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Chronic traumatic encephalopathy : ウィキペディア英語版
Chronic traumatic encephalopathy

Chronic traumatic encephalopathy (CTE), a form of encephalopathy, is a progressive degenerative disease found in people with a history of repetitive brain trauma, including symptomatic concussions as well as sub-concussive hits to the head that do not cause symptoms. The disease was previously called dementia pugilistica (DP), ''i.e.'' "punch-drunk", as it was initially found in those with a history of boxing. In the case of blast injury, a single exposure to a blast and the subsequent violent movement of the head in the blast wind can cause the condition.〔
CTE has been most commonly found in professional athletes participating in American football, association football, ice hockey, professional wrestling, stunt performing and other contact sports who have experienced repetitive brain trauma. In both cases resulting in characteristic degeneration of brain tissue and the accumulation of tau protein. Individuals with CTE may show symptoms of dementia, such as memory loss, aggression, confusion and depression, which generally appear years or many decades after the trauma. Baseline testing has been created to assess potential cognitive impairment in athletes in contact sports, but a test to determine the presence of CTE while the person is alive is not yet available.〔(Baseline Testing ) - Centers for Disease Control and Prevention Website〕
==Signs and symptoms==
Other than repeated brain trauma, the risk factors for CTE remain unknown.〔 So far, CTE can only be diagnosed posthumously. Research studies are looking into possible genetic, exposure level, and other risk factors.
Researchers who conducted a CTE pilot study at UCLA described the findings as a significant step toward being able to diagnose CTE in living patients.〔(''espn.go.com'' ), 2013/01/22.〕
Research performed at the Cleveland Clinic and at the University of Rochester has shown that in addition to concussions, sub-concussive head hits also produce measurable changes in athletes' MRI. Bazarian (University of Rochester) demonstrated persistent changes in white matter properties in athletes who did not experience a concussion during a season but had several blows to the head. This finding is consistent with the hypothesis that a number of sub-concussive events may be as damaging as a frank concussion. The MRI changes reported in this study were causally related to the presence in serum of players of auto-antibodies against the brain protein S100B. The sequence of events proposed by Janigro at the Cleveland Clinic links sub-concussion to leakage of the blood-brain barrier, extravasation of brain S100B in blood, activation of an immune response due to antigen unmasking and production of auto-antibodies. These auto-antibodies maybe pathogenic as shown for example in epileptic human brain. The link between S100B auto-antibodies and CTE needs experimental confirmation; however, antibodies against S100B or other brain protein have been found in patients affected by Alzheimer's disease.
Clinical symptoms of CTE are only beginning to be understood. They are thought to include changes in mood (i.e. depression, suicidality, apathy, anxiety), cognition (i.e. memory loss, executive dysfunction), behavior (short fuse, aggression), and in some cases motor disturbance (i.e. difficulty with balance and gait). While the pathology of CTE has been broken up into stages,〔 the clinical symptoms and clinical progression of CTE are not yet fully understood.

抄文引用元・出典: フリー百科事典『 ウィキペディア(Wikipedia)
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