2019/09/02
National Institutes for Quantum and Radiological Science and Technology
Keio University School of Medicine
Japan Agency for Medical Research and Development
Researcher Keisuke Takahata of the Department of Functional Brain Imaging, National Institute of Radiological Sciences, National Institutes for Quantum and Radiological Science and Technology (QST; President: Toshio Hirano), in a joint study with Professor Masaru Mimura and his team from the Department of Neuropsychiatry, Keio University School of Medicine, has successfully visualized in vivo the accumulation of tau protein (hereinafter "tau") in the brains of patients with various types of traumatic brain injuries. This accumulation is the cause of delayed brain damage resulting from such injuries. Furthermore, they revealed that the amount of tau accumulation in the brain is related to the onset and severity of symptoms of delayed brain damage from traumatic brain injury.
Traumatic brain injury is a general term for various symptoms caused by a physical impact to the head. Repetitive blows to the head from contact sports like boxing, or severe traumatic brain injuries, can cause a progressive neurodegenerative disease years to decades later, which is known as "delayed brain damage." Neuropathological examinations of post-mortem brains have shown that delayed brain damage from traumatic brain injury is a type of tauopathy, characterized by the excessive accumulation of tau in the brain.
Currently, delayed brain damage from traumatic brain injury has become an extremely serious social issue in many countries. The biggest reason for this is that it has been impossible to diagnose during a person's lifetime because, until now, there has been no technology to detect the accumulation of tau that causes delayed brain damage in vivo. This has made early intervention for delayed brain damage difficult and has been a major obstacle to efforts to develop treatments. Furthermore, while it was once believed that delayed brain damage was caused only in athletes like boxers who receive severe blows to the head, recent reports have revealed that it is caused by a much wider range of contact sports than previously thought, including American football and martial arts.
These issues are causing great concern for those who participate in contact sports or work in occupations with a risk of traumatic brain injury. Against this backdrop, the research group began research to develop a diagnostic technology to detect the accumulation of tau in the brain in vivo, which is the cause of delayed brain damage from traumatic brain injury.
In this study, using a positron emission tomography (PET) technology developed at QST to visualize tau in the living brain, we non-invasively measured the amount of tau accumulation in the brains of individuals who may have developed delayed brain damage from traumatic brain injury. As a result, we succeeded in detecting tau accumulation in vivo for various types of traumatic brain injuries. Furthermore, we revealed that tau accumulation in the superficial layer of the white matter, near the border with the gray matter, is associated with the symptoms of delayed brain damage, and that there is a relationship where the greater the amount of tau accumulation in the entire white matter, the more severe the psychiatric symptoms become. These results indicate that tau accumulation in the living brain, as detected by PET technology, can be an evaluation index for the early diagnosis of delayed brain damage. It is expected to contribute to the future development of therapies targeting tau accumulation in delayed brain damage.
This research was conducted with support from the Japan Agency for Medical Research and Development (AMED) under the research and development project "Research and Development of Translatable Imaging of Brain Aging Pathological Cascade and Mechanism Control" within the "Project for Elucidating the Entire Picture of Brain Function Networks through Innovative Technologies." This research was also supported by other AMED projects, including the research and development project "Elucidation and Modeling of Neural Circuits and Molecular Pathophysiology of Psychiatric Disorders," the Dementia Research and Development Project's "Construction of a Research and Development Consortium for New Imaging Diagnostics and Therapies Targeting Tau," and JSPS KAKENHI Grant Number 16K19789. The findings were published online in the British academic journal "Brain," which has published many high-impact papers in this field, on September 2, 2019, at 9:01 AM (JST).
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