In football, boxing and other fields, the players swayed their youth with fierce physical collisions, but also buried the hidden dangers of the disease. Previous studies have linked repeated brain trauma to brain disease (please read “Sports-Induced Brain Injury Studyâ€). However, the latest scientific research shows that sometimes, a brain injury may also cause Alzheimer's disease (Alzheimer's disease).
Chronic Brain Injury, a Patent for Rugby Players?
In May of this year, Junior Seau, a retired star in the National Football League (NFL)'s 20-year campaign, was found dead in the chest and later determined to be suicide. He is only 43 years old. Just last February, another super bowl guard, Dave Duerson, ended his life in the same way and donated his brain for scientific research. A few months later, the researchers found solid evidence on the 50-year-old former rugby player that he was in advanced stages of moderate chronic traumatic encephalopathy. As early as when he committed suicide, many studies have shown that occupational repeated brain injury in rugby career may lead to chronic traumatic encephalopathy (CTE).
The Brain Bank of the NFL, Boston University’s Center for Traumatic Brain Disease, points out that chronic traumatic brain disease is a progressive brain disease that occurs in athletes who have a concussion or a history of repeated head blows to their heads. It causes amnesia, depression, impaired judgment, and symptoms similar to those of Alzheimer's disease; dating back to the 1920s, the condition was called "punch-drunk syndrome," which Boxers were demented when they were young. Ten years ago, some Brain Injury Research Associations had already diagnosed the disease in a large number of dead athletes.
In recent years, there have been several incidents of NFL retired players committing suicide due to depression and other reasons. The investigation of NFL player brain damage has become more and more in depth, and the coalition has also strengthened various measures to prevent and monitor concussions.
Although Sivo did not leave behind his last words, and there is no evidence that there is a direct link between brain damage, concussion and his death, some of his teammates speculate that this is not related to his career. "The pain in his brain is a heavy price for him as a good defender. There is no doubt that this is a risk factor," said Kyle Turley, a 36 year old former winger. . Terry is one of the few athletes who are still alive and who have publicly announced that they will donate their brains for scientific research after death.
One trauma may also cause dementia
Athletes suffer from illness because of repeated head-attack attacks in their careers; however, articles published in the July issue of The Journal of Neuroscience indicate that even traumatic Traumatic brain injury (TBI) may also cause Alzheimer's disease. Serious falls or traffic accidents in life are common causes of moderate to severe TBI. But not all brain trauma can lead to TBI. According to data from the US Centers for Disease Control and Prevention, there are 1.7 million people with TBI every year; about 75% of them are concussions (the mildest form of TBI).
Moderate to severe TBI is usually caused by trauma such as serious falls or motor vehicle accidents and can cause amnesia. But not all head trauma can lead to TBI. According to the data provided by the Centers for Disease Control and Prevention, 1.7 million people suffer from TBI every year; about 75% of them are concussions (the mildest form of TBI). Currently, up to 5.1 million Americans suffer from Alzheimer's disease; Alzheimer's disease is the most common cause of dementia in adults over the age of 65.
The researchers found that a moderate to severe TBI can interfere with the regulation of Alzheimer's disease-related enzymes. This abnormality in enzyme levels causes high levels of amyloid beta, the key component of brain plaque associated with aging and Alzheimer's disease.
This study was based on previous work and used a mouse in vivo model to study a change in brain TBI. In the acute phase of the response during the first 2 days after injury, the researchers observed that the levels of two intercellular transport proteins (GGA1 and GGA3) decreased while the BACE1 enzyme levels increased.
Next, the researchers analyzed the brain samples of Alzheimer's patients and found that the levels of GGA1 and GGA3 in the brain of the patients were reduced compared with those in the brain without Alzheimer's disease, while the levels of BACE1 were increased. - Consistent with changes in mouse brain during the experiment. The researchers also found that after one week of traumatic brain injury in mice, even if GGA1 returned to normal levels, BACE1 enzyme and β-amyloid levels were still elevated, and were observed in the subacute phase (one week after wounding). Sustained amyloid beta production. In other words, after a traumatic brain injury, the protein that causes Alzheimer's disease will continue to rise for a while.
The significance of this research is to prompt scientists to develop targeted drugs against the BACE1 enzyme and delay the development of Alzheimer's disease.
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