AI Article Synopsis
- Chronic noise exposure can lead to Alzheimer's disease-like changes in the brain, such as increased tau hyperphosphorylation and β-amyloid buildup in the prefrontal cortex (PFC).
- The study focused on how chronic noise affects the corticotropin-releasing factor (CRF) system, which plays a key role in stress response and tau regulation.
- Results showed that chronic noise exposure elevated levels of corticosterone, CRF, and its receptor CRFR1, linking these changes to tau phosphorylation in PFC neurons, suggesting a potential mechanism in noise-induced cognitive decline.
Article Abstract
Chronic noise exposure has been associated with Alzheimer's disease (AD)-like pathological changes, such as tau hyperphosphorylation and β-amyloid peptide accumulation in the prefrontal cortex (PFC). Corticotropin-releasing factor (CRF) is the central driving force in the stress response and a regulator of tau phosphorylation via binding to CRF receptors (CRFR). Little is known about the CRF system in relation to noise-induced AD-like changes in the PFC. The aim of this study was to explore the effects of chronic noise exposure on the CRF system in the PFC of rats and its relationship to tau phosphorylation. Male Wistar rats were randomly divided into control and noise exposure groups. The CRF system was evaluated following chronic noise exposure (95dB sound pressure level white noise, 4h/day×30days). Chronic noise significantly accelerated the progressive overproduction of corticosterone and upregulated CRF and CRFR1 mRNA and protein, both of which persisted 7-14days after noise exposure. In contrast, CRFR2 was elevated 3-7days following the last stimulus. Double-labeling immunofluorescence co-localized p-tau with CRF in PFC neurons. The results suggest that chronic noise exposure elevates the expression of the CRF system, which may contribute to AD-like changes.
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| http://dx.doi.org/10.1016/j.jns.2016.07.049 | DOI Listing |
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