Disease
Parkinson disease
Disease classification:central nervous system disorder; hereditary disease; basal ganglia disorder; nervous system disorder; brain disorder; parkinsonian disorder
About this disease
A progressive degenerative disorder of the central nervous system characterized by loss of dopamine producing neurons in the substantia nigra and the presence of Lewy bodies in the substantia nigra and locus coeruleus. Signs and symptoms include tremor which is most pronounced during rest, muscle rigidity, slowing of the voluntary movements, a tendency to fall back, and a mask-like facial expression.
Standard definition source:MONDO:0005180 Parkinson disease · ontology version 2026-10-06
References
- Shen Zhiqiang, Ma Linlin, Mellick George D., Perše Martina. Strategies for Optimizing Genetic Mouse Models to Enhance the Understanding of Parkinson’s Disease. Biomedicines. 2026.
- Zambetta Mariana Lara, Fernandes Elayne Borges, Kim Allison, Russo Thiago Luiz, Gianlorenço Anna Carolyna, Prokai-Tatrai Katalin, Kalinderi Kallirhoe. Preclinical Parkinson’s Disease Models for Non-Motor Symptoms: Research Recommendations from a Systematic Review. Life. 2025.
- Lau Kristina, Outeiro Tiago F, Richter Franziska. Rodent models and accompanying in vitro strategies for studying the etiology and therapy of Parkinson's disease. Journal of Parkinson's Disease. 2026.
- Kin Kyohei, Yasuhara Takao, Kameda Masahiro, Date Isao. Animal Models for Parkinson’s Disease Research: Trends in the 2000s. International Journal of Molecular Sciences. 2019.
- Ugalde Valentina, Elgueta Daniela, Espinoza Sandra, Chovar-Vera Ornella, López Ernesto, Catenaccio Alejandra, Álvarez-Astudillo Francisca, Franz Dafne, Sanchez-Guajardo Vanesa, Becker María Inés, Figueroa Diego, Manjarres Zulmary, Hidalgo Sofía, Lladser Álvaro, Tapia-Rojas Cheril, Loyola Alejandra, Quezada Sergio A., Villagra Roque, Pacheco Rodrigo. Preclinical evaluation of nitrated α-synuclein-specific CAR-Treg therapy in Parkinson’s disease. Cell Reports Medicine. 2026.
- Creed Rose B., Goldberg Matthew S.. New Developments in Genetic Rat Models of Parkinson’s Disease. Movement disorders : official journal of the Movement Disorder Society. 2018.
- García‐Swinburn Roberto, Morón‐Márquez Laura, Conde‐Naranjo Carmen, García‐Roldán Ernesto, Espadas Isabel, Rodríguez‐Gil Alfonso, Ramírez‐Lorca Reposo, Villadiego Javier, Toledo‐Aral Juan José. Neuroinflammatory and Motor Alterations in LRRK2 * G2019S Transgenic Mice Without Enhanced Vulnerability to Aging or Chronic MPTP ‐Induced Nigrostriatal Neurodegeneration. Journal of Neurochemistry. 2026.
- Langston J. William. The MPTP Story. Journal of Parkinson's Disease. 2017.
- Giráldez-Pérez Rosa María, Antolín-Vallespín Mónica, Muñoz María Dolores, Sánchez-Capelo Amelia. Models of α-synuclein aggregation in Parkinson’s disease. Acta Neuropathologica Communications. 2014.
- Peng Jin, Wang Ziyu, Liu Yu, Wang Xiaohui. Striatal temporal interference stimulation alleviates motor deficits and confers neuroprotection in an MPTP-induced mouse model of Parkinson’s disease with associated improvements in mitochondrial homeostasis. Neurotherapeutics. 2026.
- Akanchise Thelma, Luo Fucen, Angelov Borislav, Deng Yuru, Fujino Takehiko, Angelova Angelina. Peptide-targeted cubosome and hexosome nanoassemblies mitigate mitochondrial dysfunction in a MitoPark model. Signal Transduction and Targeted Therapy. 2026.
