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:: دوره 12، شماره 4 - ( پاییز 1403 ) ::
دوره 12 شماره 4 صفحات 96-81 برگشت به فهرست نسخه ها
پیشرفت‌ها و چالش‌ها در مدل‌های مطالعاتی پیش بالینی بیماری‌های مغزی تحلیل برنده عصبی: بیماری‎های آلزایمر و پارکینسون
سجاد سالاری ، مریم باقری*
گروه فیزیولوژی، دانشکده پزشکی، دانشگاه علوم پزشکی ایلام، ایلام، ایران ، maryam.bagheri@medilam.ac.ir
چکیده:   (764 مشاهده)
مقدمه: بیماری‌های تخریب‌کننده عصبی مانند آلزایمر و پارکینسون، از شایع‌ترین اختلالات عصبی در افراد مسن هستند که با از بین رفتن تدریجی نورون‌های مغز مشخص می‌شوند. علیرغم پیشرفت‌های علمی قابل توجه، درمان قطعی برای این بیماری‌ها هنوز یافت نشده است. مدل‌های مطالعاتی پیش‌بالینی نقش حیاتی در درک مکانیسم‌های زیربنایی و توسعه درمان‌های نوین ایفا می‌کنند. این مقاله مروری جامع بر مدل‌های حیوانی، دارویی و ژنتیکی ارائه می‌کند که هر کدام جنبه‌هایی از رفتار، آسیب شناسی و زیست‌شناسی مولکولی مرتبط با این بیماری‌ها را شبیه‌سازی می‌کنند. علاوه بر این، بهره‌گیری از هوش مصنوعی و زبان‌های برنامه‌نویسی در تجزیه و تحلیل داده‌ها و ایجاد مدل‌های آماری شخصی‌، چشم‌اندازهای جدیدی را برای پیش‌بینی پیشرفت بیماری و طراحی درمان‌های هدفمند فراهم کرده است. مدل‌های حیوانی تراریخته برای مطالعه اثرات جهش‌های ژنتیکی مورد استفاده قرار می‌گیرند، در‌حالی‌که مدل‌های دارویی از نوروتوکسین‌هایی مانند آمیلوئید بتا و 6-هیدروکسی دوپامین برای بازسازی مسیرهای پاتوفیزیولوژیک استفاده می‌کنند. ترکیب این دو رویکرد همراه با ابزارهای هوش مصنوعی تصویری دقیق‌تر از پیچیدگی‌های بیماری را ارائه می‌دهد. نتیجه‌گیری: برای بدست آوردن درک جامع از این بیماری‌ها، توسعه مدل‌های پیشرفته‌ای که روش‌های بیولوژیکی، دارویی و هوش مصنوعی را ادغام می‌کنند، حیاتی است. این مدل‌ها می‌توانند دقت شبیه‌سازی بیماری را افزایش دهند، مسیرهای درمانی جدید را شناسایی کنند و کیفیت زندگی بیماران را بهبود بخشند.
 
واژه‌های کلیدی: نوروپاتولوژی، زوال عقل، نقص پروتئوستاز، جسم قاعده‌ای
متن کامل [PDF 1303 kb]   (270 دریافت)    
