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Mez said the results, although early, are a step towards a better understanding of the disease. "It helps us better understand biologically, mechanically, what's going on in the brain in the CTE.
"By understanding the mechanism and identifying this genetic risk factor, we have new potential targets for developing therapies," he said.
The authors stress that their conclusions need to be further developed in a larger group and replicated to allow definitive conclusions to be drawn.
Proceed with caution
Gandy, who did not participate in the study, wrote in an email that the results "were not ready for prime time".
"We must act with caution." The study shows that the gene may be associated with a reduced risk of CTE, but that CTE is a polymorphic, polyphenotypic and polygenic disease, [and] Focusing on a gene, which can reduce the risk, can be an excessive effort, "said Omalu, who was also not involved in the new research, in an email.
Mez and his team at Boston University are also studying other genes that may play a role in ETC. "If these other genes have an effect, it will probably be independent and additive to the discovery of TMEM."
Mez added that "it is likely that" several genes in the genome contribute to the risk and severity of CTEs, and that in the future, all the elements combined will improve our predictive ability. "
Today, CTE can only be diagnosed after death. This is thought to result from repeated head trauma. In football, this can happen not only from hard headaches leading to concussions, but also from repeated cracking of the brain inside the skull during fights and falls in the field. These repeated blows are called subconcussive blows and can result in an accumulation of a kind of protein called tau in the brain.
Early and prolonged exposure to repeated trauma is also considered a contributing factor to the disease. There is no treatment or treatment for the disease.
Genetic variant linked to a less severe CTE
The researchers found no association between the gene variant and the CTE. But those who had CTE and the gene variant had lower tau and brain inflammation levels than those who had a CTE but no variant.
The inflammation and accumulation of tau in the brain contribute to degeneration of the brain.
"Among people with CTE, CTE-related outcomes were more severe, they were more likely to have dementia, and they were more likely to have advanced neurodegeneration in their brains," he said. Mez.
In a study last year, researchers at Boston University detailed the discovery of a CTE in the brain of 100 of the 101 former NFL players. And although the presence of the disease is extremely high in the study, it is difficult to extrapolate the overall prevalence among football players as well as the general public, because the brains studied had a potential bias: they were given by parents because the subjects had probably had symptoms of the disease such as memory loss, confusion, depression and impulse control problems.
Understand the difference
"This research, although early, suggests the existence of some genetic risk factors, however, there was no difference between those with and without CTE." The TMEM106B gene was also associated with dementia frontotemporal, suggesting a potential overlap with a number of neurodegenerative diseases, "Manley, who did not participate in the study, wrote in an email. "More research is needed with a large number of people with and without long-term problems to fully understand their causes and effects."
Mez said, "We see a lot of former athletes who have similar exposure levels.Two college football players, who play for eight to ten years." Late in life, one from them develops a serious illness and the other can be slightly altered.
"I think it's helpful to understand this difference, and this finding begins to explain this type of difference," he said.
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