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J Neurol Sci. 2015 Feb 15;349(1-2):99-104. doi: 10.1016/j.jns.2014.12.032. Epub 2014 Dec 30.

Accumulation of amyloid in cognitive impairment after mild traumatic brain injury.

Author information

1
Department of Neurosurgery, Shuang Ho Hospital, Taipei Medical University, Taipei, Taiwan.
2
Department of Medical Imaging and Radiological Sciences, College of Medicine, Chang Gung University, Taiwan; Healthy Aging Research Center, Chang Gung University, Taoyuan, Taiwan; Department of Nuclear Medicine and Molecular Imaging Center, Chang Gung Memorial Hospital, Taiwan.
3
Department of Neurosurgery, Taipei Medical University Hospital, the Ph.D. Program for Neural Regenerative Medicine, Graduate Institute of Neural Regenerative Medicine, Taipei Medical University, Taipei, Taiwan.
4
Graduate Institute of Injury Prevention and Control, College of Public Health and Nutrition, Taipei Medical University, Taipei, Taiwan.
5
Department of Medical Imaging and Radiological Sciences, College of Medicine, Chang Gung University, Taiwan; Healthy Aging Research Center, Chang Gung University, Taoyuan, Taiwan; Department of Nuclear Medicine and Molecular Imaging Center, Chang Gung Memorial Hospital, Taiwan. Electronic address: lin4857@cgmh.org.tw.
6
Department of Neurology, Shuang Ho Hospital, Taipei Medical University, Taipei, Taiwan; Department of Neurology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan; Department of Neurology, National Defense Medical Center, Taipei, Taiwan. Electronic address: chaurjongh@tmu.edu.tw.

Abstract

Recent epidemiology studies have indicated that traumatic brain injury (TBI) can increase the risk of developing neurodegenerative diseases such as Alzheimer's disease (AD). Amyloid-β (Aβ) plaques and neurofibrillary tangles are pathological indicators of AD. The accumulation of Aβ is considered the first step of AD pathophysiology. Compelling studies have supported the hypothesis that TBI accelerates the formation and accumulation of Aβ. These findings could link TBI with AD, although the research that reported these findings had limitations, particularly regarding mild TBI (mTBI) patients. The effects of mTBI on Aβ accumulation remain uncertain because of a lack of mTBI pathology data. Using amyloid-positron emission tomography (amyloid-PET), researchers can help to determine whether mTBI increases the accumulation of Aβ, which might be involved in the pathophysiological mechanisms of mTBI in AD, and could be a target for the treatment of neurodegenerative diseases associated with TBI. In this study, we recruited 27 mTBI patients with mTBI in mean 6years before this study (21 mTBI patients without cognitive impairment, 6 mTBI patients with cognitive impairment,) and 10 controls. All of them underwent mini-mental state examination, apolipoprotein E (APOE) genotyping, and amyloid-PET. The results show an increase of amyloid accumulation and allele frequency of APOE4 in the mTBI patients with cognitive impairment. These findings indicate that amyloid accumulation is an important indicator of cognitive impairment, and amyloid-PET should be a safe and useful tool for diagnosing amyloid-related cognitive impairment. APOE allele might play a role in the occurrence of cognitive impairment after mTBI. The contribution of mTBI to the amyloid accumulation requires further study, and mTBI patients should be recruited for longitudinal research with repeated amyloid-PET studies.

KEYWORDS:

Alzheimer disease; Amyloid PET; Cognitive impairment; Genetics; Mild traumatic brain injury; Neurodegenerative diseases

PMID:
25586534
DOI:
10.1016/j.jns.2014.12.032
[Indexed for MEDLINE]

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