Parkinson's Tied to Mitochondrial Burnout (In Same Area of Brain as ME/CFS)

Cort

Founder of Health Rising and Phoenix Rising
Staff member
The really interesting thing about Parkinson's is that it effects the substantia nigra and basal ganglia in the brain - which Miller has associated with ME/CFS. It appears to effect a different part of the basal ganglia - the part that governs movement. Dopamine is a key factor in Parkinson's and it could play a role in ME/CFS.
The brain cells in Parkinson's essentially burn themselves out - an intriguing finding given the evidence of immune cell burnout in ME/CFS and the many examples of systems staying "on" too long. When the cells in Parkinson's patients die they effect movement.

"Like a motor constantly running at high speed, these neurons need to produce an incredible amount of energy to function. They appear to exhaust themselves and die prematurely. As the disease progresses, the amount of dopamine produced in the brain decreases and the symptoms - which include tremor, slowness, stiffness and impaired balance - gradually worsen, making it increasingly difficult to walk, talk, look after oneself and have a normal life.
I do wonder if there are going to be overlaps over time....
 

RuthAnn

Well-Known Member

Cort

Founder of Health Rising and Phoenix Rising
Staff member
To add to the thoughts about Parkinson's and mitochondria, here is a study showing that oxidative stress is tied to it.
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4135313/

The Role of Oxidative Stress in Parkinson’s Disease

Vera Dias, Eunsung Junn, and M. Maral Mouradian*

Along with that, and tied to that, there is iron deposition.
http://www.sciencedirect.com/science/article/pii/S0925443911001426
Neurodegeneration with brain iron accumulation — Clinical syndromes and neuroimaging
Interesting - Shungu's studies certainly indicate a high likelihood of oxidative stress in ME/CFS patients brains

Oxidative stress plays an important role in the degeneration of dopaminergic neurons in Parkinson’s disease (PD). Disruptions in the physiologic maintenance of the redox potential in neurons interfere with several biological processes, ultimately leading to cell death. Evidence has been developed for oxidative and nitrative damage to key cellular components in the PD substantia nigra. A number of sources and mechanisms for the generation of reactive oxygen species (ROS) are recognized including the metabolism of dopamine itself, mitochondrial dysfunction, iron, neuroinflammatory cells......

The brain consumes about 20% of the oxygen supply of the body, and a significant portion of that oxygen is converted to ROS [43]. ROS can be generated in the brain from several sources, both in neurons and glia, with the electron transport chain being the major contributor at the mitochondrial level [44, 45].....

Dopamine agonists have been suggested to have neuroprotective and antioxidant effects [406]. For example, pramipexole protects MES 23.5 cells against hydrogen peroxide, dopamine and L-dopa induced toxicity [407]. It also reduces lipid peroxidation and minimizes injury to the SN of MPTP lesioned mice [408]. The antioxidant effect of pramipexole independent of its dopamine receptor agonist property can be responsible for its neuroprotective action [409]. It can reduce the levels of oxygen radicals produced by MPP+ both when incubated with SH-SY5Y cells and when perfused into the rat striatum [410]. Similarly, ropinirole protects mice against 6-OHDA by increasing glutathione levels [411, 412]........

Among agents that might alleviate oxidative stress, creatine is an antioxidant involved in the inhibition of the opening of the mitochondrial permeability pore and affects mitochondrial energy production [437439]. In mice, creatine has been shown to protect against MPTP-induced dopaminergic depletion in the SN [440]. Two phase II studies of creatine in PD patients have yielded contradictory results, one failing to show efficacy [441] while the other reporting about 40% less worsening of motor Unified PD Rating Scale scores at one year [442]. In a follow up phase II NET-PD futility study, creatine use at 18 months did not show safety concerns, but the phase III trial was recently terminated due to lack of statistically significant difference from placebo [443, 444].

Other attempts to use compounds with antioxidant properties in PD have included tocopherol (vitamin E), vitamin C, Coenzyme Q10, docosahexaenoic acid (DHA), Ginkgo biloba, or polyphenols found in green tea [431, 445451]. None of these have yielded convincing evidence for neuroprotective efficacy....

Recently, ketogenic diet has been suggested as a potential therapy in neurological diseases, since the mitochondrial Complex II activator D-beta-hydroxybutyrate, a ketone body, has been shown to increase cellular GSH content, decrease intracellular ROS production induced by H2O2, inhibit apoptosis and enhance cell viability [452]. Although this diet has not been studied in animal models of PD yet, a caloric restriction diet conferred resistance to MPTP in mice, rats and rhesus monkeys [453455]. Interestingly, an uncontrolled study of five patients with PD placed on a ketogenic diet for 28 days reported a 43% improvement in their Unified PD Rating Scale scores [456].
 

RuthAnn

Well-Known Member
If one wanted a quick fix, riboflavin would be a good choice.
There are too many good links about the connection of riboflavin to Parkinson's, I couldn't decide which one to post.
Also, B2>>>thioredoxin is a good place to look.
 

RuthAnn

Well-Known Member
This is interesting:

"NO inhibits several enzymes including complexes I and IV of the mitochondrial electron transport chain, leading to ROS generation."
 

Cort

Founder of Health Rising and Phoenix Rising
Staff member
This is interesting:

"NO inhibits several enzymes including complexes I and IV of the mitochondrial electron transport chain, leading to ROS generation."
NO could be a key player in the blood vessels...I think some groups are looking at that
 

RuthAnn

Well-Known Member

Merida

Well-Known Member
@Cort
But also it is known ( have the research paper somewhere) that certain people lack enzymes involved in transporting glucose across the blood brain barrier. Ketones can cross the barrier without thus special transport, and can then be used (metabolically) for energy.

Also, there is new work being done treating Parkinson's with oral appliances that reposition the jaw back to a more normal position. Why? The jaw is a critical part of cranial function. Look on You Tube at the videos for Brendan Stack, DDS - a university trained dentist, researcher. ( I can not seem to post links from my iPad. Probably because I don't know how!!)
 

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