Skip navigation

DSpace

機構典藏 DSpace 系統致力於保存各式數位資料(如:文字、圖片、PDF)並使其易於取用。

點此認識 DSpace
DSpace logo
English
中文
  • 瀏覽論文
    • 校院系所
    • 出版年
    • 作者
    • 標題
    • 關鍵字
    • 指導教授
  • 搜尋 TDR
  • 授權 Q&A
    • 我的頁面
    • 接受 E-mail 通知
    • 編輯個人資料
  1. NTU Theses and Dissertations Repository
  2. 生命科學院
  3. 分子與細胞生物學研究所
請用此 Handle URI 來引用此文件: http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/84750
完整後設資料紀錄
DC 欄位值語言
dc.contributor.advisor王致恬zh_TW
dc.contributor.advisorChih-Tien Wangen
dc.contributor.author陳詠勳zh_TW
dc.contributor.authorYong-Hsun Chenen
dc.date.accessioned2023-03-19T22:23:44Z-
dc.date.available2024-04-03-
dc.date.copyright2022-09-13-
dc.date.issued2022-
dc.date.submitted2002-01-01-
dc.identifier.citationAuluck PK, Caraveo G, Lindquist S (2010) alpha-Synuclein: Membrane Interactions and Toxicity in Parkinson's Disease. In: ANNUAL REVIEW OF CELL AND DEVELOPMENTAL BIOLOGY, VOL 26 (Schekman R, Goldstein L, Lehmann R, eds), pp 211-233.
Bartolí R, Boix J, Odena G, De la Ossa ND, de Vega VM, Lorenzo-Zúñiga V (2013) Colonoscopy in rats: An endoscopic, histological and tomographic study. World J Gastrointest Endosc 5:226-230.
Braak H, Tredici KD, Rüb U, de Vos RAI, Jansen Steur ENH, Braak E (2003) Staging of brain pathology related to sporadic Parkinson’s disease. Neurobiology of Aging 24:197-211.
Brown JWP, Buell AK, Michaels TCT, Meisl G, Carozza J, Flagmeier P, Vendruscolo M, Knowles TPJ, Dobson CM, Galvagnion C (2016) beta-Synuclein suppresses both the initiation and amplification steps of alpha-synuclein aggregation via competitive binding to surfaces. Sci Rep 6:10.
Brundin P, Li J-Y, Holton JL, Lindvall O, Revesz T (2008) Research in motion: the enigma of Parkinson's disease pathology spread. Nature Reviews Neuroscience 9:741-745.
Chen Y, Shao Q, Yuan Y-H, Chen N-H (2018) Prion-like propagation of α-synuclein in the gut-brain axis. Brain Research Bulletin 140:341-346.
de Lau LML, Giesbergen P, de Rijk MC, Hofman A, Koudstaal PJ, Breteler MMB (2004) Incidence of parkinsonism and Parkinson disease in a general population - The Rotterdam Study. Neurology 63:1240-1244.
Dettmer U (2018) Rationally Designed Variants of alpha-Synuclein Illuminate Its in vivo Structural Properties in Health and Disease. Front Neurosci 12:14.
Dorsey ER, Sherer T, Okun MS, Bloem BR (2018) The Emerging Evidence of the Parkinson Pandemic. Journal of Parkinson's Disease 8:S3-S8.
Doty RL (2012) Olfactory dysfunction in Parkinson disease. Nature Reviews Neurology 8:329-339.
Emamzadeh FN, Surguchov A (2018) Parkinson's Disease: Biomarkers, Treatment, and Risk Factors. Front Neurosci 12:612-612.
Feigenbaum D, Lew M, Janga S, Shah MK, Mack W, Okamoto C, Hamm-Alvarez S (2018) Tear Proteins as Possible Biomarkers for Parkinson’s Disease (S3.006). Neurology 90:S3.006.
Frigerio R, Sanft KR, Grossardt BR, Peterson BJ, Elbaz A, Bower JH, Ahlskog JE, de Andrade M, Maraganore DM, Rocca WA (2006) Chemical exposures and Parkinson's disease: a population-based case-control study. Mov Disord 21:1688-1692.
