Autophagy and apoptosis dysfunction in neurodegenerative disorders.
Identifieur interne : 000085 ( France/Analysis ); précédent : 000084; suivant : 000086Autophagy and apoptosis dysfunction in neurodegenerative disorders.
Auteurs : Saeid Ghavami [Canada] ; Shahla Shojaei [Iran] ; Behzad Yeganeh [Canada] ; Sudharsana R. Ande [Canada] ; Jaganmohan R. Jangamreddy [Suède] ; Maryam Mehrpour [France] ; Jonas Christoffersson [Suède] ; Wiem Chaabane [Tunisie] ; Adel Rezaei Moghadam [Iran] ; Hessam H. Kashani [Canada] ; Mohammad Hashemi [Iran] ; Ali A. Owji [Iran] ; Marek J. Łos [Suède]Source :
- Progress in neurobiology [ 1873-5118 ] ; 2014.
English descriptors
- KwdEn :
- Animals, Apoptosis, Autophagy, Brain (pathology), Brain (physiopathology), Brain Diseases (pathology), Brain Diseases (physiopathology), Humans, Neurodegenerative Diseases (pathology), Neurodegenerative Diseases (physiopathology), Neurons (pathology), Peripheral Nervous System Diseases (pathology), Peripheral Nervous System Diseases (physiopathology).
- MESH :
- pathology : Brain, Brain Diseases, Neurodegenerative Diseases, Neurons, Peripheral Nervous System Diseases.
- physiopathology : Brain, Brain Diseases, Neurodegenerative Diseases, Peripheral Nervous System Diseases.
- Animals, Apoptosis, Autophagy, Humans.
Abstract
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.
DOI: 10.1016/j.pneurobio.2013.10.004
PubMed: 24211851
Affiliations:
- Canada, France, Iran, Suède, Tunisie
- Gouvernorat de Tunis, Manitoba, Ontario
- Toronto, Tunis, Winnipeg
- Université de Toronto, Université du Manitoba
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pubmed:24211851Le document en format XML
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Ande</name><affiliation wicri:level="4"><nlm:affiliation>Department of Internal Medicine, University of Manitoba, Winnipeg, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Internal Medicine, University of Manitoba, Winnipeg</wicri:regionArea><orgName type="university">Université du Manitoba</orgName><placeName><settlement type="city">Winnipeg</settlement><region type="state">Manitoba</region></placeName></affiliation></author><author><name sortKey="Jangamreddy, Jaganmohan R" sort="Jangamreddy, Jaganmohan R" uniqKey="Jangamreddy J" first="Jaganmohan R" last="Jangamreddy">Jaganmohan R. Jangamreddy</name><affiliation wicri:level="1"><nlm:affiliation>Department of Clinical and Experimental Medicine (IKE), Integrative Regenerative Medicine Center (IGEN), Division of Cell Biology, Linkoping University, Linkoping, Sweden.</nlm:affiliation><country xml:lang="fr">Suède</country><wicri:regionArea>Department of Clinical and Experimental Medicine (IKE), Integrative Regenerative Medicine Center (IGEN), Division of Cell Biology, Linkoping University, Linkoping</wicri:regionArea><wicri:noRegion>Linkoping</wicri:noRegion></affiliation></author><author><name sortKey="Mehrpour, Maryam" sort="Mehrpour, Maryam" uniqKey="Mehrpour M" first="Maryam" last="Mehrpour">Maryam Mehrpour</name><affiliation wicri:level="1"><nlm:affiliation>INSERM U845, Research Center "Growth & Signaling" Paris Descartes University Medical School, France.</nlm:affiliation><country xml:lang="fr">France</country><wicri:regionArea>INSERM U845, Research Center "Growth & Signaling" Paris Descartes University Medical School</wicri:regionArea><wicri:noRegion>Research Center "Growth & Signaling" Paris Descartes University Medical School</wicri:noRegion><wicri:noRegion>Research Center "Growth & Signaling" Paris Descartes University Medical School</wicri:noRegion></affiliation></author><author><name sortKey="Christoffersson, Jonas" sort="Christoffersson, Jonas" uniqKey="Christoffersson J" first="Jonas" last="Christoffersson">Jonas Christoffersson</name><affiliation wicri:level="1"><nlm:affiliation>Department of Clinical and Experimental Medicine (IKE), Integrative Regenerative Medicine Center (IGEN), Division of Cell Biology, Linkoping University, Linkoping, Sweden.