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I feel like the whole brain plasticity thing is just wishful thinking. Brain function certainly cannot be altered easily without external influences of drugs or gene expression. For all I know brain plasticity is the reason tinnitus occurs in the first place. It usually takes a traumatic event...

It's most likely the other way around. When hearing damage occurs, the brain is getting fed less sensory input. In the long term, parts of the brain receiving less stimulation wither and die leading to potential cognitive problems. The brains needs constant information to function properly.

I feel this is fairly standard practice in the R&D sector. A past advisor of mine once was approached by company for a particular problem. My advisor knew the solution right away but in order to keep his staff employed he asked for funding to do some work. The company obliged. Sometimes that's...

I sure hope the people involved in this study are aware of the Kv channels implications when it comes to hearing/tinnitus. I guess we'll know more if AUT00063 or SF34 have any effect at all.

This isn't what they meant. They meant that the parts of the brain responsible for tinnitus/chronic pain persistance are associated with higher cognitive processes. Not at all. It could very well be that the Kv channels are the faulty breakers when it comes to T noise.