Abstract

Objectives The prion protein (PrP) plays a major role in central nervous excitability, cellular adhesion, and neurite outgrowth. We hypothesized that PrP variants may act as a modulator of chronic tinnitus, a condition frequently associated with states of overexcitability in the auditory pathway. Methods 139 Caucasian patients who presented with tinnitus lasting more than 6 months were recruited from a tinnitus clinic, underwent detailed neuro-otological examinations and donated venous blood for the extraction of genomic DNA from lymphocytes. Subjects with a history of vestibular schwannoma, Meniere's disease, or pathological middle ear conditions were excluded. Tinnitus severity was graded using the Tinnitus Questionnaire (TQ). A polymorphism encoding residue 117 of PrP was genotyped by PCR-based RFLP. Results When carriers of the minor PrP allele were compared to the remaining subjects, we noted only a moderate difference in mean TQ scores (33.4 ± 4.9 vs. 37.4 ± 1.5, p > 0.05). Conclusions The present results thus do not support a significant effect of PrP variant rs8124214 on subjective ratings of tinnitus. However, functional PrP variants may act on additional outcome parameters, e.g., on the response to treatment. Future studies will need to address the interplay of these variants, and their effects on specific subgroups.

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