MAO-B-Inhibiting Nutrients and the drug Deprenyl
Monoamine oxidase (MAO) is an enzyme involved in the degradation process for various monoamines released by neurons and glial cells, including dopamine, serotonin and norepinephrine (NE).
All of which are crucial to brain function in various ways.
There are two types of MAO, Type A and Type B. Type B inhibition is what is used for anxiety, ADHD, depression, memory loss, Alzheimer’s and Parkinson’s.
MAO-B levels and activity are highly correlated and increase after chronic stress hormone exposure.
The enzyme monoamine oxidase B (MAO-B) serves a function in youth by keeping neurotransmitter levels from elevating too high. As we age past 45 years, however, MAO-B levels begin a steady rise that results the depletion in dopamine seen in elderly individuals.
MAO-B also may inflict toxic damage to brain cells via several well-defined mechanisms.
Excess MAO-B not only deprives us of our youthful emotions by depleting dopamine, but also impairs cognitive functions by decreasing acetylcholine while simultaneously accelerating brain aging.
People today should take steps to suppress MAO-B levels as they age past 45 years
Monoamine Neurotransmitters Include:
- Dopamine
- Serotonin
- Adrenaline
- Dimethyltryptamine (DMT)
- Melatonin
- Noradrenalin
- B-phenylethylamine (PEA)
- Benzylamine
Natural Products Screening for the Identification of Selective Monoamine Oxidase-B Inhibitors:
1. Gan Cao (Glycyrrhiza Uralensis Root)
MAO-B Inhibition Very High (IC50 <.07 mg/ml)
Gan Cao is a type of licorice (same genus), and is used in much the same way. Its traditional uses involves female disorders, digestive disorders, ulcers, and heart arrythmias. One of the most interesting sue of this plant, is as a “harmonizer” of other medicinal plants.
In Chinese traditional medicine this is one of the main herbs used in formulas for its ability to improve the outcomes of other plants.
The roots of Glycyrrhiza uralensis (aka Chinese licorice; family Leguminosae) is another commonly used medicinal plant in traditional Chinese and natural medicine. Our new finding that GUREE inhibits hMAO-B selectively is supported by our previous finding for its hMAO-B inhibition [17].
Interestingly, GUR was more selective than Glycyrrhiza glabra in our screen. Reported Glycyrrhiza uralensis different active constituents from other Glycyrrhiza genuses may influence its MAO-B selective inhibition [53]. GUR contains unique phytochemicals including isoprenylated phenolics [54] flavonoids, chalcones, and triterpene saponins [55].
Chalcone isoliquiritigenin, is an inhibitor for MAO-B [56] with multifunctional anti-inflammatory, antioxidant, cytoprotective [57] cellular detoxification system activator [58] and anti-apoptotic [59] anti-amyloid-β toxicity [60] neuroprotective properties. GUR total flavonoid extracts showed neurogenesis protective effect in depressed rats model [61].
The flavonoid liquiritin showed antioxidant and antiapoptotic neuroprotective effects in mice [62] and ameliorated depression in rat model [63]. Its benzopyran dehydroglyasperin-C also showed neuroprotection [64]. Xiao Yao San, a traditional herb combination containing GUR for chronic depression, was effective in both animal models and clinical trials [65,66].
Other multifunctional properties of GUR constituents included reducing pro-inflammatory cytokines, nitric oxide, reactive oxygen species, lipid peroxidation [67], and mitochondrial impairment [68]. Interestingly, GUREE reports covered its chemopreventive [69] and anti-diabetic properties [70]. Therefore, specifically investigating GUREE as a selective MAO-BI could be beneficial.
2. Psoralea Fruit Babchi (Psoralea Corylifolia)
MAO-B Inhibition Very High (IC50 <.07 mg/ml)
Psoralea fruit is a lesser known Ayurvedic and Traditional Chinese medicinal plant species. It was used in the past for conditions like vitiligo and other skin related conditions. Recently it has received a lot of attention for its MAO inhibiting properties, and is suggested to be a norepinephrine, re-uptake inhibitor.
In addition, the seeds of Psoralea corylifolia (aka, Bu Gu Zhi or Babchi; family Leguminosae) are important in traditional Chinese and Ayurvedic medicines [27]. PCSEE was one of the most potent and selective hMAO-BI using our fluorometric screening assay.
Our PCS findings are supported by our previous investigations on its hMAO-B inhibitory potency tested spectrophotometrically [17], and its selectivity for hMAO-B using a luminescence assay [28].