نوع مطالعه: مروری | موضوع مقاله: نوروفیزیوپاتولوژی
فهرست منابع
1. Bi X. Alzheimer disease: update on basic mechanisms. Journal of Osteopathic Medicine. 2010;110(s98):3-9.
2. Jellinger KA, Attems J. Prevalence of dementia disorders in the oldest-old: an autopsy study. Acta neuropathologica. 2010;119:421-33. [DOI:10.1007/s00401-010-0654-5]
3. Shah RS, Lee H-G, Xiongwei Z, Perry G, Smith MA, Castellani RJ. Current approaches in the treatment of Alzheimer's disease. Biomedicine & Pharmacotherapy. 2008;62(4):199-207. [DOI:10.1016/j.biopha.2008.02.005]
4. Förstl H, Kurz A. Clinical features of Alzheimer's disease. European archives of psychiatry and clinical neuroscience. 1999;249:288-90. [DOI:10.1007/s004060050101]
5. Wilson RS, Barral S, Lee JH, Leurgans SE, Foroud TM, Sweet RA, et al. Heritability of different forms of memory in the Late Onset Alzheimer's Disease Family Study. Journal of Alzheimer's Disease. 2011;23(2):249-55. [DOI:10.3233/JAD-2010-101515]
6. Dorszewska J, Prendecki M, Oczkowska A, Dezor M, Kozubski W. Molecular basis of familial and sporadic Alzheimer's disease. Current Alzheimer Research. 2016;13(9):952-63. [DOI:10.2174/1567205013666160314150501]
7. Waring SC, Rosenberg RN. Genome-wide association studies in Alzheimer disease. Archives of neurology. 2008;65(3):329-34. [DOI:10.1001/archneur.65.3.329]
8. Mura T, Dartigues JF, Berr C. How many dementia cases in France and Europe? Alternative projections and scenarios 2010-2050. European journal of neurology. 2010;17(2):252-9. [DOI:10.1111/j.1468-1331.2009.02783.x]
9. Parkinson J. An essay on the shaking palsy. The Journal of neuropsychiatry and clinical neurosciences. 2002;14(2):223-36. [DOI:10.1176/jnp.14.2.223]
10. Chaudhuri KR, Schapira AH. Non-motor symptoms of Parkinson's disease: dopaminergic pathophysiology and treatment. The Lancet Neurology. 2009;8(5):464-74. [DOI:10.1016/S1474-4422(09)70068-7]
11. De Lau LM, Breteler MM. Epidemiology of Parkinson's disease. The Lancet Neurology. 2006;5(6):525-35. [DOI:10.1016/S1474-4422(06)70471-9]
12. Skaper SD. Alzheimer's disease and amyloid: culprit or coincidence. Int Rev Neurobiol. 2012;102:277-316. [DOI:10.1016/B978-0-12-386986-9.00011-9]
13. Oliveira JM, Henriques AG, Martins F, Rebelo S, e Silva OAdC. Amyloid-ß Modulates Both AßPP and Tau Phosphorylation. Journal of Alzheimer's Disease. 2015;45:495-507. [DOI:10.3233/JAD-142664]
14. Haass C, Selkoe DJ. Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer's amyloid β-peptide. Nature reviews Molecular cell biology. 2007;8(2):101-12. [DOI:10.1038/nrm2101]
15. Kandel ER, Schwartz JH, Jessell TM, Siegelbaum S, Hudspeth AJ, Mack S. Principles of neural science: McGraw-hill New York; 2000.
16. Wilquet V, De Strooper B. Amyloid-beta precursor protein processing in neurodegeneration. Current opinion in neurobiology. 2004;14(5):582-8. [DOI:10.1016/j.conb.2004.08.001]
17. Krone MG, Baumketner A, Bernstein SL, Wyttenbach T, Lazo ND, Teplow DB, et al. Effects of familial Alzheimer's disease mutations on the folding nucleation of the amyloid β-protein. Journal of molecular biology. 2008;381(1):221-8. [DOI:10.1016/j.jmb.2008.05.069]
18. Miller DL, Papayannopoulos IA, Styles J, Bobin SA, Lin YY, Biemann K, et al. Peptide compositions of the cerebrovascular and senile plaque core amyloid deposits of Alzheimer′ s disease. Archives of biochemistry and biophysics. 1993;301(1):41-52. [DOI:10.1006/abbi.1993.1112]
19. AE R. β-Amyloid-(1-42) is a major component of cerebrovascular amyloid deposits: implications for the pathology of Alzheimer disease. Proc Natl Acad Sci USA. 1993;90:10836-40. [DOI:10.1073/pnas.90.22.10836]
20. Suzuki N, Iwatsubo T, Odaka A, Ishibashi Y, Kitada C, Ihara Y. High tissue content of soluble beta 1-40 is linked to cerebral amyloid angiopathy. The American journal of pathology. 1994;145(2):452.
