The protein in question, CCL11, is made in the choroid plexus, the part of the brain that produces cerebrospinal fluid. While increased levels of this protein are already linked to the inflammatory process and the aging process (the older you are, the more of it you have), having low or high amounts of CCL11 have also been linked to other brain diseases like Alzheimer’s, amyotrophic lateral sclerosis and Huntington’s disease.

Scientists are closer than ever to a test like this. Dr. Ann McKee of Boston University’s CTE Center has identified a certain protein found in brain tissue and cerebrospinal fluid. Levels of this protein are significantly higher in the brain samples and spinal fluid of people with diagnosed CTE, as opposed to people with Alzheimer’s disease or no brain disease at all.

Hernandez’s last days were marked by aggression, memory loss and impulsiveness, but it was only after his death that his loved ones got some insight into why. He was given a post-mortem diagnosis of chronic traumatic encephalopathy ― a progressive brain disease linked to repetitive head trauma, the kind that can accompany rough sports, military service or abuse.

Several CTE case series have included victims of suicide.[6, 7, 9••, 16••] However, our lack of understanding of the population incidence of CTE limits our ability to attribute a complex and multifactorial behavior such as suicide to underlying CTE proteinopathy. The issue is further complicated considering that well established risk factors for suicide and suicidal ideation such as substance use and depression [30, 31] are often comorbid in cases of CTE

Commonly noted mood features include depression, irritability, and hopelessness. Behavioral features may include impulsivity, explosivity, and aggression. Cognitive features can include memory impairment, executive dysfunction, and in severe cases dementia. Motor features, including parkinsonism, ataxia, and dysarthria, appear in a subset of cases, predominantly boxers.

Evidence to-date suggests that CTE presents clinically with symptoms in one or more of four possible domains: mood, behavior, cognition, and motor

That is, although a history of repetitive brain trauma is thought to be necessary to cause CTE (ie, all neuropathologically confirmed cases of CTE to date have had a history of repetitive brain trauma), CTE symptoms are not just the cumulative effects of this process. Furthermore, there is no clear relationship between prolonged acute concussion symptoms (eg, postconcussion syndrome) and the pathology of CTE.

CTE is characterized by the deposition of hyperphosphorylated tau (p-tau) protein as neurofibrillary tangles (NFT) beginning perivascularly and at the depths of the cortical sulci. Later stage p-tau pathology becomes more widespread, particularly dense in the medial temporal lobes, also present in the white matter, and leads to prominent neuronal loss and gliosis. The irregular and perivascular nature of the p-tau neurofibrillary tangles, the proclivity for the sulcal depths, and the marked subpial and periventricular involvement are unique features of the disease that distinguish it from other tauopathies. TAR DNA-binding protein 43 (TDP-43) is present in about 80 % of cases.