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Sulforaphane increases BDNF expression via HDAC inhibition in primary cortical neurons and 3xTg-AD mice
일차신경세포와 치매동물 모델에서 설포라판의 HDAC 활성 저해를 통한 BDNF의 증가 및 작용기작 규명

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Authors
김지성
Advisor
이기원
Major
농업생명과학대학 농생명공학부
Issue Date
2014-08
Publisher
서울대학교 대학원
Keywords
sulforaphanebrain-derived neurotrophic factorhistone deacetylaseAlzheimer’s disease
Description
학위논문 (석사)-- 서울대학교 대학원 : 농생명공학부, 2014. 8. 이기원.
Abstract
Brains of patients with Alzheimers disease (AD) contain abnormally low levels of brain-derived neurotrophic factor (BDNF), a neurotrophin that regulates learning and memory and promotes the survival of injured neurons. As recent studies indicate that sulforaphane improves learning and memory in animal models, I hypothesized that sulforaphane influences synaptic activity by regulating BDNF levels. I found that sulforaphane treatment increased BDNF levels in mouse primary cortical neurons and restored frontal cortex levels of BDNF in a triple-transgenic mouse model of AD. Also, sulforaphane inhibited histone deacetylase (HDAC) and increased acetylation of histone 3 and 4, suggesting that sulforaphane regulates BDNF expression via HDAC inhibition. Furthermore, sulforaphane increased levels of several BDNF pathway components, including tyrosine kinase receptor B (TrkB), cAMP-responsive element-binding protein (CREB), Ca2+/calmodulin-dependent protein kinase II (CaMKII), extracellular signal-regulated kinase (ERK), and Akt, as well as neuronal and synaptic molecules such as microtubule-associated protein 2 (MAP2), synaptophysin, and postsynaptic density protein-95 (PSD-95). These findings suggest that sulforaphane could be used to prevent or treat AD.
Language
English
URI
https://hdl.handle.net/10371/125881
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College of Agriculture and Life Sciences (농업생명과학대학)Dept. of Agricultural Biotechnology (농생명공학부)Theses (Master's Degree_농생명공학부)
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