21. Jarrett JT, Berger EP, Lansbury Jr PT. The carboxy terminus of the. beta. amyloid protein is critical for the seeding of amyloid formation: Implications for the pathogenesis of Alzheimer's disease. Biochemistry. 1993;32(18):4693-7. [DOI:10.1021/bi00069a001]
22. Lemere C, Blusztajn J, Yamaguchi H, Wisniewski T, Saido T, Selkoe D. Sequence of deposition of heterogeneous amyloid β-peptides and APO E in Down syndrome: implications for initial events in amyloid plaque formation. Neurobiology of disease. 1996;3(1):16-32. [DOI:10.1006/nbdi.1996.0003]
23. Bilbul M, Schipper HM. Risk profiles of Alzheimer disease. Canadian journal of neurological sciences. 2011;38(4):580-92. [DOI:10.1017/S0317167100012129]
24. Sofroniew MV. Molecular dissection of reactive astrogliosis and glial scar formation. Trends in neurosciences. 2009;32(12):638-47. [DOI:10.1016/j.tins.2009.08.002]
25. Sofroniew MV, Vinters HV. Astrocytes: biology and pathology. Acta neuropathologica. 2010;119:7-35. [DOI:10.1007/s00401-009-0619-8]
26. Perez RG, Waymire JC, Lin E, Liu JJ, Guo F, Zigmond MJ. A role for α-synuclein in the regulation of dopamine biosynthesis. Journal of Neuroscience. 2002;22(8):3090-9. [DOI:10.1523/JNEUROSCI.22-08-03090.2002]
27. Koprich JB, Johnston TH, Huot P, Reyes MG, Espinosa M, Brotchie JM. Progressive neurodegeneration or endogenous compensation in an animal model of Parkinson's disease produced by decreasing doses of alpha-synuclein. PloS one. 2011;6(3):e17698. [DOI:10.1371/journal.pone.0017698]
28. Ben Gedalya T, Loeb V, Israeli E, Altschuler Y, Selkoe DJ, Sharon R. α‐Synuclein and Polyunsaturated Fatty Acids Promote Clathrin‐Mediated Endocytosis and Synaptic Vesicle Recycling. Traffic. 2009;10(2):218-34. [DOI:10.1111/j.1600-0854.2008.00853.x]
29. Corti O, Lesage S, Brice A. What genetics tells us about the causes and mechanisms of Parkinson's disease. Physiological reviews. 2011. [DOI:10.1152/physrev.00022.2010]
30. Thomas KJ, Cookson MR. The role of PTEN-induced kinase 1 in mitochondrial dysfunction and dynamics. The international journal of biochemistry & cell biology. 2009;41(10):2025-35. [DOI:10.1016/j.biocel.2009.02.018]
31. Devine MJ, Plun-Favreau H, Wood NW. Parkinson's disease and cancer: two wars, one front. Nature Reviews Cancer. 2011;11(11):813-23. [DOI:10.1038/nrc3150]
32. Caudle WM. Occupational exposures and parkinsonism. Handbook of clinical neurology. 2015;131:225-39. [DOI:10.1016/B978-0-444-62627-1.00013-5]
33. Betarbet R, Sherer TB, MacKenzie G, Garcia-Osuna M, Panov AV, Greenamyre JT. Chronic systemic pesticide exposure reproduces features of Parkinson's disease. Nature neuroscience. 2000;3(12):1301-6. [DOI:10.1038/81834]
34. Lai B, Marion S, Teschke K, Tsui J. Occupational and environmental risk factors for Parkinson's disease. Parkinsonism & related disorders. 2002;8(5):297-309. [DOI:10.1016/S1353-8020(01)00054-2]
35. Murakami K, Miyake Y, Sasaki S, Tanaka K, Fukushima W, Kiyohara C, et al. Dietary intake of folate, vitamin B6, vitamin B12 and riboflavin and risk of Parkinson's disease: a case-control study in Japan. British Journal of Nutrition. 2010;104(5):757-64. [DOI:10.1017/S0007114510001005]
36. Shahverdi M, Sourani Z, Sargolzaie M, Modarres Mousavi M, Shirian S. An Investigation into the Effects of Water-and Fat-Soluble Vitamins in Alzheimer's and Parkinson's Diseases. The Neuroscience Journal of Shefaye Khatam. 2023;11(3):95-109. [DOI:10.61186/shefa.11.3.95]
37. Aroso M, Ferreira R, Freitas A, Vitorino R, Gomez‐Lazaro M. New insights on the mitochondrial proteome plasticity in Parkinson's disease. PROTEOMICS-Clinical Applications. 2016;10(4):416-29. [DOI:10.1002/prca.201500092]
38. Henchcliffe C, Beal MF. Mitochondrial biology and oxidative stress in Parkinson disease pathogenesis. Nature clinical practice Neurology. 2008;4(11):600-9. [DOI:10.1038/ncpneuro0924]
39. Yuan Y, Tong Q, Zhang L, Jiang S, Zhou H, Zhang R, et al. Plasma antioxidant status and motor features in de novo Chinese Parkinson's disease patients. International Journal of Neuroscience. 2016;126(7):641-6.
40. Voshavar C, Shah M, Xu L, Dutta AK. Assessment of protective role of multifunctional dopamine agonist D-512 against oxidative stress produced by depletion of glutathione in PC12 cells: implication in neuroprotective therapy for Parkinson's disease. Neurotoxicity research. 2015;28:302-18. [DOI:10.1007/s12640-015-9548-6]
41. Devore EE, Grodstein F, van Rooij FJ, Hofman A, Stampfer MJ, Witteman JC, et al. Dietary antioxidants and long-term risk of dementia. Archives of neurology. 2010;67(7):819-25. [DOI:10.1001/archneurol.2010.144]
42. Bednarczyk P. Potassium channels in brain mitochondria. Acta Biochimica Polonica. 2009;56(3):385-92. [DOI:10.18388/abp.2009_2471]
43. Fahanik-Babaei J, Eliassi A, Jafari A, Sauve R, Salari S, Saghiri R. Electro-pharmacological profile of a mitochondrial inner membrane big-potassium channel from rat brain. Biochimica et Biophysica Acta (BBA)-Biomembranes. 2011;1808(1):454-60. [DOI:10.1016/j.bbamem.2010.10.005]
44. Salari S, Ghasemi M, Fahanik-Babaei J, Saghiri R, Sauve R, Eliassi A. Evidence for a KATP channel in rough endoplasmic reticulum (rerKATP channel) of rat hepatocytes. PLoS One. 2015;10(5):e0125798. [DOI:10.1371/journal.pone.0125798]
45. Salari S, Eliassi AA, Saghiri R. Evidences on the existence of a new potassium channel in the rough endoplasmic reticulum (RER) of rat hepatocytes. Physiology and Pharmacology. 2011;15(1):16-26.
