ArticleScientific reports2018
Chronic noise exposure exacerbates AD-like neuropathology in SAMP8 mice in relation to Wnt signaling in the PFC and hippocampus.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 28 citations in OpenAlex.
- Integrating noise as a risk factor in studies of Alzheimer's disease and dementia: Guidance for epidemiologic research.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Integrating the physical environment into Alzheimer's disease and Alzheimer's disease related dementias research: A Gateway Exposome Coordinating Center (GECC) agenda on gaps and priorities.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Review
- Around-the-clock noise exposure induces hippocampus apoptosis and subsequent cognitive impairment via the PI3K/SGK1/Foxo3 signaling pathway.Journal of translational medicine · 2025Article
- Exploring the potential anti-senescence effects of soybean-derived peptide Soymetide in mice hippocampal neurons via the Wnt/β-catenin pathway.Frontiers in pharmacology · 2025Article
- Crosstalk between Oxidative Stress and Inflammation Caused by Noise and Air Pollution-Implications for Neurodegenerative Diseases.Antioxidants (Basel, Switzerland) · 2024Review
- Health position paper and redox perspectives - Disease burden by transportation noise.Redox biology · 2024Review
- Chronic noise exposure induces Alzheimer's disease-like neuropathology and cognitive impairment via ferroptosis in rat hippocampus.Environmental health and preventive medicine · 2024Article
- Research Progress on the Etiology and Pathogenesis of Alzheimer's Disease from the Perspective of Chronic Stress.Aging and disease · 2023Review
- Redox Imbalance as a Common Pathogenic Factor Linking Hearing Loss and Cognitive Decline.Antioxidants (Basel, Switzerland) · 2023Review
- Around-the-Clock Noise Induces AD-like Neuropathology by Disrupting Autophagy Flux Homeostasis.Cells · 2022Article
- Noise exposure in early adulthood causes age-dependent and brain region-specific impairments in cognitive function.Frontiers in neuroscience · 2022Article
- MicroRNA Dysregulation in the Hippocampus of Rats with Noise-Induced Hearing Loss.Oxidative medicine and cellular longevity · 2021Article
- Effect of acute noise trauma on the gene expression profile of the hippocampus.BMC neuroscience · 2020Article
- Icaritin Improves Memory and Learning Ability by Decreasing BACE-1 Expression and the Bax/Bcl-2 Ratio in Senescence-Accelerated Mouse Prone 8 (SAMP8) Mice.Evidence-based complementary and alternative medicine : eCAM · 2020Article
Corrections and comments
- Erratum issued
Authors and funding
7 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
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.
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