Fujiwara H, Hasegawa M, Dohmae N, Kawashima A, Masliah E, Goldberg MS, Shen J, Takio K, Iwatsubo T (2002) alpha-Synuclein is phosphorylated in synucleinopathy lesions. Nat Cell Biol 4:160-164.
Fukusumi H, Togo K, Sumida M, Nakamori M, Obika S, Baba K, Shofuda T, Ito D, Okano H, Mochizuki H, Kanemura Y Alpha-synuclein dynamics in induced pluripotent stem cell-derived dopaminergic neurons from a Parkinson's disease patient (PARK4) with SNCA triplication. FEBS Open Bio:13.
Gómez-Benito M, Granado N, García-Sanz P, Michel A, Dumoulin M, Moratalla R (2020) Modeling Parkinson’s Disease With the Alpha-Synuclein Protein. Frontiers in Pharmacology 11.
Gallegos S, Pacheco C, Peters C, Opazo CM, Aguayo LG (2015) Features of alpha-synuclein that could explain the progression and irreversibility of Parkinson's disease. Front Neurosci 9.
Goedert M (2015) Alzheimer’s and Parkinson’s diseases: The prion concept in relation to assembled Aβ, tau, and α-synuclein. Science 349:1255555.
Goedert M, Masuda-Suzukake M, Falcon B (2017) Like prions: the propagation of aggregated tau and α-synuclein in neurodegeneration. Brain 140:266-278.
Gonzalez-Fernandez J, Prieto-Tedejo R, Velasco-Palacios L, Jorge-Roldan S, Cubo-Delgado E (2010) Digestive disorders in Parkinson's disease: dysphagia and sialorrhea. REVISTA DE NEUROLOGIA 50:S51-S54.
Guerrero-Ferreira R, Taylor NMI, Mona D, Ringler P, Lauer ME, Riek R, Britschgi M, Stahlberg H (2018) Cryo-EM structure of alpha-synuclein fibrils. eLife 7:18.
Halliday G, Murphy K (2010) Chapter 9 - Pathology of Parkinson's Disease. In: Blue Books of Neurology (Schapira AHV, Lang AET, Fahn S, eds), pp 132-154: Butterworth-Heinemann.
Hilton D, Stephens M, Kirk L, Edwards P, Potter R, Zajicek J, Broughton E, Hagan H, Carroll C (2014) Accumulation of α-synuclein in the bowel of patients in the pre-clinical phase of Parkinson’s disease. Acta Neuropathologica 127:235-241.
Ho CY, Troncoso JC, Knox D, Stark W, Eberhart CG (2014) Beta-amyloid, phospho-tau and alpha-synuclein deposits similar to those in the brain are not identified in the eyes of Alzheimer's and Parkinson's disease patients. Brain Pathol 24:25-32.
Iwai A, Masliah E, Yoshimoto M, Ge NF, Flanagan L, Desilva HAR, Kittel A, Saitoh T (1995) THE PRECURSOR PROTEIN OF NON-A-BETA COMPONENT OF ALZHEIMERS-DISEASE AMYLOID IS A PRESYNAPTIC PROTEIN OF THE CENTRAL-NERVOUS-SYSTEM. Neuron 14:467-475.
Karampetsou M, Ardah MT, Semitekolou M, Polissidis A, Samiotaki M, Kalomoiri M, Majbour N, Xanthou G, El-Agnaf OMA, Vekrellis K (2017) Phosphorylated exogenous alpha-synuclein fibrils exacerbate pathology and induce neuronal dysfunction in mice. Sci Rep 7:16533.
Karpowicz RJ, Trojanowski JQ, Lee VMY (2019) Transmission of α-synuclein seeds in neurodegenerative disease: recent developments. Laboratory Investigation 99:971-981.
Kasuga K, Nishizawa M, Ikeuchi T (2012) α-Synuclein as CSF and Blood Biomarker of Dementia with Lewy Bodies. Int J Alzheimers Dis 2012:437025.
