Autophagy and apoptosis dysfunction in neurodegenerative disorders.
By S. Ghavami, S. Shojaei, B. Yeganeh, Sudharsana Rao Ande, Jaganmohan Reddy Jangamreddy, M. Mehrpour, Jonas Christoffersson, Wiem Chaabane, A. R. Moghadam, Hessam Kashani and 3 more. Progress in neurobiology, 2014
987 citations recorded by the source corpus.
Autophagy and apoptosis are basic physiologic processes contributing to the maintenance of cellular homeostasis. Autophagy encompasses pathways that target long-lived cytosolic proteins and damaged organelles. It involves a sequential set of events including double membrane formation, elongation, vesicle maturation and finally delivery of the targeted materials to the lysosome. Apoptotic cell death is best described through its morphology. It is characterized by cell rounding, membrane blebbing, cytoskeletal collapse, cytoplasmic condensation, and fragmentation, nuclear pyknosis, chromatin condensation/fragmentation, and formation of membrane-enveloped apoptotic bodies, that are rapidly phagocytosed by macrophages or neighboring cells. Neurodegenerative disorders are becoming increasingly prevalent, especially in the Western societies, with larger percentage of members living to an older age. They have to be seen not only as a health problem, but since they are care-intensive, they also carry a significant economic burden. Deregulation of autophagy plays a pivotal role in the etiology and/or progress of many of these diseases. Herein, we briefly review the latest findings that indicate the involvement of autophagy in neurodegenerative diseases. We provide a brief introduction to autophagy and apoptosis pathways focusing on the role of mitochondria and lysosomes. We then briefly highlight pathophysiology of common neurodegenerative disorders like Alzheimer's diseases, Parkinson's disease, Huntington's disease and Amyotrophic lateral sclerosis. Then, we describe functions of autophagy and apoptosis in brain homeostasis, especially in the context of the aforementioned disorders. Finally, we discuss different ways that autophagy and apoptosis modulation may be employed for therapeutic intervention during the maintenance of neurodegenerative disorders.
Subfields: Cell Biology, Epidemiology, Physiology
View Paper: https://www.semanticscholar.org/paper/c3f3626fdc56bad7a272982190549e090a2f93ce
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Citations in the corpus
- Oxidative stress in the aging substantia nigra and the etiology of Parkinson's disease (2019, background): “Further, selegiline‐in‐ duced neuroprotection of 6‐OHDA‐treated neurons derives from the upregulation of SOD1 and catalase expression, and the sup‐ pression of pro‐oxidant, iron‐catalyzed dopamine auto‐oxidation (Ghavami et al., 2014; Khaldy et al., 2000).”
- Compromised MAPK signaling in human diseases: an update (2015, background): “Stimulation of autophagy, a major degradation pathway for such aggregates, has thus been considered a potential therapeutic strategy for these diseases (Ghavami et al. 2014; Nixon 2013; Sarkar and Rubinsztein 2008).”