J Med Life Sci > Volume 4(1); 2006 > Article
Journal of Medicine and Life Science 2006;4(1):61-71.
DOI: https://doi.org/10.22730/jmls.2006.4.1.61    Published online June 30, 2006.
아밀로이드 베타 1-42에 의한 in vitro 및 in vivo 속후각겉질 신경로 신경세포의 사멸형태에 관한 연구
변경희1, 맹영희2, 이봉희2
1제주대학교 의과대학 해부학교실
2제주대학교 의과대학 병리학교실
A study on changes of the CNS pathway to the entorhinal cortex by amyloid beta 1-42
Kyunghee Byun1, Younghee Maeng2, Bonghee Lee2
1Department of Anatomy and Neurobiology, College of Medicine, Institute for Medical Science, Cheju National University, Ara 1 Dong, Jeju, Jeju do 690 756, Korea
2Department of Pathology, College of Medicine, Institute for Medical Science, Cheju National University, Ara 1 Dong, Jeju, Jeju do 690 756, Korea
Correspondence:  Bonghee Lee, Email: bhleel@cheju.ac.kr
Abstract
Deposition of amyloid beta protein as amyloid fibrils or non fibrillar aggregations in senile plaques characterizes the Alzheimer disease brain. Microtubule associated protein tau is abnormally phosphorylated in AD and aggregates as paired helical filaments (PHFs) in neurofibrillary tangles. The purpose of this study were 1) to identify the entorhinal cortex pathway in the normal rat brain after PRV injection, 2) whether amyloid beta 1-42 injection caused the hyperphosphorylation of tau along the entorhinal cortex CNS pathway. For analysis, rats were sacrificed at 48 hours after PRV injection or cut, at 7 days after amyloid beta 1-42 injection. Brains were processed for immunohistochemistry against PRV. tau-P, or 6E10. PRV positive neurons were observed in several CNS nuclei including hippocampus, and tau-p neurons area appeared in several nuclei including TM. These data suggest that the hyperphosphorylated tau has been increased in the CNS nuclei along entorhinal cortex pathway, and this may cause memory disturbance in Alzheimer's disease patients.
Key Words: amyloid beta, pseudorabies virus, entorhinal pathway, plaque
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