Research press release



Neuroscience: Defining features of repetitive brain trauma



今回、Sjors Scheres、Michel Goedertたちの研究グループは、3人のCTE患者(元アメリカンフットボール選手1人と元ボクシング選手2人)の死後に脳から採取したタウの構造を決定した。その結果、タウ凝集体の構造は3人とも同じだが、タウ凝集体が関係するアルツハイマー病などの他の神経変性疾患に見られるタウ凝集体の構造とは異なっていることが分かった。著者たちは、今回明らかになった構造が、CTEの診断検査法の設計に役立つ可能性があるという考えを示している。こうした知見は、脳の外傷がタウ凝集体の形成につながる仕組みへの我々の理解を深め、CTEにおけるタウの蓄積を防ぐ治療法の開発に役立つ情報をもたらしてくれる可能性がある。

Protein assemblies that appear in a neurodegenerative disorder caused by repeated blows to the head, such as sports injuries, are described online in Nature this week. Chronic traumatic encephalopathy (CTE) is characterized by the accumulation and aggregation of a protein called tau, similar to that seen in Alzheimer's disease. The new study shows that tau assemblies in CTE look slightly different from those in Alzheimer’s disease, even though it is the same tau protein that affects both. These findings demonstrate that subtle variations in the shape of tau assemblies define individual neurodegenerative diseases.

CTE affects participants of contact sports such as boxing and American football, ex-military personnel and people who have experienced physical abuse. Symptoms of CTE, such as problems with behaviour, mood, and thinking, typically do not start until long after the injuries, get worse over time and may result in dementia. Although tau protein assemblies have previously been identified as having a role in CTE progression, a detailed understanding of their structure has been lacking.

Sjors Scheres, Michel Goedert and colleagues determined the structures of tau protein from the brains of three individuals that had CTE: one American football player and two boxers. They find that the structures of the tau protein assemblies are identical in the three individuals, but differ from those seen in other neurodegenerative diseases associated with assemblies of tau protein, such as Alzheimer’s disease. The authors suggest that the newly described structure may aid in the design of diagnostic tests for CTE. The findings may improve our understanding of how brain trauma can lead to the formation of these tau proteins, which could inform the development of treatments to prevent tau accumulation in CTE.

doi: 10.1038/s41586-019-1026-5|英語の原文

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