wooow! thank you!

Contributed by Jeff T Bowles

also elevated MAO-B seems to cause parkionsons..

whenthey knocked out the MAO B gene in rodents  nothing muhc happened and they never got PArkinson's as a benefit..

what inhibts  MAO-B

a lot of supplements  especailly pterostilbene  butthe best of all is deprenyl a drug but you can get it from overses with no scrip

its what tey give to paD patients...but it quits working after awhile

but if someone took deprenyl 5 mg  a day most of their lives likely to never get parkinsons..

from perplexity 

Answer

Progesterone does not directly inhibit monoamine oxidase (MAO) enzymes, but it can indirectly modulate their activity and expression levels through its interactions with other hormones and neurotransmitter systems.Several studies have shown that estrogen, another female sex hormone, can inhibit MAO-A and MAO-B activity in various brain regions. This inhibition is thought to contribute to the neuroprotective effects of estrogen and its role in regulating mood and cognitive function.As for progesterone, its effects on MAO enzymes are more complex and depend on the presence of other hormones, particularly estrogen. Some key points:

1. Progesterone alone does not appear to significantly affect MAO-A or MAO-B activity.
2. However, when combined with estrogen, progesterone can enhance the inhibitory effects of estrogen on MAO enzymes, particularly in the hypothalamus and other brain regions involved in reproductive behavior and neuroendocrine function.
3. The fluctuations in progesterone and estrogen levels during the menstrual cycle and pregnancy can influence MAO activity, with higher progesterone levels during the luteal phase and pregnancy potentially contributing to lower MAO activity.
4. Progesterone may also modulate the expression of MAO genes, but the effects seem to be region-specific and dependent on the hormonal milieu.

In summary, while progesterone does not directly inhibit MAO enzymes, it can indirectly modulate their activity and expression levels through its interactions with estrogen and other hormonal systems, particularly in brain regions involved in reproductive function and behavior.

Based on the search results provided, several natural substances and plant-derived compounds have been found to inhibit monoamine oxidase (MAO) enzymes, particularly MAO-A and MAO-B. Here are some notable examples:

1. Alkaloids:

• Harmala alkaloids like harmine and harmaline from Peganum harmala strongly inhibit MAO-A.
• Isoquinoline alkaloids like berberine and palmatine from plants like Coptis chinensis inhibit MAO-A and MAO-B.

1. Flavonoids:

• Quercetin and its glycosides like rutin from plants like Melastoma candidum are potent MAO-A inhibitors.
• Kaempferol from Morinda citrifolia inhibits both MAO-A and MAO-B, with higher selectivity for MAO-A.
• Genistein from Glycine max selectively inhibits MAO-A.

1. Phenols and polyphenols:

• Curcumin from Curcuma longa inhibits both MAO-A and MAO-B.
• Gallic acid derivatives like myricetin rhamnosides from Diospyros kaki inhibit MAO enzymes.
• Proanthocyanidins like procyanidin B2 from grape seeds inhibit MAO-B.

1. Other compounds:

• Piperine from black pepper inhibits both MAO-A and MAO-B.
• Paeonol from Paeonia species inhibits MAO enzymes.
• Emodin from Rheum and other plants inhibits MAO.

The search results highlight that many plant-derived alkaloids, flavonoids, phenols, and other compounds exhibit potent and selective inhibition of MAO-A and/or MAO-B, making them promising candidates for further research as potential treatments for neurological disorders.

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Based on the information provided in the search results, your statement is partially correct, but requires some clarification:

1. Pterostilbene was found to be the most potent natural MAO-B inhibitor among the compounds tested, with an IC50 of 0.138 μM. This is an extremely low IC50 value, indicating high potency.
2. However, resveratrol was found to be a potent and selective inhibitor of MAO-A, not MAO-B. Its IC50 for MAO-A inhibition was 0.313 μM, which is also a very low value. Resveratrol showed much less inhibition of MAO-B.
3. Quercetin was reported to be a poor MAO inhibitor, requiring millimolar concentrations to inhibit MAO-A, which are unlikely to be reached through dietary intake. Some studies did find quercetin to inhibit MAO-A with an IC50 around 30 μM, but this is still orders of magnitude higher than pterostilbene or resveratrol for their respective targets.
4. Other flavonoids like kaempferol, genistein, and certain procyanidins from grape seeds showed moderate to good inhibition of MAO-A and/or MAO-B, but were not as potent as pterostilbene or resveratrol for their respective targets.

In summary, pterostilbene stands out as the most potent natural MAO-B inhibitor reported, while resveratrol is a very potent MAO-A inhibitor. Quercetin does not appear to be among the most effective MAO inhibitors based on the evidence provided.

Answer

Based on the search results provided, there is no direct evidence that pterostilbene supplementation has been found to prevent Parkinson's disease. The key points are:

1. There appears to be no peer-reviewed scientific research specifically studying the effects of pterostilbene in animal models of Parkinson's disease.
2. The closest relevant study found that pterostilbene protected against a decrease in dopamine release following an oxidative stressor in aging mice, but this was not in a Parkinson's disease model.
3. While pterostilbene has shown impressive neuroprotective, anti-inflammatory, and cognitive-enhancing properties in other disease models like Alzheimer's disease and stroke, its specific effects on Parkinson's disease pathology have not been investigated.
4. Pterostilbene is reported to inhibit the enzyme monoamine oxidase B (MAO-B), similar to some Parkinson's disease drugs like rasagiline and selegiline. However, this mechanism has not been directly studied in Parkinson's disease models with pterostilbene supplementation.
5. The search results highlight the potential benefits of pterostilbene for brain health, cognition, and neuroprotection, but there is a lack of direct evidence from animal or human studies demonstrating its efficacy in preventing or treating Parkinson's disease specifically.

In summary, while pterostilbene shows promise as a neuroprotective and cognitive-enhancing compound, there is currently no conclusive evidence from the provided search results that its supplementation has been found to prevent Parkinson's disease. More research is needed to investigate its potential effects on Parkinson's disease pathology and progression.

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Dr. David Perlmutter presented the effects of diabetes and Parkinson's and the astounding effect of an GLP-1.