Kim S, Kwon SH, Kam TI, Panicker N, Karuppagounder SS, Lee S, Lee JH, Kim WR, Kook M, Foss CA, Shen C, Lee H, Kulkarni S, Pasricha PJ, Lee G, Pomper MG, Dawson VL, Dawson TM, Ko HS (2019) Transneuronal Propagation of Pathologic α-Synuclein from the Gut to the Brain Models Parkinson's Disease. Neuron 103:627-641.e627.
Klettner A, Richert E, Kuhlenbäumer G, Nölle B, Bhatia KP, Deuschl G, Roider J, Schneider SA (2016) Alpha synuclein and crystallin expression in human lens in Parkinson's disease. Mov Disord 31:600-601.
Lööv C, Scherzer CR, Hyman BT, Breakefield XO, Ingelsson M (2016) α-Synuclein in Extracellular Vesicles: Functional Implications and Diagnostic Opportunities. Cellular and Molecular Neurobiology 36:437-448.
Le Couteur DG, McLean AJ, Taylor MC, Woodham BL, Board PG (1999) Pesticides and Parkinson's disease. Biomedicine & Pharmacotherapy 53:122-130.
Lebouvier T, Neunlist M, Bruley des Varannes S, Coron E, Drouard A, N'Guyen JM, Chaumette T, Tasselli M, Paillusson S, Flamand M, Galmiche JP, Damier P, Derkinderen P (2010) Colonic biopsies to assess the neuropathology of Parkinson's disease and its relationship with symptoms. PLoS One 5:e12728.
Luk Kelvin C, Kehm V, Carroll J, Zhang B, O’Brien P, Trojanowski John Q, Lee Virginia MY (2012) Pathological α-Synuclein Transmission Initiates Parkinson-like Neurodegeneration in Nontransgenic Mice. Science 338:949-953.
Meade RM, Fairlie DP, Mason JM (2019a) Alpha-synuclein structure and Parkinson's disease - lessons and emerging principles. Mol Neurodegener 14:14.
Meade RM, Fairlie DP, Mason JM (2019b) Alpha-synuclein structure and Parkinson’s disease – lessons and emerging principles. Mol Neurodegener 14:29.
Mirelman A, Bonato P, Camicioli R, Ellis TD, Giladi N, Hamilton JL, Hass CJ, Hausdorff JM, Pelosin E, Almeida QJ (2019) Gait impairments in Parkinson's disease. Lancet Neurol 18:697-708.
Mizuno Y, Hattori N, Asakawa S, Shimura H, Mori H, Shimizu N (2000) Progress in familial Parkinson's disease. JOURNAL OF CLINICAL BIOCHEMISTRY AND NUTRITION 28:143-157.
Rahimi J, Milenkovic I, Kovacs GG (2015) Patterns of Tau and α-Synuclein Pathology in the Visual System. Journal of Parkinson's Disease 5:333-340.
Rutherford NJ, Moore BD, Golde TE, Giasson BI (2014) Divergent effects of the H5OQ and G51D SNCA mutations on the aggregation of alpha-synuclein. J Neurochem 131:859-867.
Shannon KM, Keshavarzian A, Mutlu E, Dodiya HB, Daian D, Jaglin JA, Kordower JH (2012) Alpha-synuclein in colonic submucosa in early untreated Parkinson's disease. Mov Disord 27:709-715.
Stuendl A, Kunadt M, Kruse N, Bartels C, Moebius W, Danzer KM, Mollenhauer B, Schneider A (2015) Induction of α-synuclein aggregate formation by CSF exosomes from patients with Parkinson’s disease and dementia with Lewy bodies. Brain 139:481-494.
Tanaka G, Yamanaka T, Furukawa Y, Kajimura N, Mitsuoka K, Nukina N (2019) Biochemical and morphological classification of disease-associated alpha-synuclein mutants aggregates. Biochemical and Biophysical Research Communications 508:729-734.
Theillet FX, Binolfi A, Bekei B, Martorana A, Rose HM, Stuiver M, Verzini S, Lorenz D, van Rossum M, Goldfarb D, Selenko P (2016) Structural disorder of monomeric alpha-synuclein persists in mammalian cells. Nature 530:45-+.
