AD, we investigate the effects of chronic noise exposure on AD-like pathology in the senescence-accelerated mouse prone 8 (SAMP8), an excellent model of the accelerated senescence associated with AD
The 3-month-old male SAMP8 mice were randomly separated into three groups: control group, the low intensity noise exposure group (LN group) that was exposed to 88 dB sound pressure level (SPL) white noise, the high intensity noise exposure group (HN group) exposed to 98 dB SPL white noise, and the control aging group that consisted of 10 male SAMP8 mice at 8 months of age
Summary
Alzheimer’s disease (AD) is a neurodegenerative disease in which the significant pathological changes are an overproduction of amyloid beta (Aβ) and increased hyperphosphorylation of tau[1]. Chronic noise exposure in experimental animals can cause significant and persistent hyperphosphorylation of tau and formation of prominent pathological neurofibrillary tangles (NFT) of tau in the hippocampus and the prefrontal cortex (PFC), key structures in learning and memory and the initial sites of tau pathology in AD12. These results indicate that noise exposure is associated with an increased risk of developing AD. The development of AD pathogenesis is multifactorial, with aging, environmental and occupational factors implicated[13] Based on these findings, we theorized that chronic noise exposure would exacerbate aging-related. Correspondence and requests for materials should be addressed to www.nature.com/scientificreports/
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