Autophagy is a cellular degradation process that can cause the death of a cell in certain conditions. Autophagy is necessary to maintain cellular homeostasis by clearing out damaged cellular organelles and proteins through certain pathways. Mitochondria are cell organelles responsible for the constant supply of energy to maintain cellular physiology and energy metabolism.
Ashutosh Kumar et al. at the National Institute of Pharmaceutical Education and Research (NIPER), Hyderabad, India present a review on autophagy in neuronal cells. The researchers believe that autophagy on the neuronal cells can lead to neurodegenerative diseases and countering the effects of this process through targeted drugs can be beneficial in the fight against such diseases. Neuronal cells are more vulnerable to such bioenergetic depletion as most of their function crucially depends on availability of energy derived mainly from mitochondrial function. Any incidence of mitochondrial dysfunction inevitably results in neurodegeneration. Therefore, mitochondrial autophagy (mitophagy) plays an integral role in the onset of neurodegenerative diseases as the instance and failure of these pathways can have destructive effects on cellular homeostasis.
Previous studies show significant association between neurodegenerative disorders and mitochondrial dysfunction and abnormal mitophagy. Abnormal mitophagy leads to the accumulation of protein aggregates and consequential neurodegeneration. Future treatments for neurodegenerative disorders could involve drugs targeting mitochondria and autophagy-related proteins and enzymes. This review discusses the involvement of mitochondrial and autophagy dysfunction in neurodegenerative disorders specifically focusing on Alzheimer’s, Parkinson’s, and Huntington’s disease. Read full press release to find out more at: https://www.eurekalert.org/pub_releases/2018-12/bsp-aam122618.php
This article by Dr. Ashutosh Kumar et al. is published in CNS & Neurological Disorders – Drug Targets, Volume 17, Issue 9, 2018. The article is Open Access till 31st January, 2019. To obtain the article, please visit: http://www.eurekaselect.com/164678
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