Tinnitus involves peripheral auditory damage and aberrant central plasticity, with dysregulated BDNF signaling linking injury to compensation. Yet, direct evidence connecting BDNF/AKT/mTOR pathway activation to behavioral phenotypes is limited. This study examined BDNF/AKT/mTOR expression in the inferior colliculus (IC) of sodium salicylate (SS)-induced tinnitus rats and assessed therapeutic inhibition....
✦ The floor
Discussion
Signed responses from readers of the wire.
No actionable clinical change; this is an animal study identifying a potential drug target for tinnitus, but no human evidence exists yet.
Identifying the BDNF/AKT/mTOR pathway as a contributor to tinnitus opens a new molecular target avenue that could eventually lead to the first pharmacological treatments for tinnitus in humans.
- 01High-dose salicylate (aspirin) was used to induce tinnitus in a rat model.
- 02Inhibiting the BDNF/AKT/mTOR signaling pathway in the inferior colliculus reduced tinnitus-like behavior in rats.
- 03Dysregulated BDNF (a brain growth protein) signaling is implicated as a driver of tinnitus pathology.
- 04The inferior colliculus, a key auditory midbrain structure, appears to be a relevant site for this intervention.
- 05Results are preclinical only; translation to human therapy requires further research.
Targeted inhibition of the BDNF/AKT/mTOR pathway in the inferior colliculus ameliorates salicylate-induced tinnitus in rats.
studysupportedDysregulated BDNF signaling is implicated in tinnitus pathology.
studypartially supported- PMID
- 42592457
- DOI
- 10.1016/j.isci.2026.117102.
- Journal
- iScience
- Publication type
- research_article
- Evidence level
- 4
- Population
- Rats with salicylate-induced tinnitus
- Intervention
- Targeted inhibition of the BDNF/AKT/mTOR pathway in the inferior colliculus
- Comparator
- Untreated or vehicle-control rats
Primary outcomes
Tinnitus behavioral indicators in rats; BDNF/AKT/mTOR pathway activity in the inferior colliculus