46. Ghasemi M, Khodaei N, Salari S, Eliassi A, Saghiri R. Gating behavior of endoplasmic reticulum potassium channels of rat hepatocytes in diabetes. Iranian biomedical journal. 2014;18(3):165.
47. Kuum M, Veksler V, Liiv J, Ventura-Clapier R, Kaasik A. Endoplasmic reticulum potassium-hydrogen exchanger and small conductance calcium-activated potassium channel activities are essential for ER calcium uptake in neurons and cardiomyocytes. Journal of cell science. 2012;125(3):625-33. [DOI:10.1242/jcs.090126]
48. Magi S, Castaldo P, Macrì ML, Maiolino M, Matteucci A, Bastioli G, et al. Intracellular calcium dysregulation: implications for Alzheimer's disease. BioMed research international. 2016;2016. [DOI:10.1155/2016/6701324]
49. Rodriguez-Pallares J, Parga JA, Joglar B, Guerra MJ, Labandeira-Garcia JL. Mitochondrial ATP-sensitive potassium channels enhance angiotensin-induced oxidative damage and dopaminergic neuron degeneration. Relevance for aging-associated susceptibility to Parkinson's disease. Age. 2012;34:863-80. [DOI:10.1007/s11357-011-9284-7]
50. Woodruff-Pak DS. Animal models of Alzheimer's disease: therapeutic implications. Journal of Alzheimer's disease. 2008;15(4):507-21. [DOI:10.3233/JAD-2008-15401]
51. Yamada K, Nabeshima T. Animal models of Alzheimer's disease and evaluation of anti-dementia drugs. Pharmacology & therapeutics. 2000;88(2):93-113. [DOI:10.1016/S0163-7258(00)00081-4]
52. Sasaguri H, Hashimoto S, Watamura N, Sato K, Takamura R, Nagata K, et al. Recent Advances in the Modeling of Alzheimer's Disease. Front Neurosci. 2022;16:807473. [DOI:10.3389/fnins.2022.807473]
53. Sharma NS, Karan A, Lee D, Yan Z, Xie J. Advances in Modeling Alzheimer's Disease In Vitro. Advanced NanoBiomed Research. 2021;1(12):2100097. [DOI:10.1002/anbr.202100097]
54. Do Carmo S, Cuello AC. Modeling Alzheimer's disease in transgenic rats. Molecular neurodegeneration. 2013;8:1-11. [DOI:10.1186/1750-1326-8-37]
55. Martino Adami PV, Quijano C, Magnani N, Galeano P, Evelson P, Cassina A, et al. Synaptosomal bioenergetic defects are associated with cognitive impairment in a transgenic rat model of early Alzheimer's disease. Journal of Cerebral Blood Flow & Metabolism. 2017;37(1):69-84. [DOI:10.1177/0271678X15615132]
56. Futai E, Osawa S, Cai T, Fujisawa T, Ishiura S, Tomita T. Suppressor mutations for presenilin 1 familial Alzheimer disease mutants modulate γ-secretase activities. Journal of Biological Chemistry. 2016;291(1):435-46. [DOI:10.1074/jbc.M114.629287]
57. Guzmán EA, Bouter Y, Richard BC, Lannfelt L, Ingelsson M, Paetau A, et al. Abundance of Aβ 5-x like immunoreactivity in transgenic 5XFAD, APP/PS1KI and 3xTG mice, sporadic and familial Alzheimer's disease. Molecular neurodegeneration. 2014;9:1-11. [DOI:10.1186/1750-1326-9-13]
58. Zhong MZ, Peng T, Duarte ML, Wang M, Cai D. Updates on mouse models of Alzheimer's disease. Molecular neurodegeneration. 2024;19(1):23. [DOI:10.1186/s13024-024-00712-0]
59. Wolf A, Bauer B, Abner EL, Ashkenazy-Frolinger T, Hartz AM. A comprehensive behavioral test battery to assess learning and memory in 129S6/Tg2576 mice. PloS one. 2016;11(1):e0147733. [DOI:10.1371/journal.pone.0147733]
