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Autophagy and apoptosis dysfunction in neurodegenerative disorders
Saeid Ghavami1, Shahla Shojaei2, Behzad Yeganeh3
1Department of Human Anatomy and Cell Science, University of Manitoba, Winnipeg, Canada; Manitoba Institute of Child Health, Department of Physiology, University of Manitoba, Winnipeg, Canada; St. Boniface Research Centre, University of Manitoba, Winnipeg, Canada.
Progress in Neurobiology
|November 12, 2013
Summary
Autophagy and apoptosis are crucial for cell health. Deregulation of autophagy is linked to neurodegenerative diseases, suggesting therapeutic potential for these pathways.
Area of Science:
- Cellular Biology
- Neuroscience
- Pathophysiology
Background:
- Autophagy and apoptosis are fundamental cellular processes essential for maintaining homeostasis.
- Dysregulation of autophagy is implicated in the development and progression of neurodegenerative disorders.
- Neurodegenerative diseases pose a growing health and economic burden globally.
Purpose of the Study:
- To review current findings on autophagy's role in neurodegenerative diseases.
- To explore the interplay between autophagy, apoptosis, mitochondria, and lysosomes in brain homeostasis.
- To discuss therapeutic strategies targeting autophagy and apoptosis for neurodegenerative conditions.
Main Methods:
- Literature review of recent findings on autophagy and neurodegeneration.
- Focus on the roles of mitochondria and lysosomes in autophagy and apoptosis pathways.
- Examination of the pathophysiology of Alzheimer's, Parkinson's, Huntington's, and ALS.
Main Results:
- Autophagy plays a critical role in cellular homeostasis and is implicated in neurodegenerative disease pathogenesis.
- Mitochondria and lysosomes are key organelles involved in both autophagy and apoptosis.
- Specific neurodegenerative diseases exhibit distinct alterations in these cellular processes.
Conclusions:
- Modulating autophagy and apoptosis pathways offers potential therapeutic avenues for neurodegenerative disorders.
- Understanding the intricate roles of autophagy and apoptosis is vital for developing effective treatments.
- Targeting these cellular mechanisms could help manage brain homeostasis in neurodegenerative conditions.
Keywords:
ADAIFALSAMBRAAMP-activated protein kinaseAMPAAMPKAPPATGAlzheimer's diseasesApo-EAβBDNFCMAERESCRTHDHEK293HIP-1HttHuntingtin interacting proteinHuntingtin proteinHuntington's diseaseInsP(6)KsLAMPLC3LRPPRCMAP15Mitochondria dysfunctionN-methyl-d-aspartateNCCDNMDAPCDPDPINK-1PON 1–3PTEN-induced putative kinase 1Parkinson's diseasePorteopathiesRCAN-1RSVA314RSVA405RUBICONRUN domain and cysteine rich domain containingResveratrolTAR DNA-binding protein 43kDaTDP-43-kDaTrehaloseUPSUVRAGVCPX-box binding protein-1XBP-1activating molecule in Beclin-1-regulated autophagyalpha-synucleinamyloid beta precursor proteinamyloid-betaamyotrophic lateral sclerosisapolipo-protein Eapoptosis-inducing factorautophagosome-associated light chain 3autphagy related genesbrain-derived neurotrophic factorchaperon-mediated autophagyendoplasmic reticulumendosomal sorting complexes required for transporthuman embryonic kidney 293 cellsinositol hexakisphosphate kinaseslysosomal associated membrane proteinsmHttmPTPmTORmammalian target of rapamycinmicrotubule-associated protein 15mitochondrial permeability transition poremitochondrion-associated leucine-rich PPR-motif containing proteinmutant Huntingtin proteinnomenclature committee on cell deathp53pQparaxonase enzymespoly-glutamineprogrammed cell deathregulator of calcineurin-1tumor protein 53ubiquitin-proteasome systemultra-violet radiation resistance-associated genevalosin-containing proteinα-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acidα-syn
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