A brain injury can also cause senile dementia?

Many studies have shown that occupational brain injury in football career may lead to chronic traumatic encephalopathy (CTE).
NFL's "brain bank", the University of Boston's Traumatic Encephalopathy Research Center, noted that chronic traumatic encephalopathy is a progressive brain disease that occurs in athletes with a history of brain concussion or head injuries. It can lead to amnesia, depression, impaired and similar symptoms of Alzheimer's disease; back to the 20th century, 20 years, this symptom is called "boxing brain encephalopathy syndrome" (punch-drunk syndrome), it So that boxers in the age of light when there is dementia situation. As early as a decade ago, some brain damage research associations) had already diagnosed the disease in a large number of dead athletes.
In recent years, a number of NFL retired players due to depression and other causes of suicide events, for the NFL players brain damage investigation has been more and more in-depth, while the Union has also strengthened the prevention and monitoring of concussion a variety of measures.
A trauma may also cause senile dementia
Athletes suffer from pain because they have been repeatedly hit in their careers in their careers; however, the article published in The Journal of Neuroscience suggests that even a traumatic brain injury (Traumatic brain injury, TBI), may also lead to Alzheimer's disease. A serious fall or traffic accident in life is a common cause of moderate to severe TBI. But not all brain trauma can lead to TBI. Data from the US Centers for Disease Control and Prevention show that 1.7 million people have TBI each year; about 75% of them are concussion (the smallest form of TBI).
At present, as many as 5.1 million Americans suffer from Alzheimer's disease; Alzheimer's disease is the most common cause of adult dementia over 65 years of age.
The researchers found that a moderate to severe TBI would interfere with the regulation of enzymes associated with Alzheimer's disease. This abnormality in the enzyme content causes a high level of beta-amyloid protein, which is a key component in brain plaques associated with aging and Alzheimer's disease.
The study was based on previous work, using the mouse model to study a TBI changes in the brain. In the acute phase of the first 2 days of injury, the researchers observed a decrease in both intercellular transport proteins (GGA1 and GGA3) levels and elevated BACE1 levels.
Next, the researchers found that the levels of GGA1 and GGA3 in the brain of the patients were lower than those of the brains without Alzheimer's disease, while the level of BACE1 was elevated in the analysis of brain specimens from patients with Alzheimer's disease - consistent with changes in the brain of the mice in the experiment. The researchers also found that BACE1 and beta amyloid levels were elevated even after GGA1 returned to normal levels after one week of traumatic brain injury in mice and was observed in subacute (one week after trauma) Sustained beta amyloid production. In other words, after a brain trauma, causing dementia protein will continue to rise for some time