Protect Against Dopamine Deficit

Many people accept brain fog, slower brain speed, and lack of motivation as a normal part of aging.

It doesn’t have to be.

Cognitive changes can occur due to an increase in an enzyme called MAO-B (monoamine oxidase B) in the brain.

MAO-B breaks down dopamine, a neurotransmitter that is central to many aspects of cognitive functioning.¹

Overactivity of MAO-B also produces toxic compounds that damage brain cells and contribute to neurodegenerative risks.^1,2

Research has shown that inhibiting MAO-B reduces cognitive decline.^1,2

In animal studies, lowered MAO-B activity is associated with increased longevity.^3-6

Preclinical evidence has revealed that phellodendron tree bark is an inhibitor of MAO-B.⁷

By preserving healthy dopamine levels, phellodendron bark may help maintain clear thinking, cognitive function, and motivation—while reducing potential risk for neurodegeneration.

What is Dopamine?

Dopamine is a neurotransmitter that carries signals—chemical “messages”—between brain cells.¹

It is sometimes called the “feel-good” neurotransmitter. It also plays a role in various aspects of cognitive functioning, including attention, motivation, and movement.^8,9

The levels of dopamine decline by about 13% each decade after age 45.¹⁰ A meta-analysis of 95 studies including 2,611 healthy adults concluded that activity in the brain’s dopamine system decreases by an average of 3.7%–14.0% per decade age.¹¹

Low dopamine levels are associated with depression, lack of motivation and pleasure, and symptoms of drug withdrawal.^2,8

Loss of dopamine function has also been shown to play a major role in the development of some neurodegenerative diseases.¹²

How MAO-B Overactivity Damages the Brain

One potential underlying cause of low brain dopamine levels is an increase in the enzyme MAO-B, which breaks down dopamine. ¹

MAO-B activity increases in the brain as we age. ¹³

As MAO-B increases, highly toxic byproducts are formed that can damage brain cells.² This damage has been linked to brain deterioration and development of age-related neurodegenerative diseases, including Parkinson’s and Alzheimer’s.

Researchers have hypothesized that when MAO-B activity is normal, these toxic byproducts are largely neutralized by antioxidant defenses.^2,13,14

Inhibiting MAO-B overactivity prevents some of the breakdown of dopamine that occurs with aging.

Phellodendron Inhibits MAO-B

Scientists have identified, in preclinical models, phellodendron tree bark as one of the strongest and most selective plant-derived MAO-B inhibitors.^7,15

One study found that phellodendron inhibited activity up to 5.6-fold. This is comparable to deprenyl, an MAO-B-inhibiting drug used to treat Parkinson’s and depression.⁷

The ability of phellodendron to inhibit MAO-B means it has the potential to maintain dopamine levels and block the neurotoxic effects of the enzyme’s overactivity.

Phellodendron Protects Cognitive Function

Phellodendron has neuroprotective properties that go beyond MAO-B inhibition.^16-18

In one cell model of Alzheimer’s disease, phellodendron extract protected against beta-amyloid toxicity, ¹⁷ which is commonly seen in the brains of people with Alzheimer’s.

In a rodent model, phellodendron protected against neuroinflammation, amyloid production, and other changes associated with Alzheimer’s.^18,19

In humans, these mechanisms could help maintain cognitive function into older age.

Summary

With age, overactivity of the enzyme MAO-B occurs in the brain.

This may result in reduced levels of the critical neurotransmitter dopamine.

MAO-B also produces toxic compounds that damage brain cells and contribute to the risk for neurodegenerative diseases.

Phellodendron bark extract can inhibit MAO-B activity.

This may help maintain dopamine levels and prevent the neurotoxicity associated with MAO-B overactivity. Studies also show that phellodendron has other neuroprotective properties.

Those who take MAO-B-inhibiting drugs like deprenyl do not need to take phellodendron. Phellodendron is not a substitute for physician-prescribed medications.

If you have any questions on the scientific content of this article, please call a Life Extension Wellness Specialist at 1-866-864-3027.