60. Saydoff JA, Olariu A, Sheng J, Hu Z, Li Q, Garcia R, et al. Uridine prodrug improves memory in Tg2576 and TAPP mice and reduces pathological factors associated with Alzheimer's disease in related models. Journal of Alzheimer's Disease. 2013;36(4):637-57. [DOI:10.3233/JAD-130059]
61. Puzzo D, Gulisano W, Palmeri A, Arancio O. Rodent models for Alzheimer's disease drug discovery. Expert opinion on drug discovery. 2015;10(7):703-11. [DOI:10.1517/17460441.2015.1041913]
62. Calhoun ME, Kurth D, Phinney AL, Long JM, Hengemihle J, Mouton PR, et al. Hippocampal neuron and synaptophysin-positive bouton number in aging C57BL/6 mice. Neurobiology of aging. 1998;19(6):599-606. [DOI:10.1016/S0197-4580(98)00098-0]
63. Lewis J, Dickson DW, Lin W-L, Chisholm L, Corral A, Jones G, et al. Enhanced neurofibrillary degeneration in transgenic mice expressing mutant tau and APP. Science. 2001;293(5534):1487-91. [DOI:10.1126/science.1058189]
64. Boutajangout A, Authelet M, Blanchard V, Touchet N, Tremp G, Pradier L, et al. Characterisation of cytoskeletal abnormalities in mice transgenic for wild-type human tau and familial Alzheimer's disease mutants of APP and presenilin-1. Neurobiology of disease. 2004;15(1):47-60. [DOI:10.1016/j.nbd.2003.09.007]
65. Salari S, Bagheri M. A review of animal models of Alzheimer's disease: a brief insight into pharmacologic and genetic models. 2016.
66. Echeverria V, Ducatenzeiler A, Alhonen L, Janne J, Grant SM, Wandosell F, et al. Rat transgenic models with a phenotype of intracellular Aβ accumulation in hippocampus and cortex. Journal of Alzheimer's Disease. 2004;6(3):209-19. [DOI:10.3233/JAD-2004-6301]
67. Flood DG, Lin Y-G, Lang DM, Trusko SP, Hirsch JD, Savage MJ, et al. A transgenic rat model of Alzheimer's disease with extracellular Aβ deposition. Neurobiology of aging. 2009;30(7):1078-90. [DOI:10.1016/j.neurobiolaging.2007.10.006]
68. Cente M, Filipcik P, Pevalova M, Novak M. Expression of a truncated tau protein induces oxidative stress in a rodent model of tauopathy. European Journal of Neuroscience. 2006;24(4):1085-90. [DOI:10.1111/j.1460-9568.2006.04986.x]
69. Filipcik P, Zilka N, Bugos O, Kucerak J, Koson P, Novak P, et al. First transgenic rat model developing progressive cortical neurofibrillary tangles. Neurobiology of aging. 2012;33(7):1448-56. [DOI:10.1016/j.neurobiolaging.2010.10.015]
70. Zilka N, Filipcik P, Koson P, Fialova L, Skrabana R, Zilkova M, et al. Truncated tau from sporadic Alzheimer's disease suffices to drive neurofibrillary degeneration in vivo. FEBS letters. 2006;580(15):3582-8. [DOI:10.1016/j.febslet.2006.05.029]
71. Winkler J, Thal LJ, Gage FH, Fisher LJ. Cholinergic strategies for Alzheimer's disease. Journal of Molecular Medicine. 1998;76:555-67. [DOI:10.1007/s001090050250]
72. Alihosseini T, Azizi M, Abbasi N, Mohammadpour S, Bagheri M. Amelioration of amyloid beta (Aβ1-40) neurotoxicity by administration of silibinin; a behavioral and biochemical assessment. Iranian Journal of Basic Medical Sciences. 2023;26(7):791.