- Riaz Saima, Ali Shaukat, Summer Muhammad, Iqbal Amina, Ashraf Rimsha, Bibi Ramzana. Chronic Paraquat Neurotoxicity and Dopaminergic Degeneration: A Mechanistic Review. Chemistry & Biodiversity. 2026.
- Chia Shyh Jenn, Tan Eng-King, Chao Yin-Xia. Historical Perspective: Models of Parkinson’s Disease. International Journal of Molecular Sciences. 2020.
- Peshattiwar Vaibhavi, Swain Caroline, Pokharel Dipesh, Le Khoi, Kennedy Isabel, Venkiteswaran Kala, Subramanian Thyagarajan. A novel rat model of body first subtype of Parkinson’s disease. bioRxiv. 2026.
- Mao Mingyu, Wang Yan, Deng Qing, Xiang Jun, Li Wentao. Striatal small RNA remodeling in MPTP-induced Parkinson’s disease highlights coordinated downregulation of mitochondrial tsRNAs. Frontiers in Aging Neuroscience. 2026.
- Chen Chuyu, He Qianzi, Tombesi Giulia, Napier Eve, Jaconelli Matthew, Moreno-Ramos Oscar Andrés, Serio Hannah, Naaldijk Yahaira, Promes Vanessa, Schneeweis Amanda, Quinn Kaitlyn, Nasios Christopher, Greggio Elisa, Kozorovitskiy Yevgenia, Arango Daniel, Khan Amir R., Alessi Dario R., Dombeck Daniel A., Hilfiker Sabine, Awatramani Rajeshwar, Parisiadou Loukia. Leucine-rich repeat kinase 2 impairs the release sites of Parkinson’s disease vulnerable dopamine axons. Nature Communications. 2026.
- Apetz Nadine, Kordys Elena, Simon Mascha, Mang Britta, Aswendt Markus, Wiedermann Dirk, Neumaier Bernd, Drzezga Alexander, Timmermann Lars, Endepols Heike. Effects of subthalamic deep brain stimulation on striatal metabolic connectivity in a rat hemiparkinsonian model. Disease Models & Mechanisms. 2019.
- Kim Jeongah, Choe Mijeong, Jang Sangwon, Park Inah, Oh Sungjoon, Kim Eun-Kyoung, Choe Youngshik, Sun Woong, Kim Kyungjin. Pharmacological inhibition of REV-ERBα ameliorates motor deficits in the 6-OHDA-lesioned mouse model of Parkinson’s disease. Animal Cells and Systems. 2026.
- Shu Zhan, Lam Hoa A., Videlock Elizabeth J., Lindberg Iris, Maidment Nigel T.. ProSAAS overexpression arrests progression of motor deficits in a rat alpha-synuclein model of Parkinson’s disease. Translational Neurodegeneration. 2026.
- Araújo-Monteiro Luan, Soares-Silva Beatriz, Carvalhinho-Lopes Patrícia Santos, Moreira Valéria Cunha, de Campos Cruz Binatto Barbara Vitória, Pereira Ellen Games Jacob, de Lima Ana Paula Nascimento, Quintans-Junior Lucindo José, dos Santos José Ronaldo, Ribeiro Alessandra Mussi. β-Cyclodextrin-Complexed 1,8-Cineole Attenuates Motor Deficits and Preserves Tyrosine Hydroxylase Immunoreactivity in a Reserpine-Induced Mouse Model of Parkinsonism. Molecular Neurobiology. 2026.
Applicable models
Models come from published, verified disease–model relations only.
