Intracellular delivery of Parkin rescues neurons from accumulation of damaged mitochondria and pathological α-synuclein

You and your doctor should be following this research very closely because of your chance of getting Parkinsons. Does your doctor even know about that probability? It is only three years old.

Parkinson’s Disease May Have Link to Stroke March 2017 

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Intracellular delivery of Parkin rescues neurons from accumulation of damaged mitochondria and pathological α-synuclein

1. Eunna Chung¹,*,
2. Youngsil Choi¹,*,
3. Jiae Park¹,
4. Wonheum Nah¹,
5. Jaehyung Park¹,
6. Yukdong Jung¹,
7. Joonno Lee¹,
8. Hyunji Lee¹,
9. Soyoung Park¹,
10. Sunyoung Hwang¹,
11. Seongcheol Kim¹,
12. Jongseok Lee¹,
13. Dongjae Min¹,
14. Junghwan Jo¹,
15. Shinyoung Kang¹,
16. Minyong Jung¹,
17. Phil Hyu Lee²,
18. H. Earl Ruley³ and
19. Daewoong Jo¹,†

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Science Advances  29 Apr 2020:
Vol. 6, no. 18, eaba1193
DOI: 10.1126/sciadv.aba1193

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Abstract

Parkinson’s disease (PD) is a progressive neurodegenerative disorder characterized by mitochondrial dysfunction, Lewy body formation, and loss of dopaminergic neurons. Parkin, an E3 ubiquitin ligase, is thought to inhibit PD progression by removing damaged mitochondria and suppressing the accumulation of α-synuclein and other protein aggregates. The present study describes a protein-based therapy for PD enabled by the development of a cell-permeable Parkin protein (iCP-Parkin) with enhanced solubility and optimized intracellular delivery. iCP-Parkin recovered damaged mitochondria by promoting mitophagy and mitochondrial biogenesis and suppressed toxic accumulations of α-synuclein in cells and animals. Last, iCP-Parkin prevented and reversed declines in tyrosine hydroxylase and dopamine expression concomitant with improved motor function induced by mitochondrial poisons or enforced α-synuclein expression. These results point to common, therapeutically tractable features in PD pathophysiology, and suggest that motor deficits in PD may be reversed, thus providing opportunities for therapeutic intervention after the onset of motor symptoms.