Belykova M. V., Rozova K. V., Vashchenko N. M.

MELATONIN AND NEURODEGENERATION (ANALYTICAL LITERATURE REVIEW)

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About the author:

Belykova M. V., Rozova K. V., Vashchenko N. M.

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LITERATURE REVIEWS

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Scientific article

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The use of melatonin as a multifunctional drug has been substantiated by the work of many research groups. The abundance of information on melatonin as a hormone and its various preparations demonstrates the interest of the scientific community in this topic. Over the past decades, the properties of melatonin have been well studied. Every year, new possibilities for its use are revealed and its natural functions for various functional systems of the human body are determined. Many mechanisms of melatonin's influence on the development, differentiation and degradation of nerve cells have been elucidated. Our work examines the possibility of using melatonin as a non-drug adjunct in neurodegeneration with impaired brain function. Low melatonin levels have been found in people with neurological diseases. The preventive and therapeutic effects of melatonin are used in diseases such as Alzheimer's disease, Parkinson's disease, multiple sclerosis, amyotrophic lateral sclerosis, Huntington's disease, epilepsy, head ache, etc. Clinical trials of melatonin have been conducted and successful results have been reported. According to positive results obtained in experimental and clinical studies, melatonin may have preventive and therapeutic effects in neurological diseases. All major neurodegenerative diseases are also associated with oxidative stress, which is widely recognized as a potential target for protective therapy. Oxidative stress and microRNA regulatory networks also influence other processes associated with neurodegeneration, such as mitochondrial dysfunction, dysregulation of proteostasis, and increased neuroinflammation, ultimately leading to neuronal death.

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Bibliography:

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Publication of the article:

«Bulletin of problems biology and medicine», Issue 2,177, 8-18 pages, index UDC 612.018.2:612.017.2

DOI:

10.29254/2077-4214-2025-2-177-8-18