Chronic Traumatic Encephalopathy: Connecting Mechanisms to Diagnosis and Treatment

Abstract

ease (Walker & Tesco, 2013). Significant attention was directed towards chronic traumatic encephalopathy when Dr. Bennet Omalu discovered the disease in a brain autopsy of former National Football League athlete Mike Webster, whose cognitive abilities had drastically declined following his retirement. Numerous indicators of significant brain deterioration were observed in Webster’s autopsy, which was suggested to be accountable for his cognitive dysfunction in his later years (Omalu et al., 2005). Since this initial autopsy, 96% of professional athletes who have been examined for CTE by autopsy have been tested positive for the disease. Although CTE appears to be most prevalent among American football athletes, it is not restricted to this group of individuals. It is suggested that any individual who has been subjected to extensive brain injury throughout their life, including victims of abuse, can develop CTE (Baugh et al., 2012). Although many great strides have been made in the progression of research on CTE, there is still much that remains unclear about the disease. Currently, there is no formal diagnosis that can be made while the individual is still alive. A post-mortem diagnosis can be performed by an autopsy, which allows for the identification of neuropathological markers of the disease. These markers include the presence of TAR DNA-binding protein 43 (TDP-43), a diffuse spread of hyperphosphorylated tau protein, and enlarged ventricles (Gavett, Stern, & McKee, 2011). FurtherINTRODUCTION Chronic traumatic encephalopathy (CTE) is a neurodegenerative disease that is commonly observed in professional athletes, military veterans, and other individuals who have been subjected to repetitive brain injuries. Approximately 42 million people worldwide suffer from brain injury every year, which increases their risk of developing chronic traumatic encephalopathy later in life (Gardner & Yaffe, 2015). The main symptoms associated with the disease are profound memory loss, motor deterioration, unexplained aggression, depression, and suicidality. These cognitive and behavioral symptoms are also accompanied by biological changes in the brain. Similar to Alzheimer’s disease, CTE is primarily characterized by an accumulation of tangles of protein, although the distribution of these tangles throughout the brain is unique to each disChronic Traumatic Encephalopathy: Connecting Mechanisms to Diagnosis and Treatment