73. Kowall NW, Beal MF, Busciglio J, Duffy LK, Yankner BA. An in vivo model for the neurodegenerative effects of beta amyloid and protection by substance P. Proceedings of the National Academy of Sciences. 1991;88(16):7247-51. [DOI:10.1073/pnas.88.16.7247]
74. Bagheri M, Rezakhani A, Nyström S, Turkina MV, Roghani M, Hammarström P, et al. Amyloid beta1-40-induced astrogliosis and the effect of genistein treatment in rat: a three-dimensional confocal morphometric and proteomic study. PLoS One. 2013;8(10):e76526. [DOI:10.1371/journal.pone.0076526]
75. Bagheri M, Joghataei M-T, Mohseni S, Roghani M. Genistein ameliorates learning and memory deficits in amyloid β (1-40) rat model of Alzheimer's disease. Neurobiology of Learning and Memory. 2011;95(3):270-6. [DOI:10.1016/j.nlm.2010.12.001]
76. Ghofrani S, Joghataei M-T, Mohseni S, Baluchnejadmojarad T, Bagheri M, Khamse S, et al. Naringenin improves learning and memory in an Alzheimer's disease rat model: Insights into the underlying mechanisms. European Journal of Pharmacology. 2015;764:195-201. [DOI:10.1016/j.ejphar.2015.07.001]
77. Bagheri M, Rezakhani A, Roghani M, Joghataei MT, Mohseni S. Protocol for three-dimensional confocal morphometric analysis of astrocytes. JoVE (Journal of Visualized Experiments). 2015(106):e53113. [DOI:10.3791/53113-v]
78. Lecanu L, Papadopoulos V. Modeling Alzheimer's disease with non-transgenic rat models. Alzheimer's research & therapy. 2013;5:1-9. [DOI:10.1186/alzrt171]
79. Montazeri A, Akhlaghi M, Barahimi AR, Jahanbazi Jahan Abad A, Jabbari R. The role of metals in neurodegenerative diseases of the central nervous system. The Neuroscience Journal of Shefaye Khatam. 2020;8(2):130-46. [DOI:10.29252/shefa.8.2.130]
80. Pilcher H. Alzheimer's disease could be "type 3 diabetes". The Lancet Neurology. 2006;5(5):388-9. [DOI:10.1016/S1474-4422(06)70434-3]
81. Laursen B, Mørk A, Kristiansen U, Bastlund JF. Hippocampal P3-like auditory event-related potentials are disrupted in a rat model of cholinergic degeneration in Alzheimer's disease: reversal by donepezil treatment. Journal of Alzheimer's Disease. 2014;42(4):1179-89. [DOI:10.3233/JAD-131502]
82. Farajpour H, Banimohamad-Shotorbani B, Rafiei-Baharloo M, Lotfi H. Application of Artificial Intelligence in Regenerative Medicine. The Neuroscience Journal of Shefaye Khatam. 2023;11(4):94-107. [DOI:10.61186/shefa.11.4.94]
83. Petrella JR, Jiang J, Sreeram K, Dalziel S, Doraiswamy P, Hao W, et al. Personalized Computational Causal Modeling of the Alzheimer Disease Biomarker Cascade. The journal of prevention of Alzheimer's disease. 2024;11(2):435-44. [DOI:10.14283/jpad.2023.134]
84. Ke M, Chong CM, Zhu Q, Zhang K, Cai CZ, Lu JH, et al. Comprehensive Perspectives on Experimental Models for Parkinson's Disease. Aging Dis. 2021;12(1):223-46. [DOI:10.14336/AD.2020.0331]
85. Shadrina M, Slominsky P. Modeling Parkinson's Disease: Not Only Rodents? Front Aging Neurosci. 2021;13:695718. [DOI:10.3389/fnagi.2021.695718]
86. Blesa J, Phani S, Jackson-Lewis V, Przedborski S. Classic and new animal models of Parkinson's disease. BioMed Research International. 2012;2012. [DOI:10.1155/2012/845618]
87. Klivenyi P, Vecsei L. Pharmacological Models of Parkinson's Disease in Rodents. Neurodegeneration: Methods and Protocols. 2011:211-27. [DOI:10.1007/978-1-61779-328-8_14]
88. Ruffy R, Leonard M. Chemical cardiac sympathetic denervation hampers defibrillation in the dog. Journal of cardiovascular electrophysiology. 1997;8(1):62-7. [DOI:10.1111/j.1540-8167.1997.tb00609.x]
89. Valette H, Deleuze P, Syrota A, Delforge J, Crouzel C, Fuseau C, et al. Canine myocardial beta-adrenergic, muscarinic receptor densities after denervation: a PET study. Journal of Nuclear Medicine. 1995;36(1):140-6.
