Deans' stroke musings: Intracellular delivery of Parkin rescues neurons from accumulation of damaged mitochondria and pathological α-synuclein

Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Wednesday, May 6, 2020

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

The latest here:

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

Eunna Chung¹,*,
Youngsil Choi¹,*,
Jiae Park¹,
Wonheum Nah¹,
Jaehyung Park¹,
Yukdong Jung¹,
Joonno Lee¹,
Hyunji Lee¹,
Soyoung Park¹,
Sunyoung Hwang¹,
Seongcheol Kim¹,
Jongseok Lee¹,
Dongjae Min¹,
Junghwan Jo¹,
Shinyoung Kang¹,
Minyong Jung¹,
Phil Hyu Lee²,
H. Earl Ruley³ and
Daewoong Jo¹,†

See all authors and affiliations

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

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.