Vitamin K2 Is A Mitochondrial Electron Carrier That Rescues Pink1 Deficiency

paymanz

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http://www.ncbi.nlm.nih.gov/pubmed/22582012


Human UBIAD1 localizes to mitochondria and converts vitamin K(1) to vitamin K(2). Vitamin K(2) is best known as a cofactor in blood coagulation, but in bacteria it is a membrane-bound electron carrier. Whether vitamin K(2) exerts a similar carrier function in eukaryotic cells is unknown. We identified Drosophila UBIAD1/Heix as a modifier of pink1, a gene mutated in Parkinson's disease that affects mitochondrial function. We found that vitamin K(2) was necessary and sufficient to transfer electrons in Drosophila mitochondria. Heix mutants showed severe mitochondrial defects that were rescued by vitamin K(2), and, similar to ubiquinone, vitamin K(2) transferred electrons in Drosophila mitochondria, resulting in more efficient adenosine triphosphate (ATP) production. Thus, mitochondrial dysfunction was rescued by vitamin K(2) that serves as a mitochondrial electron carrier, helping to maintain normal ATP production.
 
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Parkinson's disease is essentially a metabolic disease of energy production
[http://www.vib.be/en/news/Pages/New-discoveries-place-lack-of-energy-at-the-basis-of-Parkinson%E2%80%99s-Disease.aspx]. Respiration-boosting near infrared light [http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0078562] as well as a mitochondrial electron carrier, vitamin K2,
[http://www.ncbi.nlm.nih.gov/pubmed/22582012] both rescue Parkinson's disease models based on this theory.

Both infrared light and vitamin K2 rescue or work around pink1 models.
<<This study also found that mutant LRRK2 causes mitochondrial degradation by autophagy in the dendrites of neurons, which led to shortening of the dendrites. PINK1 suppressed the autophagy induction elicited by mutant LRRK2 and prevented the mitochondrial degradation and neurite shortening. Furthermore, mutant LRRK2 caused a delay in calcium clearance after neuronal iv depolarization. This prolonged elevation in intracellular calcium caused mitochondrial depolarization followed by degradation.>> [http://d-scholarship.pitt.edu/10539/]

Glutamate-induced neuron death requires mitochondrial calcium uptake.
[http://www.ncbi.nlm.nih.gov/pubmed/10196525]

Dopamine protects neurons against glutamate-induced excitotoxicity
[http://www.nature.com/cddis/journal/v4/n1/full/cddis2012194a.html]

Mutant LRRK2 enhances glutamatergic synapse activity and evokes excitotoxic dendrite degeneration. [http://www.ncbi.nlm.nih.gov/pubmed/24874075]

<<Pregnenolone and progesterone protect against nerve damage (5) by the excitotoxic amino acids (glutamic acid, aspartic acid, monosodium glutamate, aspartame, etc.), while estrogen (6) and cortisol (7) are nerve-destroying, acting through the excitotoxic amino acids. Excitotoxins destroy certain types of nerve, especially the dopaminergic and cholinergic types, leaving the noradrenergic types (8), paralleling the changes that occur in aging. The clustering of oligodendrocytes around deteriorating nerve cells could represent an adaptive attempt to provide pregnenolone to injured nerve cells.>> [http://raypeat.com/articles/articles/multiple-sclerosis.shtml]

<<In Parkinson’s disease, the benefits seen from increasing the concentration of dopamine could result from dopamine’s antagonism to serotonin; anti-serotonin drugs can alleviate the symptoms, and 5-hydroxytryptophan can worsen the symptoms (Chase, et al., 1976). Other movement disorders, including akathisia and chorea, can be produced by serotonin. In autism, repetitive motions are a common symptom, and serotonin is high in the blood serum and platelets of autistic children and their relatives. Irritable bowel syndrome, another kind of “movement disorder,” can be treated effectively with anti-serotonin agents. This syndrome is very common in women, with premenstrual exacerbations, when estrogen is highest. One of the side effects of oral contraceptives is chorea, uncontrollable dancing movements. Some research has found increased serotonin in people with Huntington’s chorea (Kish, et al., 1987), and positive results with bromocriptine have been reported (Agnoli, et al., 1977).The neurosteroid, allopregnanolone, for which progesterone is the precursor, facilitates the inhibitory action of GABA, which is known to be deficient in some disorders of mood and movement. This suggests that progesterone will be therapeutic in the movement disorders, as it is in various mood problems. Progesterone has some specific antiserotonin actions (e.g., Wu, et al., 2000).>> [http://raypeat.com/articles/articles/serotonin-depression-aggression.shtml]

<<genomewide association studies have found an association between LRRK2 and Crohn's disease as well as with Parkinson's disease, suggesting that the two diseases share common pathways.>> [http://en.wikipedia.org/wiki/LRRK2]

