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The issue of mitochondrial dysfunction in tinnitus, along with specific damage to proteins involved in the motility of SC of OHC, calls for an in-depth analysis of metabolic dysfunctions in degenerative tinnitus and presbyacusis, which may relate to the sophisticated mechanisms of sound transduction of the inner ear with molecular dysfunctions leading to altered sound perception in the course of inner ear degeneration

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However, the mechanisms by which type 2 responses promote behavioural outputs have yet to be established

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