Tran Hien T, Chung Charlotte H-Y, Iba M, Zhang B, Trojanowski John Q, Luk Kelvin C, Lee Virginia MY (2014) α-Synuclein Immunotherapy Blocks Uptake and Templated Propagation of Misfolded α-Synuclein and Neurodegeneration. Cell Reports 7:2054-2065.
Tuttle MD, Comellas G, Nieuwkoop AJ, Covell DJ, Berthold DA, Kloepper KD, Courtney JM, Kim JK, Barclay AM, Kendall A, Wan W, Stubbs G, Schwieters CD, Lee VMY, George JM, Rienstra CM (2016) Solid-state NMR structure of a pathogenic fibril of full-length human alpha-synuclein. Nat Struct Mol Biol 23:409-415.
Twelves D, Perkins KSM, Counsell C (2003) Systematic review of incidence studies of Parkinson's disease. Mov Disord 18:19-31.
Urwyler P, Nef T, Killen A, Collerton D, Thomas A, Burn D, McKeith I, Mosimann UP (2014) Visual complaints and visual hallucinations in Parkinson's disease. Parkinsonism & Related Disorders 20:318-322.
Veys L, Vandenabeele M, Ortuño-Lizarán I, Baekelandt V, Cuenca N, Moons L, De Groef L (2019) Retinal α-synuclein deposits in Parkinson's disease patients and animal models. Acta Neuropathol 137:379-395.
Wakabayashi K, Tanji K, Mori F, Takahashi H (2007) The Lewy body in Parkinson's disease: molecules implicated in the formation and degradation of alpha-synuclein aggregates. Neuropathology 27:494-506.
Wang F, Tang W, Lazear H, Bennett J, Enquist L, Friedman H (2005) Herpes Simplex Virus Type 1 Glycoprotein E Is Required for Axonal Localization of Capsid, Tegument, and Membrane Glycoproteins. Journal of virology 79:13362-13372.
Wang L, Das U, Scott David A, Tang Y, McLean Pamela J, Roy S (2014) α-Synuclein Multimers Cluster Synaptic Vesicles and Attenuate Recycling. Current Biology 24:2319-2326.
Wang W, Perovic I, Chittuluru J, Kaganovich A, Nguyen LTT, Liao JL, Auclair JR, Johnson D, Landeru A, Simorellis AK, Ju SL, Cookson MR, Asturias FJ, Agar JN, Webb BN, Kang CH, Ringe D, Petsko GA, Pochapsky TC, Hoang QQ (2011) A soluble alpha-synuclein construct forms a dynamic tetramer. Proc Natl Acad Sci U S A 108:17797-17802.
-
dc.identifier.urihttp://tdr.lib.ntu.edu.tw/jspui/handle/123456789/84750-
dc.description.abstract帕金森氏症 (PD) 是第二常見的神經退化性疾病,並且具有全身症性狀包含運動、嗅覺、腸道和視覺問題, PD 病因是由於中腦黑質緻密部 (SNc) 中多巴胺能神經元的喪失,在死亡的多巴胺能神經元中發現了大量的 α-突觸核蛋白 (α-Syn) 聚集體,稱為路易體,聚集的 α-Syn 標誌是在於其絲氨酸 129 位點 (pS129) 磷酸化的程度增加。近期研究表明,使用人類α-Syn (hα-Syn) 預形成的原纖維 (PFF) 注入十二指腸可以使其傳播到大腦並引起 PD 病理特徵,以此為動物模型中的 hα-Syn 傳播提供了證據;然而隨著 PD 研究的進展,hα-Syn 傳播的機制仍理解不多。在這項研究中,我們使用已建立的 PD 大鼠模型,經由活體內電穿孔技術表達對照質體(偽手術組)、人類野生型 α-Syn (hWT) 或其突變體 [α-Syn-A53T (hA53T ); α-Syn-A30P、E46K、H50Q、G51D、A53T (hPenta)],發現轉染後 1-3 個月後所有 hα-Syn 質體均誘導PD 症狀以及 hα-Syn 聚集體,我們更進一步探討了 hα-Syn 從大腦傳播到其他器官的潛在機制和時間進程,在轉染後 1 個月,hα-Syn 從右側 SNc 傳播到左側大腦、小腦、十二指腸、盲腸和乙狀結腸等腸道消化器官,但在這些器官中未檢測到 hα-Syn 聚集體的形成,這些數據表明 hα-Syn 可能在轉染後 1 個月從腦傳播到胃腸 (GI) 系統;相比之下,在轉染 3 個月後,我們除了在上述器官中發現 hα-Syn 聚集體,亦在其他器官中也發現了新形成的 hα-Syn 聚集體,包括嗅球、視神經和視網膜,有趣的是,特別在左側視神經(尤其是 hPenta)中發現了豐富的 hα-Syn 聚集體,鑑於視網膜主要投射到大腦的對側,hα-Syn 聚集體可能從右腦逆行傳播,通過左側視神經最後到達左側視網膜,表明 hα-Syn 聚集體可能通過視覺迴路傳播,最後我們也發現血漿中之細胞外囊泡(EV)在轉染後 3 個月後含有 hα-Syn 聚集體。綜上所述,從大腦到腸道的傳播要早於眼睛,並且來自血漿 EV 中的 hα-Syn 也可以作為早期檢測 PD 的診斷方法。zh_TW
