It is crucial to understand that most of the damage caused by brain injury does not occur upon initial impact to the head, but rather as a consequence of secondary brain injury.
In the hours, days, weeks, and months following TBI, the increased permeability of the neuronal membrane allows for an excessive influx of metal ions and circulating free radicals. This situation produces a series of protein degradation cascades and oxidation, leading to widespread molecular damage and neuronal cell death.
In short, the damaged area after the initial trauma expands if not treated, a process, which can last for years. Currently, there are no drugs or therapies that can stop the post-TBI biochemical cascade.
The company will verify its novel concept in several animal models of neurodegenerative conditions, including head trauma and stroke, in the hope of obtaining highly promising results. A series of tests has demonstrated that the regulated reduction of different free metal ions induces the effective neuroprotection of the affected tissues in the injured brain and encourages the naturally occurring process of brain detoxification.