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系統識別號 U0026-1506202023594200
論文名稱(中文) miR-34c, 高脂肪飲食和神經退化性疾病的相關研究
論文名稱(英文) The study of miR-34c, high-fat diet and neurodegenerative diseases
校院名稱 成功大學
系所名稱(中) 臨床醫學研究所
系所名稱(英) Institute of Clinical Medicine
學年度 108
學期 2
出版年 109
研究生(中文) 高毓佳
研究生(英文) Yu-Chia Kao
學號 S98001119
學位類別 博士
語文別 中文
論文頁數 114頁
口試委員 指導教授-蔡坤哲
共同指導教授-王亮超
召集委員-江伯敏
口試委員-李旺祚
口試委員-周一鳴
中文關鍵字 脂肪  高脂飲食  肥胖  微核糖核酸-34  過氧化體增生活化受體  SIRT (NAD-依賴性去乙醯化酶)  PGC-1α過氧化體增生活化受體γ共同活化子-1α  神經退化性疾病  阿茲海默症  巴金森氏症 
英文關鍵字 Lipid  high-fat diet  obesity  miR-34  PPAR  SIRT  PGC-1α  neurodegenerative diseases  Alzheimer’s disease  Parkinson’s disease 
學科別分類
中文摘要 神經退化性疾病縱然在部分病患有遺傳傾向,環境因素亦可藉由表觀遺傳(epigenetic)之調控影響疾病的危險性和影響病程進展,此一論文旨在研究轉錄後及轉譯後調控方式一為微核糖核酸,另一為飲食對前兩大神經退化性疾病阿茲海默症和巴金森氏症的影響。微核糖核酸(miRNAs)逐漸被視為神經退化性疾病的關鍵調控因子。在第一個研究中我們假設表現於海馬迴的微核糖核酸-34c於老鼠會引發如同人類阿茲海默症之記憶障礙,我們證實微核糖核酸-34c過量表現於海馬迴神經元會對神經樹突長度和神經樹突棘密度造成負向影響,將微核糖核酸-34c感染載入之海馬迴神經元相較未被感染載入之神經元平均神經樹突較短且有較少之絲狀偽足(filopodia)。神經樹突和突觸為神經傳導乃至記憶形成和儲存的基本結構,神經樹突的破壞足以引發阿茲海默症。
飲食對健康至關重要且為簡易可調整的因子,流行病學及動物實驗顯示代謝性疾病包含肥胖和神經退化性疾病的相關性。第二個實驗旨在研究飲食引發之肥胖對巴金森氏症之影響,著重於多巴胺路徑和腦部過氧化體增生活化受體。高脂飲食造成老鼠腦部黑質多巴胺神經元數量降低,高脂飲食亦促發神經發炎造成黑質和紋狀體星形膠質細胞增生,腦部黑質之神經樹突棘減少顯示長期高脂飲食改變多巴胺神經之神經可塑性。高脂飲食餵食之老鼠其腦部黑質和腹側被蓋區之所有過氧化體增生活化受體子型(α, β/δ, γ)之數量皆比一般飲食之對照組減少,其中又以α子型之減少最為顯著。
英文摘要 For neurodegenerative diseases, despite of genetic predisposition in some individuals, environmental factors affect disease risk and progression through epigenetic regulation. Our thesis aims to investigate the impacts of post-transcriptional and post-translational control schemes - one via microribonucleic acid (miRNAs), and another through diet, on the top two neurodegenerative diseases - Alzheimer’s and Parkinson’s disease. miRNAs are increasingly recognized as key regulators in neurodegenerative diseases. Our first study hypothesized that miR-34c, a miRNA expressed in mammalian hippocampus, could induce memory impairment akin to that of patients with Alzheimer’s disease (AD) in mice. We showed that miR-34c overexpression in hippocampal neurons negatively regulated dendritic length and spine density. Hippocampal neurons transfected with miR-34c had shorter dendrites on average and fewer filopodia and spines than those not transfected with miR-34c. Because dendrites and synapses are key sites for signal transduction and fundamental structures for memory formation and storage, disrupted dendrites can contribute to AD.
Diets are critical for health and are easily modifiable factor. Several epidemiologic and animal studies have revealed correlations between metabolic disorders including obesity and neurodegenerative diseases. Our second study aimed to assess the effect of diet-induced obesity on Parkinson’s disease (PD) with emphasis on the dopaminergic pathway and brain peroxisome proliferator-activated receptors (PPARs). In mice, a high-fat diet (HFD) resulted in fewer dopaminergic neurons in the substantia nigra (SN). HFD also induced neuroinflammation, with increased astrogliosis in the SN and striatum. Dendritic spine density in the SN of HFD-exposed mice decreased, which suggested that prolonged HFD altered dopaminergic neuroplasticity. All three PPAR subtype (PPAR-α, PPAR-β/δ, PPAR-γ) levels were significantly reduced in the SN and the ventral tegmental area (VTA) of HFD mice when compared to those in normal-diet controls, and the PPAR-α showed the most prominent reduction.
論文目次 Abstract. I
中文摘要. II
Acknowledgement. III
Abbreviation. IV-VI
Content. VII
Chapter 1. Introduction
1.1. Neurodegenerative Diseases. 1
1.2. Alzheimer’s Disease and Aβ Theory. 1-4
1.3. Parkinson’s Disease. 4
1.4. Epigenetics. 4-5
1.5. miRNAs. 5
1.6. Epigenetic Control of Alzheimer’s Disease. 6
1.7. Epigenetic Control of Parkinson’s Disease. 6-7
1.8. Lipids and Alzheimer’s Disease. 7-8
1.9. Lipids and Parkinson’s Disease. 8
Chapter 2. Association between miRNA-34c and Neuroplasticity. 9-19
Chapter 3. Association between High Fat Diet and Proliferator-Activated Receptors in the Midbrain Dopaminergic Neurons. 20-33
Chapter 4.
4.1. miR-34 and SIRT. 34-43
4.2. PPAR. 44-46
4.3. PGC-1α. 47-60
Chapter 5. Conclusion. 61-63
References. 64-103
Figures. 104-114
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