</nlm:affiliation><country xml:lang="fr">Suède</country><wicri:regionArea>Department of Clinical and Experimental Medicine (IKE), Integrative Regenerative Medicine Center (IGEN), Division of Cell Biology, Linkoping University, Linkoping</wicri:regionArea><wicri:noRegion>Linkoping</wicri:noRegion></affiliation></author><author><name sortKey="Chaabane, Wiem" sort="Chaabane, Wiem" uniqKey="Chaabane W" first="Wiem" last="Chaabane">Wiem Chaabane</name><affiliation wicri:level="3"><nlm:affiliation>Department of Clinical and Experimental Medicine (IKE), Integrative Regenerative Medicine Center (IGEN), Division of Cell Biology, Linkoping University, Linkoping, Sweden; Department of Biology, Faculty of Sciences, Tunis University, Tunis, Tunisia.</nlm:affiliation><country xml:lang="fr">Tunisie</country><wicri:regionArea>Department of Clinical and Experimental Medicine (IKE), Integrative Regenerative Medicine Center (IGEN), Division of Cell Biology, Linkoping University, Linkoping, Sweden; Department of Biology, Faculty of Sciences, Tunis University, Tunis</wicri:regionArea><placeName><settlement type="city">Tunis</settlement><region nuts="2">Gouvernorat de Tunis</region></placeName></affiliation></author><author><name sortKey="Moghadam, Adel Rezaei" sort="Moghadam, Adel Rezaei" uniqKey="Moghadam A" first="Adel Rezaei" last="Moghadam">Adel Rezaei Moghadam</name><affiliation wicri:level="1"><nlm:affiliation>Young Researchers Club, Ardabil Branch, Islamic Azad University, Ardabil, Iran.</nlm:affiliation><country xml:lang="fr">Iran</country><wicri:regionArea>Young Researchers Club, Ardabil Branch, Islamic Azad University, Ardabil</wicri:regionArea><wicri:noRegion>Ardabil</wicri:noRegion></affiliation></author><author><name sortKey="Kashani, Hessam H" sort="Kashani, Hessam H" uniqKey="Kashani H" first="Hessam H" last="Kashani">Hessam H. Kashani</name><affiliation wicri:level="4"><nlm:affiliation>Department of Human Anatomy and Cell Science, University of Manitoba, Winnipeg, Canada; Manitoba Institute of Child Health, Department of Physiology, University of Manitoba, Winnipeg, Canada.</nlm:affiliation><country xml:lang="fr">Canada</country><wicri:regionArea>Department of Human Anatomy and Cell Science, University of Manitoba, Winnipeg, Canada; Manitoba Institute of Child Health, Department of Physiology, University of Manitoba, Winnipeg</wicri:regionArea><orgName type="university">Université du Manitoba</orgName><placeName><settlement type="city">Winnipeg</settlement><region type="state">Manitoba</region></placeName></affiliation></author><author><name sortKey="Hashemi, Mohammad" sort="Hashemi, Mohammad" uniqKey="Hashemi M" first="Mohammad" last="Hashemi">Mohammad Hashemi</name><affiliation wicri:level="1"><nlm:affiliation>Department of Clinical Biochemistry, School of Medicine, Zahedan University of Medical Sciences, Zahedan, Iran; Cellular and Molecular Biology Research Center, Zahedan University of Medical Sciences, Zahedan, Iran.</nlm:affiliation><country xml:lang="fr">Iran</country><wicri:regionArea>Department of Clinical Biochemistry, School of Medicine, Zahedan University of Medical Sciences, Zahedan, Iran; Cellular and Molecular Biology Research Center, Zahedan University of Medical Sciences, Zahedan</wicri:regionArea><wicri:noRegion>Zahedan</wicri:noRegion></affiliation></author><author><name sortKey="Owji, Ali A" sort="Owji, Ali A" uniqKey="Owji A" first="Ali A" last="Owji">Ali A. Owji</name><affiliation wicri:level="1"><nlm:affiliation>Department of Biochemistry, Recombinant Protein Laboratory, Medical School, Shiraz University of Medical Sciences, Shiraz, Iran. Electronic address: aaowji@yahoo.com.</nlm:affiliation><country xml:lang="fr">Iran</country><wicri:regionArea>Department of Biochemistry, Recombinant Protein Laboratory, Medical School, Shiraz University of Medical Sciences, Shiraz</wicri:regionArea><wicri:noRegion>Shiraz</wicri:noRegion></affiliation></author><author><name sortKey="Los, Marek J" sort="Los, Marek J" uniqKey="Los M" first="Marek J" last="Łos">Marek J. Łos</name><affiliation wicri:level="1"><nlm:affiliation>Department of Clinical and Experimental Medicine (IKE), Integrative Regenerative Medicine Center (IGEN), Division of Cell Biology, Linkoping University, Linkoping, Sweden. Electronic address: mjelos@gmail.com.