90. Penttinen AM, Suleymanova I, Albert K, Anttila J, Voutilainen MH, Airavaara M. Characterization of a new low‐dose 6‐hydroxydopamine model of Parkinson's disease in rat. Journal of neuroscience research. 2016;94(4):318-28. [DOI:10.1002/jnr.23708]
91. Javoy F, Sotelo C, Herbet A, Agid Y. Specificity of dopaminergic neuronal degeneration induced by intracerebral injection of 6-hydroxydopamine in the nigrostriatal dopamine system. Brain research. 1976;102(2):201-15. [DOI:10.1016/0006-8993(76)90877-5]
92. Baluchnejadmojarad T, Roghani M, Nadoushan MRJ, Bagheri M. Neuroprotective effect of genistein in 6‐hydroxydopamine hemi‐parkinsonian rat model. Phytotherapy Research: An International Journal Devoted to Pharmacological and Toxicological Evaluation of Natural Product Derivatives. 2009;23(1):132-5. [DOI:10.1002/ptr.2564]
93. Vazifehkhah S, Karimzadeh F. Parkinson Disease: from Pathophysiology to the Animal Models. The Neuroscience Journal of Shefaye Khatam. 2016;4(3):91-102. [DOI:10.18869/acadpub.shefa.4.3.91]
94. Kowall NW, Hantraye P, Brouillet E, Beal MF, McKee AC, Ferrante RJ. MPTP induces alpha-synuclein aggregation in the substantia nigra of baboons. Neuroreport. 2000;11(1):211-3. [DOI:10.1097/00001756-200001170-00041]
95. Fornai F, Schlüter OM, Lenzi P, Gesi M, Ruffoli R, Ferrucci M, et al. Parkinson-like syndrome induced by continuous MPTP infusion: convergent roles of the ubiquitin-proteasome system and α-synuclein. Proceedings of the National Academy of Sciences. 2005;102(9):3413-8. [DOI:10.1073/pnas.0409713102]
96. Nikokalam Nazif N, Khosravi M, Ahmadi R, Bananej M, Majd A. Neuroprotective Effect of Quercetin in 1-Methyl-4-Phenyl-1, 2, 3, 6-Tetrahydropyridine-Induced Model of Parkinson's Disease. The Neuroscience Journal of Shefaye Khatam. 2019;8(1):1-10. [DOI:10.29252/shefa.8.1.1]
97. Day BJ, Patel M, Calavetta L, Chang L-Y, Stamler JS. A mechanism of paraquat toxicity involving nitric oxide synthase. Proceedings of the National Academy of Sciences. 1999;96(22):12760-5. [DOI:10.1073/pnas.96.22.12760]
98. Berry C, La Vecchia C, Nicotera P. Paraquat and Parkinson's disease. Cell Death & Differentiation. 2010;17(7):1115-25. [DOI:10.1038/cdd.2009.217]
99. McCormack AL, Thiruchelvam M, Manning-Bog AB, Thiffault C, Langston JW, Cory-Slechta DA, et al. Environmental risk factors and Parkinson's disease: selective degeneration of nigral dopaminergic neurons caused by the herbicide paraquat. Neurobiology of disease. 2002;10(2):119-27. [DOI:10.1006/nbdi.2002.0507]
100. Thiffault C, Langston JW, Di Monte DA. Increased striatal dopamine turnover following acute administration of rotenone to mice. Brain research. 2000;885(2):283-8. [DOI:10.1016/S0006-8993(00)02960-7]
101. Rappold PM, Cui M, Chesser AS, Tibbett J, Grima JC, Duan L, et al. Paraquat neurotoxicity is mediated by the dopamine transporter and organic cation transporter-3. Proceedings of the National Academy of Sciences. 2011;108(51):20766-71. [DOI:10.1073/pnas.1115141108]
102. Inden M, Kitamura Y, Takeuchi H, Yanagida T, Takata K, Kobayashi Y, et al. Neurodegeneration of mouse nigrostriatal dopaminergic system induced by repeated oral administration of rotenone is prevented by 4‐phenylbutyrate, a chemical chaperone. Journal of neurochemistry. 2007;101(6):1491-504. [DOI:10.1111/j.1471-4159.2006.04440.x]
103. Sherer TB, Kim J-H, Betarbet R, Greenamyre JT. Subcutaneous rotenone exposure causes highly selective dopaminergic degeneration and α-synuclein aggregation. Experimental neurology. 2003;179(1):9-16. [DOI:10.1006/exnr.2002.8072]
104. Höglinger GU, Féger J, Prigent A, Michel PP, Parain K, Champy P, et al. Chronic systemic complex I inhibition induces a hypokinetic multisystem degeneration in rats. Journal of neurochemistry. 2003;84(3):491-502. [DOI:10.1046/j.1471-4159.2003.01533.x]
105. Pan-Montojo F, Anichtchik O, Dening Y, Knells L, Pursche S, Jung R, et al. Progression of Parkinson's disease pathology is reproduced by intragastric administration of rotenone in mice. Nature Precedings. 2010:1-. [DOI:10.1038/npre.2010.3352.3]
