Noise and Alzheimer's disease

Belojević, Goran · 2023 · Crossref

DOI: 10.58424/annnurs.y9e.cdx.n73

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Summary

This narrative review investigates the potential causal relationship between chronic noise exposure and Alzheimer’s disease (AD), positioning noise as an emerging environmental risk factor. The study is motivated by the global burden of AD and recent evidence suggesting that environmental noise contributes to cognitive impairment and neurodegeneration. The author aims to synthesize existing animal and human studies to elucidate the pathological mechanisms linking noise exposure to AD pathology, including amyloid-beta accumulation and tau hyperphosphorylation. The methodology involved a systematic search of the PubMed database for English-language papers published up to April 2023, using keywords related to noise, cognition, memory, and dementia. The review categorizes findings into animal studies, human studies, and pathological concepts. Animal experiments primarily utilized rodents exposed to various noise levels (e.g., 70–100 dB) and durations, assessing behavioral changes, neurotransmitter levels, and neuropathological markers. Human studies included epidemiological cohorts, experimental exposure trials, and brain imaging analyses to evaluate cognitive performance and dementia risk associated with traffic, aircraft, and occupational noise. Findings from animal studies demonstrate that chronic noise exposure induces cognitive deficits, anxiety-like behaviors, and significant neuropathological changes. These include hippocampal cell necrosis and apoptosis, increased amyloid-beta production, tau hyperphosphorylation, and neuroinflammation characterized by elevated proinflammatory cytokines. Mechanistically, noise exposure activates the hypothalamic-pituitary-adrenal axis, leading to elevated corticosterone levels, and disrupts glutamate-NMDA receptor signaling, resulting in excitotoxicity and oxidative stress. In humans, epidemiological data indicate a dose-response relationship between noise exposure and dementia risk. A meta-analysis reported a relative risk of 1.18 for AD per 25 dB increase in noise. Cohort studies in Denmark and other regions showed increased hazard ratios for AD and mild cognitive impairment associated with road and railway noise levels above 50–65 dB. However, some studies found no significant association, highlighting inconsistencies potentially due to confounding factors like air pollution or uncontrolled hearing status. Brain imaging studies revealed correlations between traffic noise and white matter volume changes in the corpus callosum. The review concludes that there is biological plausibility for noise as a risk factor for AD, mediated by both hearing-loss-related mechanisms (social isolation, cognitive load) and direct neurotoxic pathways (oxidative stress, excitotoxicity, neuroinflammation). The author suggests that noise countermeasures could serve as preventive strategies for AD. Future research is recommended to investigate the efficacy of hearing aids in slowing cognitive decline and to conduct intervention studies in industrial settings with better control of confounding variables.

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• cognitive impairment