Chronic Noise Exposure Causes Persistence Of Tau Hyperphosphorylation And Formation Of NFT Tau In The Rat Hippocampus And Prefrontal Cortex

Background: The non-auditory effects of noise exposure on the central nervoussystem have been established both epidemiologically and experimentally. Chronicnoise exposure (CNE) has been associated with tau hyperphosphorylation andAlzheimer disease (AD)-like pathological changes. However, experimental evidenceis still limited.Objectives：The aim of the current study was to explore the aftereffects of CNE ontau phosphorylation in rat hippocampus and cortex.Methods: Forty eight male Wistar rats were randomly assigned to a noise-exposedgroup and a control group. At different time points (day0, day3, day7, or day14)after the end of the last noise exposure,12rats (6in the noise-exposed group and6inthe control group) were sacrificed through decapitation. The levels of RIPA-solubleand RIPA-insoluble phosphorylated tau at Ser202, Ser396, Ser404, and Ser422inthe hippocampus and cortex were measured after CNE (100dB SPL white noise,4hr/day×14days).Results: Exposure to white noise for14consecutive days significantly increasedphosphorylated tau at Ser202, Ser396, Ser404, and Ser422in the hippocampus andcortex, which are the sites typically phosphorylated in Alzheimer brains. Tauhyperphosphorylation persisted for7days to14days after the cessation of noiseexposure. These alterations were also concomitant with the generation of pathologicalneurofibrillary tangle (NFT) tau3or7days after the end of the stimulus.Conclusions: These results show, for the first time, that CNE not only leads to a longlasting increase of non-NFT hyperphosphorylated tau but also to delayed formation ofpathological NFT tau in the hippocampus and cortex that may contribute to functionaldeficits in memory.