C57BL/6 MPTP 黑质纹状体变性参考模型(文献参考)
MPTP 诱导黑质纹状体多巴胺能变性研究的文献参考模型;适用性限于化学诱导范式下的神经退行性表型与近交品系间反应比较
Verified applicability
Full model record6-OHDA 损伤帕金森样模型(大鼠,文献参考)
6-OHDA 损伤范式下多巴胺能进行性退变研究的文献参考模型;适用性限于该损伤模型范围
Verified applicability
Full model recordA53T 人α-突触核蛋白转基因研究模型(文献参考)
A53T 人α-突触核蛋白转基因研究的文献参考模型;适用性限于突触核蛋白病相关研究范围,不等同于完整帕金森病
Verified applicability
Full model recordMitoPark mouse
MitoPark 小鼠用于研究线粒体 DNA 维持、年龄依赖性黑质纹状体退变、运动与情感表型及线粒体靶向干预。
Verified applicability
Full model recordParkin knockout mouse
Parkin 敲除小鼠用于研究 Parkin 在丝裂自噬和 dopamine 神经元维持中的作用;基线神经退变较轻,适用于机制与应激易感性研究。
Verified applicability
Full model recordDJ-1 knockout mouse
DJ-1 敲除小鼠用于研究 DJ-1 抗氧化功能及对 MPTP/氧化应激的易感性;基线表型较轻。
Verified applicability
Full model recordRotenone-treated mouse
鱼藤酮暴露小鼠用于研究线粒体复合体 I 抑制、α-突触核蛋白蓄积及黑质纹状体多巴胺能变性。
Verified applicability
Full model recordA30P alpha-synuclein transgenic mouse (Thy1 promoter)
Thy1-A30P α-突触核蛋白转基因小鼠用于研究年龄依赖性精细运动障碍、α-突触核蛋白聚集和突触功能异常。
Verified applicability
Full model recordMPTP-lesioned non-human primate
MPTP 损伤非人灵长类用于研究帕金森样运动障碍、左旋多巴诱导的运动障碍及多巴胺替代治疗。
Verified applicability
Full model recordalpha-synuclein PFF-injected C57BL/6J mouse
纹状体注射 α-突触核蛋白预制纤维用于研究模板化聚集、病理传播、免疫清除及多巴胺能易感性。
Verified applicability
Full model recordMPTP-treated Swiss mouse
MPTP 处理 Swiss 小鼠用于研究品系依赖的黑质生化和结构改变;其多巴胺能神经元丢失通常弱于 C57BL/6。
Verified applicability
Full model record6-OHDA-lesioned C57BL/6 mouse
单侧纹状体 6-OHDA 损伤 C57BL/6 小鼠用于研究遗传修饰、神经炎症和运动不对称。
Verified applicability
Full model recordReserpine-treated mouse
利血平处理小鼠用于研究 VMAT2 介导的单胺耗竭、可逆性帕金森样运动障碍和药物反应。
Verified applicability
Full model recordLRRK2 G2019S knock-in mouse
LRRK2 G2019S 敲入小鼠用于研究内源表达水平下 LRRK2 对多巴胺轴突释放和突触功能的调节。
Verified applicability
Full model record6-OHDA-lesioned Sprague-Dawley rat
6-OHDA 损伤 Sprague-Dawley 大鼠用于研究黑质纹状体变性机制、神经保护、DBS 和运动/非运动表型。
Verified applicability
Full model recordRotenone-treated Wistar rat
鱼藤酮处理 Wistar 大鼠用于研究线粒体复合体 I 功能障碍、α-突触核蛋白病理和神经保护。
Verified applicability
Full model recordPINK1 knockout mouse
PINK1 敲除小鼠用于研究线粒体质量控制与遗传性帕金森病机制;多数品系基线无明显黑质纹状体退变。
Verified applicability
Full model recordParaquat plus maneb-treated mouse
百草枯联合代森锰暴露小鼠用于研究环境农药相关的多巴胺能易感性和基因—环境交互。
Verified applicability
Full model recordLPS-induced hemiparkinsonian rat
单侧纹状体 LPS 注射大鼠用于研究微胶质激活、神经炎症驱动的多巴胺能神经元变性和抗炎保护。
Verified applicability
Full model record6-OHDA-lesioned Wistar rat
