Human Neural Stem Cells Overexpressing Choline Acetyltransferase Restore Cognitive Function of Kainic Acid-Induced Learning and Memory Deficit Animals
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- Dongsun Park
- College of Veterinary Medicine, Chungbuk National University, Cheongju, Republic of Korea
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- Seong Soo Joo
- Division of Marine Molecular Biotechnology, Gangneung-Wonju National University, Gangneung, Republic of Korea
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- Tae Kyun Kim
- College of Veterinary Medicine, Chungbuk National University, Cheongju, Republic of Korea
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- Sun Hee Lee
- College of Veterinary Medicine, Chungbuk National University, Cheongju, Republic of Korea
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- Hyomin Kang
- College of Veterinary Medicine, Chungbuk National University, Cheongju, Republic of Korea
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- Hong Jun Lee
- Medical Research Institute, Chung-Ang University Medical School, Seoul, Republic of Korea
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- Inja Lim
- Department of Physiology, Chung-Ang University Medical School, Seoul, Republic of Korea
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- Akinori Matsuo
- Molecular Neuroscience Research Center, Shiga University of Medical Science, Ohtsu, Japan
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- Ikuo Tooyama
- Molecular Neuroscience Research Center, Shiga University of Medical Science, Ohtsu, Japan
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- Yun-Bae Kim
- College of Veterinary Medicine, Chungbuk National University, Cheongju, Republic of Korea
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- Seung U. Kim
- Medical Research Institute, Chung-Ang University Medical School, Seoul, Republic of Korea
説明
<jats:p> Alzheimer disease (AD) is a progressive neurodegenerative disease, which is characterized by loss of memory and cognitive function. In AD patients dysfunction of the cholinergic system is the main cause of cognitive disorders, and decreased activity of choline acetyltransferase (ChAT), an enzyme responsible for acetylcholine (ACh) synthesis, is observed. In the present study we investigated if brain transplantation of human neural stem cells (NSCs) genetically modified to encode ChAT gene improves cognitive function of kainic acid (KA)-induced learning deficit rats. Intrahippocampal injection of KA to hippocampal CA3 region caused severe neuronal loss, resulting in profound learning and memory deficit. F3.ChAT human NSCs transplanted intracerebroventricularly improved fully the learning and memory function of KA-induced learning deficit animals, in parallel with the elevation of ACh levels in cerebrospinal fluid. F3.ChAT human NSCs migrated to the KA-induced injury site (CA3) and differentiated into neurons and astrocytes. The present study demonstrates that human NSCs expressing ChAT have lesion-tropic property and improve cognitive function of learning deficit model rats with hippocampal injury by increasing ACh level. </jats:p>
収録刊行物
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- Cell Transplantation
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Cell Transplantation 21 (1), 365-371, 2012-01-01
SAGE Publications
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詳細情報 詳細情報について
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- CRID
- 1360283695733424128
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- ISSN
- 15553892
- 09636897
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- データソース種別
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- Crossref
- KAKEN
