지원사업
학술연구/단체지원/교육 등 연구자 활동을 지속하도록 DBpia가 지원하고 있어요.
커뮤니티
연구자들이 자신의 연구와 전문성을 널리 알리고, 새로운 협력의 기회를 만들 수 있는 네트워킹 공간이에요.
논문 기본 정보
- 자료유형
- 학술저널
- 저자정보
- 발행연도
- 2020.1
- 수록면
- 230 - 248 (19page)
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초록· 키워드
오류제보하기
Traumatic brain injury (TBI) causes disability and death, accelerating the progression towards Alzheimer’s disease and Parkinson’s disease (PD). TBI causes serious motor and cognitive impairments, as seen in PD that arise during the period of the initial insult. However, this has been understudied relative to TBI induced neuroinflammation, motor and cognitive decline that progress towards PD. Neuronal ubiquitin-C-terminal hydrolaseL1 (UCHL1) is a thiol protease that breaks down ubiquitinated proteins and its level represents the severity of TBI. Previously, we demonstrated the molecular action of glia maturation factor (GMF); a proinflammatory protein in mediating neuroinflammation and neuronal loss. Here, we show that the weight drop method induced TBI neuropathology using behavioral tests, western blotting, and immunofluorescence techniques on sections from wild type (WT) and GMF-deficient (GMF-KO) mice. Results reveal a significant improvement in substantia nigral tyrosine hydroxylase and dopamine transporter expression with motor behavioral performance in GMF-KO mice following TBI. In addition, a significant reduction in neuroinflammation was manifested, as shown by activation of nuclear factor-kB, reduced levels of inducible nitric oxide synthase, and cyclooxygenase-2 expressions. Likewise, neurotrophins including brain-derived neurotrophic factor and glial-derived neurotrophic factor were significantly improved in GMF-KO mice than WT 72 h post-TBI. Consistently, we found that TBI enhances GFAP and UCHL-1 expression and reduces the number of dopaminergic TH-positive neurons in WT compared to GMF-KO mice 72 h post-TBI. Interestingly, we observed a reduction of THpositive tanycytes in the median eminence of WT than GMF-KO mice. Overall, we found that absence of GMF significantly reversed these neuropathological events and improved behavioral outcome. This study provides evidence that PD-associated pathology progression can be initiated upon induction of TBI.
목차
등록된 정보가 없습니다.
참고문헌 (121)
참고문헌 신청
Menon DK / 2010 / Position statement : definition of traumatic brain injury / Arch Phys Med Rehabil 91:1637~1640
Taylor CA / 2017 / Traumatic brain injury-related emergency department visits, hospitalizations, and deaths-United States, 2007 and 2013 / MMWR Surveill Summ 66:1~16
Faul M / 2010 / Traumatic brain injury in the United States: national estimates of prevalence and incidence, 2002–2006 / Inj Prev 16(Suppl 1):A268
Skolnick BE / 2014 / A clinical trial of progesterone for severe traumatic brain injury / N Engl J Med 371:2467~2476
Coronado VG / 2012 / Trends in traumatic brain injury in the U.S. and the public health response:1995-2009 / J Safety Res 43:299~307
Taylor CA / 2017 / Traumatic brain injury-related emergency department visits, hospitalizations, and deaths-United States, 2007 and 2013 / MMWR Surveill Summ 66:1~16
Faul M / 2010 / Traumatic brain injury in the United States: national estimates of prevalence and incidence, 2002–2006 / Inj Prev 16(Suppl 1):A268
Skolnick BE / 2014 / A clinical trial of progesterone for severe traumatic brain injury / N Engl J Med 371:2467~2476
Coronado VG / 2012 / Trends in traumatic brain injury in the U.S. and the public health response:1995-2009 / J Safety Res 43:299~307
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