dc.description.abstractParkinson’s disease (PD) is a second common neurodegenerative disease with systemic symptoms, including motor, olfactory, defecation, and visual defects. PD results from the loss of dopaminergic (DA) neurons in substantial nigra par compacta (SNc) of the midbrain. The enormous aggregates of alpha-synuclein (α-Syn), called Lewy bodies, are found in the dead DA neurons. The hallmark of the aggregated α-Syn is the increase in phosphorylation at serine 129 (pS129). Emerging studies indicated the human α-Syn (hα-Syn)-preformed fibrils (PFF) can propagate from mouse duodenum to brain and cause the PD pathological features, providing the evidence for hα-Syn propagation in animal models. However, how hα-Syn may propagate as PD progression remains unclear. In this study, we established the PD rat model using in vivo electroporation to transfect the right SNc with the control plasmid (sham control), human wild-type α-Syn (hWT), or its mutants [α-Syn-A53T (hA53T); α-Syn-A30P,E46K,H50Q,G51D,A53T (hPenta)]. After 1-3 months post transfection, all hα-Syn plasmids induced the progressive PD symptoms as well as α-Syn aggregates. Further, we explored the time course of hα-Syn propagation from brain to other organs. At 1 month post transfection, hα-Syn propagates from the right SNc to the left cerebrum, cerebellum, and guts such as duodenum, cecum, and sigmoid colon, with no-detectable hα-Syn aggregates in these organs. These suggest that hα-Syn may propagate from brain to the gastrointestinal (GI) system at 1 month post transfection. By contrast, after 3 months post transfection, we found α-Syn aggregates in the organs mentioned above. Moreover, α-Syn aggregates were found in some other organs, including olfactory bulbs, optic nerves, and retinas. Particularly, abundant hα-Syn aggregates were found in the left optic nerves (especially for hPenta). Given that retinas mainly project to the contralateral side of brain, hα-Syn aggregates may retrogradely propagate from the right brain, through the left optic nerves, and finally to the left retinas, indicating that hα-Syn aggregates may propagate through visual circuits. Furthermore, we found that plasma may contain extracellular vesicles (EVs) harboring hα-Syn and hα-Syn aggregates after 3 months post transfection. Taken together, the propagation from brain to gut is earlier than to eyes. The hα-Syn in the EVs from plasma may also serve as a diagnosis way to detect PD at the early stage.en
dc.description.provenanceMade available in DSpace on 2023-03-19T22:23:44Z (GMT). No. of bitstreams: 1
U0001-0209202210542400.pdf: 8573760 bytes, checksum: 85b19dfa0b65c83a19ba3bbd381365d1 (MD5)
Previous issue date: 2021
en
dc.description.tableofcontents口試委員會證明書 i
致謝 ii
中文摘要 iii
Abstract v
Abbreviations vii
Content x
Introduction 1
Parkinson’s disease 1
Prevalence of Parkinson’s disease 1
Etiology of Parkinson’s disease 1
Pathology of Parkinson’s disease 2
Alpha-Synuclein (-Syn) 3
The structure and function of αSyn 3
Aggregation of α-Syn 5
Mutations of α-Syn 6
Transportation of α-Syn 7
Propagation of -Syn 8
Propagation of α-Syn in the central nervous system 8
Propagation of α-Syn in the peripheral nervous system 9
Purpose of the study 11
Materials and Methods 12
Animals 12
Plasmids 12
Stereotaxic surgery 14
