2004 Fiscal Year Final Research Report Summary
Prevention of neurodegeneration after head injury by activated maicroglia with antisense method
| Project/Area Number |
15591537
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | Nagoya City University |
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Principal Investigator |
AIHARA Noritaka Nagoya City University, Garduae School of Medical Sciences, Research Associate, 大学院・医学研究科, 講師 (00264739)
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| Co-Investigator(Kenkyū-buntansha) |
YAMADA Kazuo Nagoya City University, Garduae School of Medical Sciences, Professor, 大学院・医学研究科, 教授 (90150341)
MASE Mitsuhito Nagoya City University, Garduae School of Medical Sciences, Associate Professor, 大学院・医学研究科, 助教授 (60238920)
KATANO Hiroyuki Nagoya City University, Garduae School of Medical Sciences, Associate Professor, 大学院・医学研究科, 助教授 (30295612)
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| Project Period (FY) |
2003 – 2004
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| Keywords | activated microglia / traumatic brain injury / Brain-deraived neurotrophic factor / myelencephalon-specific protease / hjigher cortical dysfunction / MAPK / degenerarting neuron / CMRO2 |
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| Research Abstract |
In order to clarify after the pathophysiological of cognitive impairment after traumatic brain injury. Fifty-two patients with mild traumatic brain injury were devided into three groups based on magneteic resonance images (MRI). Findings. Regional cerebral blood flow (CBF), oxygen extraction fraction (OEF), and cerebral metabolic rate of oxygen (CMRO2) were measured by PET. Higher cortical dysfunction was evaluated using Wechsler Adult Intelligence Scale-Revised (WAIS R). We concluded that the severity of higher cortical dysfmction is correlated with decrease of CMR02. To elucidated temporal pattern of histological changes in diffuse brain injury, we developed the rat diffuse brain injurt model We examined the histological changes after difi'use brain injury using silver impregnation method for selcive demonstration of collapsed neurons. Quantitative evaluation revealed that the number of dark axons at the cerebral peduncles invreased during the experimental peropd. We revealed that axon progressively degenerate after diffse brain injury in rat model. Activated microglia infiltrates in degenerated neuron. Activated microglia were evaluated phosphorylation of p38 mitogen-activated protein kinase (MAPK). Activated microglia produce Brain-deraived neurotrophic factor (BDNF), but the amount of BDNF is insufficient for the rescue of degenerarting neuron. We also examined the expression of myelencephalon-specific protease (MSP) after rat brain injury model. The gene of MSP is a member of the kallikrein gene fatnihy and in rats is expressed mainly in the central nervous system. MSP was expressed mainly in oligodendrocytes. We suggest that the expression of MSP may be related to turnover of myelin-associated proteins and extracelluar matrix proteins after brain injury. The regulation of active MSP may be important in the physiological or pathological changes involved in remyelination or demyelination.
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Research Products
(10 results)