106. Aschner M, Guilarte TR, Schneider JS, Zheng W. Manganese: recent advances in understanding its transport and neurotoxicity. Toxicology and applied pharmacology. 2007;221(2):131-47. [DOI:10.1016/j.taap.2007.03.001]
107. Bowman AB, Kwakye GF, Hernández EH, Aschner M. Role of manganese in neurodegenerative diseases. Journal of trace elements in medicine and biology. 2011;25(4):191-203. [DOI:10.1016/j.jtemb.2011.08.144]
108. Sadeghi L, Babadi VY, Tanwir F. Manganese dioxide nanoparticle induces Parkinson like neurobehavioral abnormalities in rats. Bratislavske Lekarske Listy. 2018;119(6):379-84. [DOI:10.4149/BLL_2018_070]
109. Bouabid S, Tinakoua A, Lakhdar‐Ghazal N, Benazzouz A. Manganese neurotoxicity: behavioral disorders associated with dysfunctions in the basal ganglia and neurochemical transmission. Journal of neurochemistry. 2016;136(4):677-91. [DOI:10.1111/jnc.13442]
110. Pickrell AM, Pinto M, Hida A, Moraes CT. Striatal dysfunctions associated with mitochondrial DNA damage in dopaminergic neurons in a mouse model of Parkinson's disease. Journal of Neuroscience. 2011;31(48):17649-58. [DOI:10.1523/JNEUROSCI.4871-11.2011]
111. Meredith GE, Sonsalla PK, Chesselet M-F. Animal models of Parkinson's disease progression. Acta neuropathologica. 2008;115:385-98. [DOI:10.1007/s00401-008-0350-x]
112. Kay DM, Factor SA, Samii A, Higgins DS, Griffith A, Roberts JW, et al. Genetic association between α‐synuclein and idiopathic parkinson's disease. American Journal of Medical Genetics Part B: Neuropsychiatric Genetics. 2008;147(7):1222-30. [DOI:10.1002/ajmg.b.30758]
113. Miklya I, Göltl P, Hafenscher F, Pencz N. The role of parkin in Parkinson's disease. Neuropsychopharmacologia Hungarica: a Magyar Pszichofarmakologiai Egyesulet lapja= official journal of the Hungarian Association of Psychopharmacology. 2014;16(2):67-76.
114. Tan EK, Skipper LM. Pathogenic mutations in Parkinson disease. Human mutation. 2007;28(7):641-53. [DOI:10.1002/humu.20507]
115. Khan E, Hasan I, Haque ME. Parkinson's Disease: Exploring Different Animal Model Systems. Int J Mol Sci. 2023;24(10). [DOI:10.3390/ijms24109088]
116. Ahmadi R, Sohrabian L. The Effect of Ghrelin Agonist, Exercise, and Nicotine on Catalepsy in an Animal Model of Parkinson's Disease. The Neuroscience Journal of Shefaye Khatam. 2017;5(3):28-34. [DOI:10.18869/acadpub.shefa.5.3.28]
117. Dehay B, Bezard E. New animal models of Parkinson's disease. Movement disorders. 2011;26(7):1198-205. [DOI:10.1002/mds.23546]
118. Bayersdorfer F, Voigt A, Schneuwly S, Botella JA. Dopamine-dependent neurodegeneration in Drosophila models of familial and sporadic Parkinson's disease. Neurobiology of disease. 2010;40(1):113-9. [DOI:10.1016/j.nbd.2010.02.012]
119. Alexander AG, Marfil V, Li C. Use of Caenorhabditis elegans as a model to study Alzheimer's disease and other neurodegenerative diseases. Frontiers in genetics. 2014;5:95895. [DOI:10.3389/fgene.2014.00279]
120. Cui X, Li X, Zheng H, Su Y, Zhang S, Li M, et al. Human midbrain organoids: a powerful tool for advanced Parkinson's disease modeling and therapy exploration. npj Parkinson's Disease. 2024;10(1):189. [DOI:10.1038/s41531-024-00799-8]
121. Seghatoleslam M, Hosseini M. Potential of stem cells in the treatment of nervous system disorders. Neurosci J Shefaye Khatam. 2015;3(1):99-114. [DOI:10.18869/acadpub.shefa.3.1.99]



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Salari S, Bagheri M. Advancements and Challenges in Preclinical Study Models of Neurodegenerative Brain Diseases: Alzheimer's and Parkinson's Diseases. Shefaye Khatam 2024; 12 (4) :81-96
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سالاری سجاد، باقری مریم. پیشرفت‌ها و چالش‌ها در مدل‌های مطالعاتی پیش بالینی بیماری‌های مغزی تحلیل برنده عصبی: بیماری‎های آلزایمر و پارکینسون. مجله علوم اعصاب شفای خاتم. 1403; 12 (4) :81-96

URL: http://shefayekhatam.ir/article-1-2506-fa.html



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