Heart perfusion and brain fixation 16
Cryosection 17
Immunofluorescence staining 18
Brain and optic nerves 18
Eye balls 19
Preparation of tissue lysate 20
Western blotting 21
Preparation of the extracellular vesicles (EVs) 22
Dot blotting 23
Results 25
The immunoreactivity of human α-Syn after transfection. 25
The immunoreactivity of α-Syn aggregates after transfection. 26
Overexpressing hPenta may induce the higher level of aggregated α-Syn in right cerebrum of rats in comparison with hWT, hA53T, or Ctrl. 26
Ectopic hα-Syn propagates across the other side of brain and forms aggregates at 3 months post transfection. 28
Aggregated hα-Syn propagates to olfactory bulbs at 3 months post transfection. 29
hα-Syn propagates to cerebellum at 1 month and forms aggregates at 3 months post transfection. 30
Signals of aggregated hα-Syn appears in optic nerves after 3 months post transfection. 31
Ectopic hα-Syn propagates to retinas and forms the aggregates after 3 months post transfection. 32
Ectopic hα-Syn accumulates in eye cups but not lens after 3 months post transfection. 34
Ectopic hα-Syn propagates to the digestive system after 1 month post transfection and forms the aggregates after 3 months post transfection. 35
Aggregated hα-Syn was detected in plasma but not CSF after 3 months post transfection. 37
Discussion 39
The size of hα-Syn and pS129 in immunoblotting 40
The hPenta mutant serves as a powerful factor in PD progression. 41
The hα-Syn propagation by EVs 42
Pros and cons of the established rats PD model in our studies and future work 43
Conclusion 45
References 46
Figure 1. Hallmarks of Parkinson’s disease (PD) and alpha-Synuclein (α-Syn). 52
Figure 2. Stereotaxic surgery and in vivo electroporation. 54
Figure 3. Schematic flowchart for the experimental protocol. 56
Figure 4. Pathological α-Syn in the central nervous system. 58
Figure 5. The Triton-insoluble fraction of tissue lysates. 60
Figure 6. The schematic diagram to extract the extracellular vesicles (EVs) from the bio-fluids of transfected rats. 62
Figure 7. Aggregated hα-Syn accumulates in the right substantia nigra (SNc) at 3 months post transfection. 64
Figure 8. hα-Syn propagates to the left SNc and forms the aggregates at 3 months post transfection. 66
Figure 9. The immunoreactivity of monomeric/misfolded hα-Syn in the right cerebrum at 1 month or 3 months post transfection. 68
Figure 10. The immunoreactivity of monomeric/misfolded hα-Syn in the left cerebrum at 1 month or 3 months post transfection. 70
Figure 11. The immunoreactivity of monomeric/misfolded hα-Syn in the olfactory bulbs at 1 month or 3 months post transfection. 72
Figure 12. The immunoreactivity of monomeric/misfolded hα-Syn in the cerebellum at 1 month or 3 months post transfection. 74
Figure 13. The visual pathway in the vertebrates. 76
Figure 14. The immunoreactivity of monomeric/misfolded hα-Syn in the optic nerves at 1 month post transfection. 78
Figure 15. The hα-Syn propagates from brain to optic nerves at 3 months post transfection. 80
Figure 16. The aggregated hα-Syn in optic nerves at 3 months post transfection. 82
Figure 17. The aggregated hα-Syn propagates to the retinas at 3 months post transfection. 83
