During work in 2016 to verify the triggering of cytokines as the mechanism of action for TUG, I found that TUG had triggered TNF-alpha. It was during this time that I became aware of the work of Dr. Goldberg and others attempting neuroregeneration. They were using mTOR. I read that mTOR was triggered by TNF-alpha. I speculated that it might be possible to direct a focused ultrasound at the optic nerve to induce mTOR for neuroprotection.
Looking into the literature (mostly orthopedic) a number of papers indicated quite a few beneficial biochemical pathways, besides TNF-alpha, that are neuroprotective and that are triggered by low power ultrasound.
A couple months ago my Indian colleague sent some images of patients treated by TUG that seemed to show a slight decrease in the cup disc ratio after treatment. I decided to look at those patients I had treated during my clinical trials back in 2010 to 2012 to see if there was a similar beneficial effect. (I have not treated patients since 2014 with TUG due to lack of funds for clinical trials.)
Review of patients treated with TUG during that time frame and with images on the same HRT instrument revealed that in many cases there was a significant increase in the RNFL (retinal nerve fiber layer) occurring after the treatment, especially in those patients who I treated with TUG multiple times to reduce significantly high intraocular pressure.
There is an expectation that with glaucoma patients there is a gradual attrition of the RNFL. I was finding, in many of my patients, an increase in the RNFL thickness. This is very unusual.
When the RNFL (retinal nerve fiber layer) thins, it indicates loss of nerve cells from the optic nerve. The significant increase in the RNFL noted above hopefully indicates neuroregeneration.
The present TUG device has shown promise that it is effective for neuroregeneration. (Therefore, I may no longer need to develop another new device that uses focused ultrasound aimed at the optic nerve.)
I am now trying to raise funds to do a confirmatory clinical trial to verify my findings.
I imagine that my findings of an increased thickness of the RNFL that I have seen represent the possibility of neuroprotection. With an expectation that we see a thinning of this layer over time with glaucoma, and this thinning is a marker for degeneration, I feel that the thickening I see represents the strong support for neuroprotection or more.