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.

Thursday, April 23, 2020

The pivotal role of Ubiquitin-activating enzyme E1 (UBA1) in neuronal health and neurodegeneration

I couldn't make heads or tails out of this, enzymatic ubiquitylation cascade, so go ask your doctor. Should we initiate or suppress this and how do we do it? 

The pivotal role of Ubiquitin-activating enzyme E1 (UBA1) in neuronal health and neurodegeneration

Justin J.Yerburyab


Highlights

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UBA1 is the ubiquitin activator and as such functions at the apex of the enzymatic ubiquitylation cascade.
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UBA1 activity is vital to many aspects of neural function, including growth and development, neuronal excitability, neurotransmission, and long-term potentiation.
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Alteration of UBA1 level, location or activity is associated with neurological disorders including mutations causing spinal muscular atrophy.
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UBA1 modulation may provide potential therapeutic targets for neurological disorders.

Abstract

Ubiquitin-activating enzyme E1, UBA1, functions at the apex of the enzymatic ubiquitylation cascade, catalysing ubiquitin activation. UBA1 is thus of fundamental importance to the modulation of ubiquitin homeostasis and to all downstream ubiquitylation-dependent cellular processes, including proteolysis through the ubiquitin-proteasome system and selective autophagy. The proteasome-dependent and -independent functions of UBA1 contribute significantly to a range of processes crucial to neuronal health. The significance of UBA1 activity to neuronal health is clear in light of accumulating evidence implicating impaired UBA1 activity in a range of neurodegenerative conditions, including Parkinson’s disease, Alzheimer’s disease, Huntington’s disease and spinal muscular atrophy. Moreover, ubiquitylation-independent functions of UBA1 of importance to neuronal functioning have been proposed. Here, we summarise findings supporting the significant role of UBA1 in regulating neuronal functioning, and discuss the detrimental consequences of UBA1 impairment that contribute to neuronal dysfunction and degeneration.

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