Figure 18. The hα-Syn is majorly detected at the IPL and GCL of retina at 3 months post transfection. 86
Figure 19. The aggregated hα-Syn accumulates in the retina and the eye cup at 3 months post transfection. 88
Figure 20. The immunoreactivity of monomeric/misfolded hα-Syn in the eye cups at 1 month or 3 months post transfection. 90
Figure 21. The immunoreactivity of monomeric/misfolded hα-Syn in the lens at 1 month or 3 months post transfection. 92
Figure 22. The propagation of α-Syn through the brain-gut axis. 94
Figure 23. The immunoreactivity of monomeric/misfolded hα-Syn in the duodenum at 1 month or 3 months post transfection. 96
Figure 24. The immunoreactivity of monomeric/misfolded hα-Syn in the cecum at 1 month or 3 months post transfection. 98
Figure 25. The immunoreactivity of monomeric/misfolded hα-Syn in the sigmoid colon at 1 month or 3 months post transfection. 100
Figure 26. α-Syn propagates through cell-to-cell transmission. 102
Figure 27. Human α-Syn is not detectable in the microvesicles and exosomes from CSF of the rats at 1 month or 3 months post transfeciton. 104
Figure 28. Human α-Syn may be carried by the microvesicles and exosomes from plasma of the rats at 1 month or 3 months post transfection. 106
Figure 29. Summary of the results. 108
Appendix 109
Supplementary data 1. The decreased trend of the fecal weights is similar to the PD symptoms at 3 months post transfection. 109
2022 The 37th Joint Annual Conference of Biomedical Science Abstract 110
2022 The 37th Joint Annual Conference of Biomedical Science poster 111
The 2022 abstract of Institute of Molecular and Cell Biology poster competition 112
The 2022 Institute of Molecular and Cell Biology poster competition 113
-
dc.language.isozh_TW-
dc.subject帕金森氏症zh_TW
dc.subject胞外囊泡zh_TW
dc.subjectα-突觸核蛋白傳播zh_TW
dc.subject活體電穿孔zh_TW
dc.subject多巴胺神經元zh_TW
dc.subjectα-Syn propagationen
dc.subjectdopaminergic neuronsen
dc.subjectextracellular vesiclesen
dc.subjectParkinson’s diseaseen
dc.subjectin vivo electroporationen
dc.titleα突觸核蛋白聚集體在中樞神經系統和其他器官中的傳播機制zh_TW
dc.titleThe mechanism underlying propagation of α-Synuclein aggregates in the central nervous system and other organsen
dc.typeThesis-
dc.date.schoolyear110-2-
dc.description.degree碩士-
dc.contributor.oralexamcommittee周申如;盧主欽;徐立中zh_TW
dc.contributor.oralexamcommitteeShen-Ju Chou;Juu-Chin Lu;Li-Chung Hsuen
dc.subject.keyword帕金森氏症,多巴胺神經元,活體電穿孔,α-突觸核蛋白傳播,胞外囊泡,zh_TW
dc.subject.keywordParkinson’s disease,dopaminergic neurons,in vivo electroporation,α-Syn propagation,extracellular vesicles,en
dc.relation.page118-
dc.identifier.doi10.6342/NTU202203095-
dc.rights.note同意授權(限校園內公開)-
dc.date.accepted2022-09-05-
dc.contributor.author-college生命科學院-
dc.contributor.author-dept分子與細胞生物學研究所-
dc.date.embargo-lift2027-09-01-
顯示於系所單位:分子與細胞生物學研究所

文件中的檔案:
檔案 大小格式 
ntu-110-2.pdf
  未授權公開取用
8.37 MBAdobe PDF檢視/開啟
顯示文件簡單紀錄


系統中的文件,除了特別指名其著作權條款之外,均受到著作權保護,並且保留所有的權利。

社群連結
聯絡資訊
10617臺北市大安區羅斯福路四段1號
No.1 Sec.4, Roosevelt Rd., Taipei, Taiwan, R.O.C. 106
Tel: (02)33662353
Email: ntuetds@ntu.edu.tw
意見箱
相關連結
館藏目錄
國內圖書館整合查詢 MetaCat
臺大學術典藏 NTU Scholars
臺大圖書館數位典藏館
本站聲明
© NTU Library All Rights Reserved