Abstract

Autophagy involves the breakdown of complete organelles and macromolecules in the cytoplasm of eukaryotic cells, especially proteins with extended half-lives. During this degrading phase, therapeutic, pharmacological, and fasting approaches are important. All eukaryotic cells engage in autophagy, which is an ancient and evolutionarily conserved phenomenon. It has been discovered in mammals, including humans, as well as the yeast Saccharomyces cerevisiae and the fl y Drosophila melanogaster. Its signifi cance in cell and dysfunction impairing the autophagy process that is connected to a broad array of serious illnesses, including neuronal and metabolic brain diseases. Only a concise summary of the various forms of autophagy and its molecular mechanisms, as well as how they relate to neuronal health, will be provided in this work. Negative regulations are frequently used to defi ne the regulatory networks that govern the autophagy process. This study, however, focuses on alternative strategies to promote autophagy. Metabolic neurodegenerative diseases can be treated by activating this mechanism via a variety of drugs or mechanisms. These points are covered and discussed in this article.

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