Of the 1.5 million cases of TBI in the US annually, about 80,000 result in some degree of disability. And although most of the current interest in the disease is associated with sports and athletics, much greater numbers of cases stem from accidents (auto, bicycle, falls) and assaults. The majority of funding for TBI research is directed towards understanding the pathophysiology of disease and developing methods or equipment to decrease the likelihood of traumatic brain injury occurring as a consequence of violent or repeated insults to the head.
Our goal is to successfully treat both the acute and chronic forms of TBI with the same therapeutic agent even though the two are generally considered to be distinct entities. The product we are developing to accomplish that end is an oxidized form of streptolysin O, the exotoxin of group A streptococci that causes the pain of a sore throat. We call it SLO.
After over ten years of in vitro experiments, in vivo evaluation in both laboratory and domestic animals, and human anecdotal experience, we have shown SLO to be a potent agent for preventing scars and for ameliorating scars present for as long as six decades. The question has been one of whether the same SLO that has such a profound effect on both internal and external scars could likewise influence brain “scars” where little or no collagen is present.
A small number of ex-NFL players, professional boxers, and accident victims were treated with sublingual drops of SLO for periods ranging from two months to nearly a year. Patients included some football players with an estimated quarter million hits to their head and a woman in a severe auto accident 30 years prior to initiating SLO therapy. All showed significant improvement.
To better understand the in vivo mechanism(s) of action of SLO, the molecule was evaluated in an accepted mouse model for the acute form of TBI. Injured mice treated with SLO showed a statistically significant improvement in the Morris Water Maze Test for memory versus injured and untreated animals. To a slightly lesser degree the treated mice also demonstrated improved balance. And as with humans, there were no adverse effects.
Histopathologic examination of the brains of treated vs untreated animals shows that the former group had considerably less microglial infiltrations in the area of the hippocampus than did the injured and untreated group. This, combined with genomic data, strongly suggests that in the acute disease there is a decided inhibition of inflammation induced by SLO, and consequently there would be a decrease in gliosis and thus in what would be considered brain scarring.
In these early studies it would appear that SLO can prevent scarring in the acute phase of TBI and decrease scars in the brain that is chronically compromised – in both cases permitting improved function and consequent improved health.
Recorded at the Society for Scientific Exploration Conference in Boulder, Colorado 2016.
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Published on November 22, 2018