<<Recently we have delineated that oral feeding of cinnamon (Cinnamonum verum) powder produces sodium benzoate (NaB) in blood and brain of mice.>> [http://www.ncbi.nlm.nih.gov/pubmed/24946862]

<<Sodium benzoate reduces ammonia content in the blood by conjugating with glycine to form hippuric acid, which is rapidly excreted by the kidneys.>> [http://www.rxlist.com/ammonul-drug/clinical-pharmacology.htm]

<<Ammonia is produced by stimulated nerves, and normally its elimination helps to eliminate and control the excitotoxic amino acids, glutamate and aspartate. The production of urea consumes aspartic acid, converting it to fumaric acid, but this requires carbon dioxide, produced by normal mitochondrial function. A deficiency of carbon dioxide would reduce the delivery of oxygen to the brain by constricting blood vessels and changing hemoglobin's affinity for oxygen (limiting carbon dioxide production), and the failure to consume aspartate (in urea synthesis) and glutamate (as alpha-ketoglutarate) and aspartate (as oxaloacetate) in the Krebs cycle, means that as energy becomes deficient, excitation tends to be promoted.>> [http://raypeat.com/articles/articles/epilepsy-progesterone.shtml]

<<Increased intracellular calcium, in association with excess nitric oxide and excitatory amino acids, is involved in several neurodegenerative diseases, including ALS, Alzheimers disease, Parkinsons disease, Huntingtons chorea, and epilepsy. Magnesium, nicotine, progesterone, and many other substances are known to protect against excitotoxic calcium overload, but there is no coherent effort in the health professions to make rational use of the available knowledge.>> [http://raypeat.com/articles/articles/calcium.shtml]
 

haidut

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Such_Saturation said:
Parkinson's disease is essentially a metabolic disease of energy production
[http://www.vib.be/en/news/Pages/New-discoveries-place-lack-of-energy-at-the-basis-of-Parkinson%E2%80%99s-Disease.aspx]. Respiration-boosting near infrared light [http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0078562] as well as a mitochondrial electron carrier, vitamin K2,
[http://www.ncbi.nlm.nih.gov/pubmed/22582012] both rescue Parkinson's disease models based on this theory.

Both infrared light and vitamin K2 rescue or work around pink1 models.
<<This study also found that mutant LRRK2 causes mitochondrial degradation by autophagy in the dendrites of neurons, which led to shortening of the dendrites. PINK1 suppressed the autophagy induction elicited by mutant LRRK2 and prevented the mitochondrial degradation and neurite shortening. Furthermore, mutant LRRK2 caused a delay in calcium clearance after neuronal iv depolarization. This prolonged elevation in intracellular calcium caused mitochondrial depolarization followed by degradation.>> [http://d-scholarship.pitt.edu/10539/]

Glutamate-induced neuron death requires mitochondrial calcium uptake.
[http://www.ncbi.nlm.nih.gov/pubmed/10196525]

Dopamine protects neurons against glutamate-induced excitotoxicity
[http://www.nature.com/cddis/journal/v4/n1/full/cddis2012194a.html]

Mutant LRRK2 enhances glutamatergic synapse activity and evokes excitotoxic dendrite degeneration. [http://www.ncbi.nlm.nih.gov/pubmed/24874075]

<<Pregnenolone and progesterone protect against nerve damage (5) by the excitotoxic amino acids (glutamic acid, aspartic acid, monosodium glutamate, aspartame, etc.), while estrogen (6) and cortisol (7) are nerve-destroying, acting through the excitotoxic amino acids. Excitotoxins destroy certain types of nerve, especially the dopaminergic and cholinergic types, leaving the noradrenergic types (8), paralleling the changes that occur in aging. The clustering of oligodendrocytes around deteriorating nerve cells could represent an adaptive attempt to provide pregnenolone to injured nerve cells.>> [http://raypeat.com/articles/articles/multiple-sclerosis.shtml]

<<In Parkinson’s disease, the benefits seen from increasing the concentration of dopamine could result from dopamine’s antagonism to serotonin; anti-serotonin drugs can alleviate the symptoms, and 5-hydroxytryptophan can worsen the symptoms (Chase, et al., 1976). Other movement disorders, including akathisia and chorea, can be produced by serotonin. In autism, repetitive motions are a common symptom, and serotonin is high in the blood serum and platelets of autistic children and their relatives. Irritable bowel syndrome, another kind of “movement disorder,” can be treated effectively with anti-serotonin agents. This syndrome is very common in women, with premenstrual exacerbations, when estrogen is highest. One of the side effects of oral contraceptives is chorea, uncontrollable dancing movements. Some research has found increased serotonin in people with Huntington’s chorea (Kish, et al., 1987), and positive results with bromocriptine have been reported (Agnoli, et al., 1977).The neurosteroid, allopregnanolone, for which progesterone is the precursor, facilitates the inhibitory action of GABA, which is known to be deficient in some disorders of mood and movement. This suggests that progesterone will be therapeutic in the movement disorders, as it is in various mood problems. Progesterone has some specific antiserotonin actions (e.g., Wu, et al., 2000).>> [http://raypeat.com/articles/articles/serotonin-depression-aggression.shtml]

