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.

Saturday, April 17, 2021

Nitric oxide and dopamine metabolism converge via mitochondrial dysfunction in the mechanisms of neurodegeneration in Parkinson's disease

 

         

Because of the usefulness of nitric oxide in your recovery, your doctor is responsible for adjusting your nitric oxide protocol with this in mind.  Or does your doctor incompetently not even have a nitric oxide protocol?

 

Your risk of Parkinsons here:

Parkinson’s Disease May Have Link to Stroke March 2017

The latest here:

Nitric oxide and dopamine metabolism converge via mitochondrial dysfunction in the mechanisms of neurodegeneration in Parkinson's disease

 

Abstract

The molecular mechanisms underlying the degeneration and neuronal death associated with Parkinson's disease (PD) are not clearly understood. Several pathways and models have been explored in an overwhelming number of studies. Overall, from these studies, mitochondrial dysfunction and nitroxidative stress have emerged as major contributors to degeneration of dopaminergic neurons in PD. In addition, an excessive or inappropriate production of nitric oxide (NO) and an abnormal metabolism of dopamine have been independently implicated in both processes. However, the participation of NO in reactions with dopamine relevant to neurotoxicity strongly suggests that dopamine or its metabolites may be potential targets for NO, affecting the physiological chemistry of both, NO and dopamine. In this short review, we provide a critical and integrative appraisal of the nitric oxide-dopamine pathway we have previously suggested and that might be operative in PD. This pathway emphasizes a connection between abnormal dopamine and NO metabolism, which may potentially converge in an integrated mechanism with toxic cellular outcomes. In particular, it encompasses the synergistic interaction of NO with 3,4-dihydroxyphenylacetic acid (DOPAC), a major dopamine metabolite, leading to dopaminergic cell death via mechanisms that involve mitochondrial dysfunction, gluthathione depletion and nitroxidative stress.

Keywords

Parkinson's disease
Nitric oxide
DOPAC
Mitochondrial dysfunction
Nitroxidative stress
Glutathione
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