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Evidence that formulations of the selective MAO-B inhibitor, selegiline, which bypass first-pass metabolism, also inhibit MAO-A in the human brain.

Author: AlexoffDavid L, Apelskog-TorresKaren, CarterPauline, FahnStanley, FowlerJoanna S, GilmorMichelle, HubbardBarbara, JayneMillard, KingPayton, LoganJean, McCall-PerezFred, MuenchLisa, SheaColleen, ShumayElena, TelangFrank, VolkowNora D, WangGene-Jack, XuYouwen

Clinical TrialA clinical trial is a planned study conducted on humans to evaluate the efficacy and safety of pharmaceuticals, medical devices, and treatment methods. It aims to explore the possibilities of new treatments and improve the health of patients.
Journal ArticleAn article published in an academic or professional journal that reports original research or scholarly analysis.
Research Support, N.I.H., ExtramuralResearch funding provided by the NIH to external research institutions and researchers.
Research Support, Non-U.S. Gov'tResearch funding provided by government agencies outside the United States.
Research Support, U.S. Gov't, Non-P.H.S.Research funding provided by US government agencies other than the Public Health Service.

Overview

This study provides the first direct evidence of brain MAO-A inhibition in humans by high-dose Zydis selegiline, an orally disintegrating formulation of selegiline. Selegiline is a MAO-B inhibitor used for Parkinson's disease. The study uses positron emission tomography to demonstrate that high-dose Zydis selegiline inhibits both MAO-A and MAO-B in the brain.
Paper Details　
Original Abstract of the Article :
Selegiline (L-deprenyl) is a selective, irreversible inhibitor of monoamine oxidase B (MAO-B) at the conventional dose (10 mg/day oral) that is used in the treatment of Parkinson's disease. However, controlled studies have demonstrated antidepressant activity for high doses of oral selegiline and fo...See full text at original site
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引用元：
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4289953/

データ提供：米国国立医学図書館（NLM）

Selegiline Formulations: Beyond MAO-B Inhibition in the Human Brain

Selegiline, a medication commonly used to treat Parkinson's disease, is known to selectively inhibit monoamine oxidase B (MAO-B). However, studies have suggested that high doses of selegiline, as well as transdermal formulations, might also inhibit MAO-A in the human brain.

This study provides direct evidence that Zydis selegiline, a buccal formulation of selegiline, inhibits MAO-A in the human brain. The study used positron emission tomography (PET) imaging to measure MAO-A activity in healthy men after receiving different doses of Zydis selegiline. The results confirmed that higher doses of Zydis selegiline inhibited MAO-A, highlighting the potential for this formulation to have broader therapeutic effects.

Selegiline: Expanding Therapeutic Potential

This study expands our understanding of selegiline's effects on the brain. It provides direct evidence that formulations of selegiline that bypass first-pass metabolism, such as Zydis selegiline, can inhibit MAO-A in the human brain. This finding suggests that selegiline may have broader therapeutic potential than previously thought, potentially impacting its use in treating conditions beyond Parkinson's disease.

Implications for Neuropharmacology

This study has significant implications for the field of neuropharmacology. It challenges the traditional understanding of selegiline's selectivity and suggests that specific formulations may have broader effects on the brain. These findings can inform the development of new therapeutic strategies and may lead to the exploration of selegiline's potential in treating other neurological conditions.

Dr.Camel's Conclusion

Selegiline, like a desert oasis, offers a source of relief for those suffering from Parkinson's disease. This study reveals that different formulations of selegiline can have broader effects on the brain, suggesting that this medication may hold the key to unlocking new therapeutic possibilities. It's like discovering a hidden spring in the desert, offering fresh hope for treating neurological conditions and expanding the therapeutic landscape.
Date :
  1. Date Completed 2016-03-15
  2. Date Revised 2021-10-21
Further Info :

Pubmed ID

25249059

DOI: Digital Object Identifier

PMC4289953

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Languages

English

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