Abstract
BackgroundChronic noise exposure is one environmental hazard that is associated with genetic susceptibility factors that increase Alzheimer’s disease (AD) pathogenesis. However, the comprehensive understanding of the link between chronic noise stress and AD is limited. Herein, we investigated the effects of chronic noise exposure on AD-like changes in senescence-accelerated mouse prone 8 (SAMP8).MethodsA total of 30 male SAMP8 mice were randomly divided into the noise-exposed group, the control group, and aging group (positive controls), and mice in the exposure group were exposed to 98 dB SPL white noise for 30 consecutive days. Transcriptome analysis and AD-like neuropathology of hippocampus were examined by RNA sequencing and immunoblotting. Enzyme-linked immunosorbent assay and real-time PCR were used to further determine the differential gene expression and explore the underlying mechanisms of chronic noise exposure in relation to AD at the genome level.ResultsChronic noise exposure led to amyloid beta accumulation and increased the hyperphosphorylation of tau at the Ser202 and Ser404 sites in young SAMP8 mice; similar observations were noted in aging SAMP8 mice. We identified 21 protein-coding transcripts that were differentially expressed: 6 were downregulated and 15 were upregulated after chronic noise exposure; 8 genes were related to AD. qPCR results indicated that the expression of Arc, Egr1, Egr2, Fos, Nauk1, and Per2 were significantly high in the noise exposure group. These outcomes mirrored the results of the RNA sequencing data.ConclusionsThese findings further revealed that chronic noise exposure exacerbated aging-like impairment in the hippocampus of the SAMP8 mice and that the protein-coding transcripts discovered in the study may be key candidate regulators involved in environment-gene interactions.
Highlights
Alzheimer’s disease (AD) is the most common form of dementia, accounting for 50–56% of autopsy and clinical cases [1]
Chronic noise exacerbates AD-like neuropathology in senescence-accelerated mouse prone 8 (SAMP8) mice To explore the effects of chronic noise exposure on Amyloid beta (Aβ) in the hippocampus, we determined the concentrations of soluble and insoluble Aβ1-40 and Aβ1-42 in the brain components by using a mouse Enzyme-linked immunosorbent assay (ELISA) kit
Tau phosphorylation levels were assessed by quantitative immunoblot analyses of cortical extracts from individual mouse in each group after the end of the 30-day experiment period (Fig. 1e, f). In comparison with those in the control group, the levels of tau phosphorylated at Ser202 and Ser404 in the noise group were significantly increased (Fig. 1g, h). These data suggested that chronic noise exposure accelerated AD-like pathological alterations in the SAMP8 mice
Summary
Alzheimer’s disease (AD) is the most common form of dementia, accounting for 50–56% of autopsy and clinical cases [1]. It is marked by a progressive loss of memory and cognitive function, overproduction of amyloid beta (Aβ), and increased hyperphosphorylation of tau [1, 2]. AD-like pathological changes, such as aggregation of Aβ and the phosphorylation of tau protein, are associated with aging [8, 9]. Chronic noise exposure is one environmental hazard that is associated with genetic susceptibility factors that increase Alzheimer’s disease (AD) pathogenesis. We investigated the effects of chronic noise exposure on AD-like changes in senescence-accelerated mouse prone 8 (SAMP8)
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
