Welcome to Francis Academic Press

Academic Journal of Medicine & Health Sciences, 2023, 4(10); doi: 10.25236/AJMHS.2023.041005.

The Transmission of Pathological α-Synuclein


Funing Zhang1, Yi Liu2

Corresponding Author:
Funing Zhang

1Ipswich School, United Kingdom

2Beijing National Day School, Beijing, China


Parkinson's disease (PD) is a chronic neurodegenerative disorder. The main pathogenesis is the degeneration and death of dopamine neurons in the substantia nigra caused by a large accumulation of α-synuclein (Syn) and incorrect protein folding. Parkinson’s disease is characterized by abundant α-synuclein neuronal inclusions, while the stereotypical progression of α-synuclein pathology through the brain over time suggests that there may be a physical transmission of pathological α-synuclein from one area of the brain to another. In thisstudy, our goal is to prove the transmission of pathological α-synuclein by comparing brain slices of mice in different stages. Genetic type #24 KI-SNCA-tdT (+/-) mice were used as the model, freezing mouse brain sections (CPu+SNc brain region), immunohistochemical staining of mouse brain sections, laser copolymerization microscopy and other experimental techniques were used. We focus on phosphorylated alpha-synuclein and abnormal aggregation of fibrous alpha-synuclein lewy bodies. Finally, we concluded that phosphorylated alpha-synuclein (pSyn) could be transmitted from the Dorsal striatum to the SNc brain region via a neural circuit consisting of dopamine neurons. This leads to the formation of Lewy bodies in dopamine neurons in the SNc brain region, causing neuropathy that leads to Parkinson's disease.


Parkinson’s disease, α-synuclein, Lewy Body

Cite This Paper

Funing Zhang, Yi Liu. The Transmission of Pathological α-Synuclein. Academic Journal of Medicine & Health Sciences (2023) Vol. 4, Issue 10: 38-41. https://doi.org/10.25236/AJMHS.2023.041005.


[1] Goedert M, Jakes R, Spillantini M G. The synucleinopathies: twenty years on [J]. Journal of Parkinson's disease, 2017, 7(s1): S51-S69.

[2] Tian J, Hou Z D, Ren X P. Behavioral phenotype and pathological characteristics of α-synucleofibrillar induced mouse model of Parkinson's disease [J]. Journal of Wenzhou Medical University, 2019, 49(03):157-161.

[3] Braak H, Del Tredici K, Rüb U, et al. Staging of brain pathology related to sporadic Parkinson’s disease [J]. Neurobiology of aging, 2003, 24(2): 197-211. 

[4] Jankovic J. Parkinson’s disease: clinical features and diagnosis [J]. Journal of neurology, neurosurgery & psychiatry, 2008, 79(4): 368-376. 

[5] Magrinelli F, Picelli A, Tocco P, et al. Pathophysiology of motor dysfunction in Parkinson’s disease as the rationale for drug treatment and rehabilitation[J]. Parkinson’s disease, 2016. 

[6] Samii A, Nutt J G, Ransom B R. Parkinson's disease [J]. The Lancet, 2004, 363(9423): 1783-1793. 

[7] Henderson M X, Trojanowski J Q, Lee V M Y. α-Synuclein pathology in Parkinson’s disease and related α-synucleinopathies[J]. Neuroscience letters, 2019, 709: 134316.

[8] Luk K C, Kehm V, Carroll J, et al. Pathological α-synuclein transmission initiates Parkinson-like neurodegeneration in nontransgenic mice[J]. Science, 2012, 338(6109): 949-953. 

[9] Tu L, Zhang N, Conde K M, et al. Free-floating immunostaining of mouse brains [J]. JoVE (Journal of Visualized Experiments), 2021 (176): e62876.

[10] Evilsizor M N, Ray-Jones H F, Lifshitz J, et al. Primer for immunohistochemistry on cryosectioned rat brain tissue: example staining for microglia and neurons [J]. JoVE (Journal of Visualized Experiments), 2015 (99): e52293.