References

1. Behl T, Kaur D, Sehgal A, et al. Role of Monoamine Oxidase Activity in Alzheimer’s Disease: An Insight into the Therapeutic Potential of Inhibitors. Molecules. 2021 Jun 18;26(12).
2. Finberg JPM, Rabey JM. Inhibitors of MAO-A and MAO-B in Psychiatry and Neurology. Frontiers in Pharmacology. 2016 2016-October-18;7.
3. Kitani K, Kanai S, Ivy GO, et al. Assessing the effects of deprenyl on longevity and antioxidant defenses in different animal models. Ann N Y Acad Sci. 1998 Nov 20;854:291-306.
4. Kitani K, Minami C, Isobe K, et al. Why (--)deprenyl prolongs survivals of experimental animals: increase of anti-oxidant enzymes in brain and other body tissues as well as mobilization of various humoral factors may lead to systemic anti-aging effects. Mech Ageing Dev. 2002 Apr 30;123(8):1087-100.
5. Knoll J, Dallo J, Yen TT. Striatal dopamine, sexual activity and lifespan. Longevity of rats treated with (-)deprenyl. Life Sci. 1989;45(6):525-31.
6. Knoll J, Miklya I. Longevity study with low doses of selegiline/(-)-deprenyl and (2R)-1-(1-benzofuran-2-yl)-N-propylpentane-2-amine (BPAP). Life Sci. 2016 Dec 15;167:32-8.
7. Zarmouh NO, Messeha SS, Elshami FM, et al. Natural Products Screening for the Identification of Selective Monoamine Oxidase-B Inhibitors. European J Med Plants. 2016 May;15(1).
8. Available at: https://www.nih.gov/news-events/nih-research-matters/dopamine-affects-how-brain-decides-whether-goal-worth-effort. Accessed November, 21, 2022.
9. Blum K, Oscar-Berman M, Barh D, et al. Dopamine Genetics and Function in Food and Substance Abuse. J Genet Syndr Gene Ther. 2013 Feb 10;4(121).
10. Knoll J. Deprenyl (selegiline): the history of its development and pharmacological action. Acta Neurol Scand Suppl. 1983;95:57-80.
11. Karrer TM, Josef AK, Mata R, et al. Reduced dopamine receptors and transporters but not synthesis capacity in normal aging adults: a meta-analysis. Neurobiology of Aging. 2017 2017/09/01/;57:36-46.
12. Klein MO, Battagello DS, Cardoso AR, et al. Dopamine: Functions, Signaling, and Association with Neurological Diseases. Cell Mol Neurobiol. 2019 Jan;39(1):31-59.
13. Kumar MJ, Andersen JK. Perspectives on MAO-B in aging and neurological disease: where do we go from here? Mol Neurobiol. 2004 Aug;30(1):77-89.
14. Naoi M, Maruyama W, Inaba-Hasegawa K. Type A and B monoamine oxidase in age-related neurodegenerative disorders: their distinct roles in neuronal death and survival. Curr Top Med Chem. 2012;12(20):2177-88.
15. Mazzio E, Deiab S, Park K, et al. High throughput screening to identify natural human monoamine oxidase B inhibitors. Phytother Res. 2013 Jun;27(6):818-28.
16. Sun Y, Lenon GB, Yang AWH. Phellodendri Cortex: A Phytochemical, Pharmacological, and Pharmacokinetic Review. Evid Based Complement Alternat Med. 2019;2019:7621929.
17. Xian YF, Lin ZX, Ip SP, et al. Comparison the neuropreotective effect of Cortex Phellodendri chinensis and Cortex Phellodendri amurensis against beta-amyloid-induced neurotoxicity in PC12 cells. Phytomedicine. 2013 Jan 15;20(2):187-93.
18. Kim Y JI, Lee S. . Effects of Phellodendron amurense extract on the Alzheimer’s disease model. Journal of Physiology & Pathology in Korean Medicine. 2005;19:130-8.
19. Lee B, Sur B, Shim I, et al. Phellodendron amurense and Its Major Alkaloid Compound, Berberine Ameliorates Scopolamine-Induced Neuronal Impairment and Memory Dysfunction in Rats. Korean J Physiol Pharmacol. 2012 Apr;16(2):79-89.