Previous PCS screened extracts for active constituents revealed that the ethanolic extract composes more medically active compounds than some other PCS extracts, which makes it a better candidate for novel phytomedicines [29].
PSCEE is rich in benzopyrone structure constituents including coumarins and flavonoids. PCS furocoumarins psoralen and isopsoralen showed rat MAOs activities inhibitions [30], which were supported by total furocoumarins potent antidepressant effects on mice [31]. PCS also contains isoflavones, which have been used as dietary supplements in various diseases, including osteoporosis, cognitive dysfunction, cardiovascular disease, and inflammation [32], which are close to PCS multifaceted properties [33–35].
We previously investigated bavachinin and genistein flavonoids constituents of PCS. Bavachinin exhibited a selective hMAO-B inhibition [28] while isoflavone genistein was similarly potent but less selective against hMAO-B [36].
Moreover, PCSEE contains monoterpenes that protected against the MAO-B substrate 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) SN cell damage and MPTP-induced motor deficits in PD model [37], inhibited DA and norepinephrine (NE) transporters [38], and showed antidepressant effects with catecholamine neurotransmitters regulation [39,40].
The PCS extracts were also neuroprotective against the MPTP precursor MPP+ [38] and the nitropropionic acid (3-NP) induced cytotoxicity and mitochondrial dysfunction [41].
Although the seeds are used in dermatological disorders health supplements [33] and increasingly investigated on in vitro and animal models, the extract and its phytochemicals clinical effects on degenerative diseases are yet to be clinically considered.
From our results, the observed association between PCS constituents MAO-B inhibitions and the extracts neuroprotection in the previous reports suggests more investigations for potential beneficial PCS phytochemicals for PD.
3. Ferula assafoetida roots
MAO-B Inhibition Very High (IC50 <0.07 mg/ml)
This resin has been used as a spice and a phytomedicine around the globe for centuries. In the folklore medicine, it is mostly used in asthma, gastrointestinal disorders, and neuronal disorders [20].
In recent reports, the resin improved memory and learning in rats [21], and exhibited neuroprotection and nerve stimulation in mice peripheral neuropathy [22], and anticonvulsant properties [23].
FAR contains bioactive phytochemicals such as polysulfides, sesquiterpenes, sesquiterpene-coumarins, diterpenes, phenolics, and flavonoids [20,24]. Its coumarin umbelliprenin showed anti-inflammatory properties [20], while ferulic acid showed anti-atherosclerotic, antioxidant, and neuroprotective properties [25] and became a candidate for AD [26].
Therefore, investigations on the resin concerning PD need to be considered.
4. Amur Cork Tree (Phellodendron Amurense)
MAO-B Inhibition Very High (IC50 <.07 mg/ml)
Amur cork tree is one of the 50 fundamental Chinese herbs. It’s commonly used for it’s sedative, muscle relaxant, antiarrhythmic, positive inotropic, hypotensive, and antibacterial actions.
Phellodendron amurense (aka Amur cork tree; family Rutaceae) is a meagerly investigated Chinese medicinal plant. In our study, its bark ethanolic extract clearly was a selective hMAO-BI as its potent inhibition was previously spectrophotometrically confirmed [17].
The plant constituted alkaloids such as phellodendron, palmatine, jatrorrhizine, and berberine [42,43] where the later displayed safe antidepressant-like activities in mice by the possible mechanism MAO-A inhibition and increasing DA, NE and serotonin brain levels [44,45].
PAB is high in the flavone tetramethyl-o-scutellarin, and the triterpenoids limonoids [42]. Limonoid obacunone was found neuroprotective in glutamate-induced neurotoxicity in vitro [46].
In clinical studies, PAB extract supplement safely reduced cortisol [47], and relieved mild anxiety in women [48]. Also, PAB inhibited pro-inflammatory cytokines [49,50] and protected from prostate tumors progression [51], property found in some MAO-AIs [52].
Based on our results and literature, there is a lack of knowledge on MAO-B inhibition and selectivity benefits of PAB extracts and phytochemicals. Further studies on PABEE as MAO-BI source for PD are highly recommended.
Natural Products Screening for the Identification of Selective Monoamine Oxidase-B Inhibitors
DEPRENYL
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The Most Sought-After Anti-Aging Drug
February 2016
By William Faloon
In the 1980s-1990s, published studies in Europe showed remarkable life span increases in animals given a drug called deprenyl.
In elderly rats treated with deprenyl, remaining life span doubled in response to the drug. Aged dogs given deprenyl had twice the survival rate compared with placebo-treated dogs. Mice that were immune-suppressed lived up to about 200% longer on deprenyl. (Most elderly humans suffer immune suppression).
