کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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5812044 | 1115025 | 2013 | 4 صفحه PDF | دانلود رایگان |

Recent work has implicated environmental stimuli as contributing to the risk of developing Alzheimer's disease (AD). Noise is one of the most important environmental health hazards for humans. Here, we propose that noise exposure, especially chronic noise exposure, can cause AD-like neuropathological changes, and that persistence of these changes have an etiological association with the development of AD. Noise can induce tau hyperphosphorylation, formation of neurofibrillary tangles (NFT) and increase β-amyloid (Aβ) and amyloid precursor protein (APP) and thus could be pivotal to AD pathogenesis and progression. The aberrant accumulation of NFT and Aβ could promote synaptic malfunction and apoptosis of neurons, which eventually could lead to Alzheimer dementia. Noise-induced excitotoxicity and oxidative stress are associated with AD-like neuropathology and an increasing risk for the development of AD. Noise can induce excitotoxicity and oxidative stress which might be one of the mechanisms how noise exposure could increase AD risk. To test this hypothesis, epidemiological studies should be carried out. On the other hand, in addition to its potential risk for the development of AD, noise exposure has many other harmful effects which warrant that actions should be taken to protect the public health from noise hazards without waiting for the results of these studies.
Journal: Medical Hypotheses - Volume 81, Issue 4, October 2013, Pages 623-626