According to clinical data, traumatic brain injury is a major cause of cognitive impairment that affects a very large population worldwide. Despite rising awareness of the debilitating and lifelong advancing consequences of traumatic brain injury (TBI), currently there are no treatments that slow the degenerative process. In fact, TBI survivors are currently treated with extensive cognitive and physical rehabilitation, along with medications that can alleviate symptoms, yet do not stop or slow degeneration.
For the first time, researchers have found that the process of this chronic health condition can be pharmacologically reversed in animal models. This offers an important proof of principle in the field and a potential path to new therapy. The findings of the study carried out by researchers at the School of Medicine, Case Western Reserve University and Harrington Discovery Institute, University Hospitals recently published in the Proceedings of the National Academy of Sciences.
TBI associated with age-related dementia, according to clinical knowledge
“In fact, TBI can have lifelong detrimental effects on a number of aspects of health,” explains the senior author of the study. Meanwhile, cognitive dysfunction, sensorimotor impairment, or emotional dysregulation such as anxiety and depression are commonly associated long-term outcomes of TBI. In addition, the risk of developing age-related forms of dementia such as Parkinson’s diseases and Alzheimer’s significantly increased with TBI.
Hence, the team set out to establish if reversing lifelong chronic neurodegeneration and associated cognitive defects after TBI is possible, which was earlier never demonstrated. For this, the team use a mouse model that imitated concussive impact in middle-aged people who suffered from TBI a decades prior. Also, an energy-elevating neuroprotective compound administered known as P7C3-A20, which was previously shown to have therapeutic value for acute TBI.