</nlm:affiliation><country xml:lang="fr">Suède</country><wicri:regionArea>Department of Clinical and Experimental Medicine (IKE), Integrative Regenerative Medicine Center (IGEN), Division of Cell Biology, Linkoping University, Linkoping</wicri:regionArea><wicri:noRegion>Linkoping</wicri:noRegion></affiliation></author></analytic><series><title level="j">Progress in neurobiology</title><idno type="eISSN">1873-5118</idno><imprint><date when="2014" type="published">2014</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Apoptosis</term><term>Autophagy</term><term>Brain (pathology)</term><term>Brain (physiopathology)</term><term>Brain Diseases (pathology)</term><term>Brain Diseases (physiopathology)</term><term>Humans</term><term>Neurodegenerative Diseases (pathology)</term><term>Neurodegenerative Diseases (physiopathology)</term><term>Neurons (pathology)</term><term>Peripheral Nervous System Diseases (pathology)</term><term>Peripheral Nervous System Diseases (physiopathology)</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Brain</term><term>Brain Diseases</term><term>Neurodegenerative Diseases</term><term>Neurons</term><term>Peripheral Nervous System Diseases</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Brain</term><term>Brain Diseases</term><term>Neurodegenerative Diseases</term><term>Peripheral Nervous System Diseases</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Apoptosis</term><term>Autophagy</term><term>Humans</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">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.</div></front></TEI><affiliations><list><country><li>Canada</li><li>France</li><li>Iran</li><li>Suède</li><li>Tunisie</li></country><region><li>Gouvernorat de Tunis</li><li>Manitoba</li><li>Ontario</li></region><settlement><li>Toronto</li><li>Tunis</li><li>Winnipeg</li></settlement><orgName><li>Université de Toronto</li><li>Université du Manitoba</li></orgName></list><tree><country name="Canada"><region name="Manitoba"><name sortKey="Ghavami, Saeid" sort="Ghavami, Saeid" uniqKey="Ghavami S" first="Saeid" last="Ghavami">Saeid Ghavami</name></region><name sortKey="Ande, Sudharsana R" sort="Ande, Sudharsana R" uniqKey="Ande S" first="Sudharsana R" last="Ande">Sudharsana R. Ande</name><name sortKey="Kashani, Hessam H" sort="Kashani, Hessam H" uniqKey="Kashani H" first="Hessam H" last="Kashani">Hessam H. Kashani</name><name sortKey="Yeganeh, Behzad" sort="Yeganeh, Behzad" uniqKey="Yeganeh B" first="Behzad" last="Yeganeh">Behzad Yeganeh</name></country><country name="Iran"><noRegion><name sortKey="Shojaei, Shahla" sort="Shojaei, Shahla" uniqKey="Shojaei S" first="Shahla" last="Shojaei">Shahla Shojaei</name></noRegion><name sortKey="Hashemi, Mohammad" sort="Hashemi, Mohammad" uniqKey="Hashemi M" first="Mohammad" last="Hashemi">Mohammad Hashemi</name><name sortKey="Moghadam, Adel Rezaei" sort="Moghadam, Adel Rezaei" uniqKey="Moghadam A" first="Adel Rezaei" last="Moghadam">Adel Rezaei Moghadam</name><name sortKey="Owji, Ali A" sort="Owji, Ali A" uniqKey="Owji A" first="Ali A" last="Owji">Ali A. Owji</name></country><country name="Suède"><noRegion><name sortKey="Jangamreddy, Jaganmohan R" sort="Jangamreddy, Jaganmohan R" uniqKey="Jangamreddy J" first="Jaganmohan R" last="Jangamreddy">Jaganmohan R. Jangamreddy</name></noRegion><name sortKey="Christoffersson, Jonas" sort="Christoffersson, Jonas" uniqKey="Christoffersson J" first="Jonas" last="Christoffersson">Jonas Christoffersson</name><name sortKey="Los, Marek J" sort="Los, Marek J" uniqKey="Los M" first="Marek J" last="Łos">Marek J. Łos</name></country><country name="France"><noRegion><name sortKey="Mehrpour, Maryam" sort="Mehrpour, Maryam" uniqKey="Mehrpour M" first="Maryam" last="Mehrpour">Maryam Mehrpour</name></noRegion></country><country name="Tunisie"><region name="Gouvernorat de Tunis"><name sortKey="Chaabane, Wiem" sort="Chaabane, Wiem" uniqKey="Chaabane W" first="Wiem" last="Chaabane">Wiem Chaabane</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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