Not only were life spans lengthened, but some deprenyl-supplemented animals displayed more youthful energy levels, as related to sexual activity.
This outpour of scientific data from Europe had aging Americans clamoring to get their hands on deprenyl. It started being used in Europe to treat Parkinson’s disease in the 1970s, but the FDA did not approve deprenyl until 1989.
When deprenyl was finally approved, it cost Americans 4 times more money than what Europeans were paying for the identical drug. Unwilling to pay this extortionist price, Americans began ordering personal-use supplies from Europe.
The FDA struck back and launched criminal investigations against those seeking to make deprenyl more affordable. The FDA did this at the behest of the drug company that owned the patent on deprenyl.
One individual made a liquid form of deprenyl that sold quite well until he was arrested by the FDA and sent to prison for almost 13 years. Back in those days, deprenyl was the most sought-after anti-aging drug.
Some of our supporters still use deprenyl, though getting a physician to prescribe it for anti-aging purposes is sometimes impossible. This article will describe how Americans can now derive the anti-aging mechanism of deprenyl in a low-cost nutrient.
Deprenyl is a drug the FDA approved to treat early-stage Parkinson’s disease. It was enthusiastically greeted by neurologists when first approved in the United States, but its therapeutic effect on advanced Parkinson’s patients was disappointing.
That’s because a significant drop in dopamine occurs before symptoms of Parkinson’s disease become evident. Therefore, most Parkinson’s patients have already lost so many dopamine-producing neurons that deprenyl is of little value.
Deprenyl enhances the anti-Parkinson effects of standard drugs. Its primary mechanism is to inhibit an enzyme in the brain that destroys dopamine.
Longevity enthusiasts realized 30 years ago that if low-dose deprenyl is initiated before the onset of Parkinson’s symptoms, the brain might be protected against Parkinson’s and other neurodegenerative diseases.
By inhibiting this dopamine-degrading enzyme, it was theorized, people might not only live longer, but behave younger.
This same enzyme (MAO-B) may be involved in the destruction of dopamine-producing neurons.
Dopamine Levels in the Brain
Prior to age 45 in people, dopamine levels remain fairly stable. After that, dopamine in the human brain decreases by about 13% each decade.
When the dopamine-producing neuron content in the brain reaches about 30% of normal, Parkinson’s symptoms may be present.
When dopamine levels reach 10% of normal, death ensues.
This has led to the hypothesis that if we live long enough, we will all develop Parkinson’s symptoms due to dopamine depletion in our brains.
How Deprenyl Works in the Brain
Monoamine oxidase B (MAO-B) is an enzyme in the brain that degrades neurotransmitters like dopamine.
As humans age, MAO-B levels begin to increase and degrade precious dopamine and other neurotransmitters.
Deprenyl is a selective inhibitor of MAO-B. As little as 5 mg twice a week of deprenyl is all aging humans may need to maintain their dopamine at youthful levels.
Parkinson’s patients were prescribed 10 mg a day of deprenyl. The inventor of the drug (Dr. Joseph Knoll) believed this dose was too high.
It was long ago hypothesized that low-dose deprenyl might help prevent degenerative brain diseases and improve the quality of life. This is evidenced by increased “mounting frequency” in old male rats treated with deprenyl compared to untreated controls.
Dopamine is a primary “feel-good” neurotransmitter that progressively depletes as humans age. By restoring dopamine and other neurotransmitter levels using low-dose deprenyl, aging humans may regain some of their youthful sense of well-being.
Deprenyl has demonstrated intriguing anti-aging properties. Animals given relatively low doses of the drug live much longer than control groups not receiving deprenyl.
Need to Suppress MAO-B in Aging Brains
The enzyme monoamine oxidase B (MAO-B) serves a function in youth by keeping neurotransmitter levels from elevating too high. As we age past 45 years, however, MAO-B levels begin a steady rise that results the depletion in dopamine seen in elderly individuals.
MAO-B also may inflict toxic damage to brain cells via several well-defined mechanisms.
Excess MAO-B not only deprives us of our youthful emotions by depleting dopamine, but also impairs cognitive functions by decreasing acetylcholine while simultaneously accelerating brain aging.
People today should take steps to suppress MAO-B levels as they age past 45 years. Those who are already taking low-dose deprenyl (5 mg twice a week) may be deriving enormous benefits by protecting against MAO-B toxicity.
The problem is that most doctors will not prescribe deprenyl to non-Parkinson’s patients. Insurance companies are unlikely pay for “off-label” use.
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