双侧 6-OHDA 损伤 Wistar 大鼠用于研究非运动症状、疼痛、情感障碍及 DBS/神经保护。
Verified applicability
Full model recordLRRK2 G2019S transgenic mouse
LRRK2 G2019S 转基因小鼠用于研究 LRRK2 过表达驱动的神经炎症、运动与情感表型及环境毒素交互。
Verified applicability
Full model recordMPTP-treated mouse (strain not specified)
MPTP诱导小鼠用于帕金森病相关运动功能和黑质纹状体损伤研究;本记录不指定原文未报告的品系。
Verified applicability
Full model recordA53T alpha-synuclein transgenic mouse
A53T α-突触核蛋白表达(转基因或 AAV 递送)用于研究聚集、传播、突触功能障碍和运动表型;不同启动子/载体分别解释,M83 另列。
Verified applicability
Full model record6-OHDA-lesioned mouse
6-OHDA损伤小鼠用于研究黑质纹状体损伤及神经保护;本条来源未限定品系,不代表某一特定近交系。
Verified applicability
Full model recordAAV-human alpha-synuclein overexpression mouse
AAV 介导的人 α-突触核蛋白过表达用于研究黑质多巴胺能病理、传播和神经保护。
Verified applicability
Full model recordBAC human SNCA transgenic rat
BAC 人 SNCA 转基因大鼠用于研究人 α-突触核蛋白表达及年龄依赖性病理。
Verified applicability
Full model recordLRRK2 R1441G BAC transgenic mouse
LRRK2 R1441G BAC 转基因小鼠用于研究 LRRK2 过表达对多巴胺传递和运动表型的影响。
Verified applicability
Full model recordSnca G51D knock-in mouse
Snca G51D 敲入小鼠用于研究 G51D α-突触核蛋白病理、纤毛和突触改变。
Verified applicability
Full model recordTCE-treated Lewis rat
三氯乙烯暴露 Lewis 大鼠用于研究环境毒素相关的多巴胺能毒性。
Verified applicability
Full model recordRotenone-treated rat
鱼藤酮暴露大鼠用于研究帕金森病相关线粒体功能障碍及多巴胺能损伤;全身毒性、死亡率及表型变异限制其适用性。
Verified applicability
Full model recordParaquat-treated mouse
百草枯暴露小鼠用于研究帕金森病相关氧化应激和多巴胺能毒性;不能等同于完整复现人类疾病。
Verified applicability
Full model recordParaquat-treated rat
百草枯暴露Sprague-Dawley大鼠用于研究帕金森病相关抗氧化防御受损及中脑GPx变化;该依据不证明完整运动表型或稳定黑质退变。
Verified applicability
Full model recordAAV-human alpha-synuclein overexpression rat
人α-突触核蛋白过表达大鼠用于研究运动不对称及TH阳性神经元损伤。
Verified applicability
Full model recordE46K alpha-synuclein BAC transgenic rat
E46K BAC转基因大鼠用于研究α-突触核蛋白聚集及毒素易感性;文献未见12月龄明确多巴胺能神经元丢失或明显运动缺陷。
Verified applicability
Full model recordLRRK2 R1441C knock-in mouse
LRRK2 R1441C敲入小鼠用于研究多巴胺传递和D2受体功能;不代表已出现自发多巴胺能退变或α-突触核蛋白积累。
Verified applicability
Full model recordPINK1 knockout rat
PINK1敲除大鼠用于研究年龄相关多巴胺能损伤、运动功能及α-突触核蛋白病理,表型具有研究条件依赖性。
Verified applicability
Full model recordParkin knockout rat
Parkin敲除大鼠用于研究帕金森病相关蛋白稳态及蛋白组机制;文献未显示明确行为缺陷或多巴胺能神经元丢失。
Verified applicability
Full model recordDJ-1 knockout rat
DJ-1敲除大鼠用于研究帕金森病相关多巴胺能退变和运动功能,表型随年龄及研究条件变化。
Verified applicability
Full model recordalpha-synuclein PFF-injected rat
α-突触核蛋白PFF大鼠用于研究病理传播和黑质多巴胺能损伤;所引研究未见明显运动缺陷。
Verified applicability
Full model record