Amyloid Accumulation After Mild Traumatic Brain Injury

Overview

We are extending the researches of Taiwan neurosurgery traumatic brain injury (TBI) database which is led by Professor WT Chiu in Taipei Medical University and will recruit mild TBI (mTBI) participants who have ever been registered in the database. This database has been established for over 15 years and contains the information of over 150000 patients. It is one of the largest TBI database in the world. TBI usually results from traffic accidents, falls or violence events. Most of the victims are young people and the victims suffer from life-threatening and mental-physical deficits. Mild TBI (mTBI) usually was neglected before because its symptoms, signs are mild and mTBI patients usually were not obtained enough initial treatment. Therefore, mTBI might result in long-term cognitive and affective impairments, such as depression, indifference, anxiety, memory impairment, loss of attention and executive function. These late effects not only decrease the life quality of patients and their family but also increase the social and medical burden. Recent epidemiology studies have pointed out that TBI would increase the risk for dementia, especially Alzheimer disease (AD) by 2-4 times. However, the association between TBI severity, number of repeats, genetic factors and onset of AD remains further investigation. Amyloid-β (Aβ) plaques and neurofibrillary tangles are the pathological hallmarks for AD. Accumulation of Aβ is considered to be the first step of pathophysilogy of AD. Compelling researches have supported TBI accelerates the formation and accumulation of Aβ. These findings could link TBI with AD but the previous researches had limitations. There was lack of mTBI pathology data so the impacts of mTBI on Aβ accumulation were still obscure. By amyloid-PET, we could study the effects of mTBI on the accumulation of Aβ and this tool could be helpful for understanding the real impacts and pathophysiological mechanisms of mTBI on AD.

We will conduct amyloid PET, cognitive examination and APOE genotyping for the individuals who had traumatic brain injury (TBI) in 1 year, 5 years, 10 years and 15 years ago. Age-gender-matched controls without TBI will be recruited. The main aim of this study is to evaluate the impact of TBI on amyloid accumulation in the brain. In the mean time, we also will test the effects of APOE genotypes in amyloid accumulation after TBI and the clinical relevants, in terms of cognitive function.