<<genomewide association studies have found an association between LRRK2 and Crohn's disease as well as with Parkinson's disease, suggesting that the two diseases share common pathways.>> [http://en.wikipedia.org/wiki/LRRK2]

<<Recently we have delineated that oral feeding of cinnamon (Cinnamonum verum) powder produces sodium benzoate (NaB) in blood and brain of mice.>> [http://www.ncbi.nlm.nih.gov/pubmed/24946862]

<<Sodium benzoate reduces ammonia content in the blood by conjugating with glycine to form hippuric acid, which is rapidly excreted by the kidneys.>> [http://www.rxlist.com/ammonul-drug/clinical-pharmacology.htm]

<<Ammonia is produced by stimulated nerves, and normally its elimination helps to eliminate and control the excitotoxic amino acids, glutamate and aspartate. The production of urea consumes aspartic acid, converting it to fumaric acid, but this requires carbon dioxide, produced by normal mitochondrial function. A deficiency of carbon dioxide would reduce the delivery of oxygen to the brain by constricting blood vessels and changing hemoglobin's affinity for oxygen (limiting carbon dioxide production), and the failure to consume aspartate (in urea synthesis) and glutamate (as alpha-ketoglutarate) and aspartate (as oxaloacetate) in the Krebs cycle, means that as energy becomes deficient, excitation tends to be promoted.>> [http://raypeat.com/articles/articles/epilepsy-progesterone.shtml]

<<Increased intracellular calcium, in association with excess nitric oxide and excitatory amino acids, is involved in several neurodegenerative diseases, including ALS, Alzheimers disease, Parkinsons disease, Huntingtons chorea, and epilepsy. Magnesium, nicotine, progesterone, and many other substances are known to protect against excitotoxic calcium overload, but there is no coherent effort in the health professions to make rational use of the available knowledge.>> [http://raypeat.com/articles/articles/calcium.shtml]

Speaking of red light and brain function - I get unmatched mental clarity and calm if I take a hefty dose of MB and then sit under red light for a few hours. Neither MB nor red light on their own can give me that effect. I think there are studies on PubMed saying this "photosensitization" exercise may be effective for many conditions. I guess if you can radiate the entire body it should have a systemic pro-metabolic effect.
 
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Sometimes I would take the methylene blue and end up measuring something on the stopwatch exactly the same even three times in a row, to the hundredth of a second.
 
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paymanz

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haidut said:
post 83428 Speaking of red light and brain function - I get unmatched mental clarity and calm if I take a hefty dose of MB and then sit under red light for a few hours. Neither MB nor red light on their own can give me that effect. I think there are studies on PubMed saying this "photosensitization" exercise may be effective for many conditions. I guess if you can radiate the entire body it should have a systemic pro-metabolic effect.
how safe is it to use MB and red light in combination . it seems like there is a risk of DNA damage, at least is higher doses. what dosage you think is safe?

i just saw this one www.ncbi.nlm.nih.gov/pubmed/19218330 , also if MB+light can kill micro organisms then it probably can do same to our cells...
 
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haidut

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paymanz said:
post 106793
haidut said:
post 83428 Speaking of red light and brain function - I get unmatched mental clarity and calm if I take a hefty dose of MB and then sit under red light for a few hours. Neither MB nor red light on their own can give me that effect. I think there are studies on PubMed saying this "photosensitization" exercise may be effective for many conditions. I guess if you can radiate the entire body it should have a systemic pro-metabolic effect.
how safe is it to use MB and red light in combination . it seems like there is a risk of DNA damage, at least is higher doses. what dosage you think is safe?

i just saw this one http://www.ncbi.nlm.nih.gov/pubmed/19218330 , also if MB+light can kill micro organisms then it probably can do same to our cells...

In low doses of about 1mg I think MB does not have cytotoxic effects when combined with red light.
 
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Nighteyes

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Such_Saturation said:
post 83388 One of the side effects of oral contraceptives is chorea, uncontrollable dancing movements

For some reason I had to read this line several times - thinking I had read it wrong :lol:

Certainly not a funny disorder, my brain has just entered friday mode i guess...
 
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