Noise and Alzheimer's disease

Abstract

Alzheimer's disease (AD) is the most common form of degenerative dementia and the seventh leading cause of death. Numerous influencing factors for AD have been investigated: aging, female gender, genetics, unhealthy diet, hearing loss, unhealthy lifestyle, physical inactivity, insufficient sleep, head injury, depression, hypertension, and environmental factors (air pollution, aluminum, silicon, selenium, pesticides, lack of sunbathing, electric and magnetic fields). Recent animal and human studies point to a possible relationship between noise exposure and AD. The aim of this narrative review is to present basic pathological concepts of this relationship. Possible mediating factors that explain the influence of noise on AD are sleep disturbance, excitotoxicity, oxidative stress injury in the auditory cortex and hippocampus, and systemic inflammation. Studies on animals point to cognitive dysfunctions related to noise exposure: anxiety-like behavior, impaired learning and memory, increased glutamate levels in the hippocampus and reduced expression of N-methyl-D-aspartic acid receptor 2B. Neuropathological changes in animals exposed to noise include necrosis and apoptosis of hippocampal cells, accumulation of amyloid b, tau hyperphosphorylation and peroxidative damage in the hypothalamus and the auditory cortex, and the elevated expression of proinflammatory cytokines and microglial activation in the auditory cortex and hippocampus. Human brain scan studies have pointed to the positive relationship between traffic noise exposure and white matter volume in the body of the corpus callosum at the level of the auditory cortex. In conclusion, there is a biological plausibility of the noise-AD relationship, and noise countermeasures may be regarded as the prevention of AD.