New approaches for Parkinson's treatment? Researchers study metabolic changes

Veet

Well-Known Member
"Without DJ1, neurons cannot absorb enough glutamine and this affects serine production. Both amino acids are important for producing glutathione, which is used to neutralise free radicals," explains Dr. Johannes Meiser, lead author for the study. "In the absence of DJ1, this defence mechanism does not work effectively and oxidative stress occurs. This prematurely ages the cells."

The research team was also able to show that mutations in the DJ1 gene can also negatively affect other cells in the brain. Microglial cells, which are responsible for the immune reaction in the brain, become 'hyperactive' when the DJ1 gene is defective. "Normally, microglial cells are only activated when something in the brain needs to be cleaned up, for instance during inflammation," explains Hiller. "However, if these cells are constantly active, as we discovered happens with the DJ1 defect, this weakens the underlying neurons."
 

Croatoan

Well-Known Member
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3620453/

In both idiopathic and genetic cases of PD, oxidative stress is thought to be the common underlying mechanism that leads to cellular dysfunction and demise.

The metabolism of DA itself contributes to oxidative stress, resulting in modification of intracellular macromolecules whose functions are important for cell survival. Mitochondrial dysfunction and the consequent increase in reactive oxygen species also trigger a sequence of events that leads to cell demise.
 

Cort

Founder of Health Rising and Phoenix Rising
Staff member
https://www.sciencedaily.com/releases/2016/03/160302083559.htm

Researchers are studying the causes of premature aging of neurons in Parkinson’s patients with a defective DJ1 (PARK7) gene. The genetic defect causes changes in the cellular metabolism meaning that neurons are subjected to oxidative stress and an increased immune response in the brain.
That could be big given the basal ganglia problems found in ME/CFS, FM and Parkinson's and the possiible issues with cellular metabolism and oxidative stress found in all three. Nice catch - look forward to reviewing this further.
I expect a study result to come out in the not too distant future suggesting ME/CFS may have more Parkinson's-like components.
 

RuthAnn

Well-Known Member
That could be big given the basal ganglia problems found in ME/CFS, FM and Parkinson's and the possiible issues with cellular metabolism and oxidative stress found in all three. Nice catch - look forward to reviewing this further.
I expect a study result to come out in the not too distant future suggesting ME/CFS may have more Parkinson's-like components.
I didn't know basal ganglia issues are found in ME/CFS!

I didn't see this, you have an article about it.

http://www.cortjohnson.org/blog/2014/09/15/unrewarding-reward-basal-ganglia-inflammation-fatigue-chronic-fatigue-syndrome/

I was just reading about basal ganglia issues at Linus Pauling institute while reading about biotin.
http://lpi.oregonstate.edu/mic/vitamins/biotin

This is what it says about basal ganglia disease, and while we may not have the inherited disease, it is currently being tested for use with MS, which we may not have, either. But usually it seems that in order to find information something you have to look at studies for extreme conditions.

"Biotin is used in the treatment of an inherited disorder of thiamin transport, called biotin-responsive basal ganglia disease, and is currently being tested in trials to limit or reverse functional disabilities in individuals with multiple sclerosis. (More information)"
 

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