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Author: Sandeep Kumar Barodia
Publisher: Frontiers Media SA
ISBN: 2889633349
Category :
Languages : en
Pages : 132
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Book Description
Several pathogenic mechanisms are involved in the pathogenesis of Parkinson’s Disease (PD), a neurodegenerative disease characterized by the loss of substantial nigra (SN) dopamine (DA) neurons. Alterations in calcium (Ca2+) homeostasis, cellular proteostasis, axonal transport, mitochondrial function, and neuroinflammation are linked to PD. However, research involving inter-organelle communication and their significance as precise mechanisms underlying neuronal death in PD remain to be elucidated. Evidence showed that perturbations in the mitochondria-endoplasmic reticulum (ER) network play an important role in the pathogenesis of PD. Alterations in the mitochondria-ER interface have been reported in PARK2 knockout mice and patients harboring PARK2 mutations. Enhanced parkin levels maintain mitochondria-ER cross-talk and assure regulated Ca2+ transfer to sustain cell bioenergetics. Several familial PD-related proteins, including Parkin and PINK1, may lead to modifications in the mitochondria-ER signaling. Interestingly, mitochondria-ER tethering suppresses mitophagy and parkin/PINK1-dependent mechanism regulates the destruction of mitochondria-ER contact sites by catalyzing a rapid burst of Mfn2 phospho-ubiquitination to trigger p97-dependent disassembly of Mfn2 complexes from the outer mitochondrial membrane. Mitofusin-mediated ER stress elicited neurodegeneration in Pink1/Parkin models of PD. α-Synuclein, a presynaptic protein, can bind to the ER-mitochondria tethering protein vesicle-associated membrane protein-associated protein B (VAPB) to disrupt Ca2+ homeostasis and mitochondrial ATP production. It has been reported that ER stress and mitochondrial cell death pathways might mediate A53T mutant α-synuclein-induced toxicity. Mitochondria-ER signaling mechanism is poorly characterized in neurons and its association in neuronal pathophysiology remains uncertain. The presence of mitochondria-ER contacts in neurons, preferentially at synapses, suggests a potential role in regulating synaptic activity. Alterations in mitochondria-ER associations are expected to be potentially detrimental to neurons, especially to SN DA neurons. Compounds from an unbiased chemical screen reverse both ER-to-Golgi trafficking defects and associated mitochondrial dysfunction in different PD models. In addition, a dibenzoylmethane derivative protects DA neurons against ER stress. Thus, mitochondria-ER signaling may represent a possible upstream drug target as potential therapeutic strategy for PD. In this Research Topic, we bring together knowledge that emphasizes the importance of mitochondria-ER communication and its impact to further dissect the pathogenic mechanisms in PD.
Author: Sandeep Kumar Barodia
Publisher: Frontiers Media SA
ISBN: 2889633349
Category :
Languages : en
Pages : 132
Get Book Here
Book Description
Several pathogenic mechanisms are involved in the pathogenesis of Parkinson’s Disease (PD), a neurodegenerative disease characterized by the loss of substantial nigra (SN) dopamine (DA) neurons. Alterations in calcium (Ca2+) homeostasis, cellular proteostasis, axonal transport, mitochondrial function, and neuroinflammation are linked to PD. However, research involving inter-organelle communication and their significance as precise mechanisms underlying neuronal death in PD remain to be elucidated. Evidence showed that perturbations in the mitochondria-endoplasmic reticulum (ER) network play an important role in the pathogenesis of PD. Alterations in the mitochondria-ER interface have been reported in PARK2 knockout mice and patients harboring PARK2 mutations. Enhanced parkin levels maintain mitochondria-ER cross-talk and assure regulated Ca2+ transfer to sustain cell bioenergetics. Several familial PD-related proteins, including Parkin and PINK1, may lead to modifications in the mitochondria-ER signaling. Interestingly, mitochondria-ER tethering suppresses mitophagy and parkin/PINK1-dependent mechanism regulates the destruction of mitochondria-ER contact sites by catalyzing a rapid burst of Mfn2 phospho-ubiquitination to trigger p97-dependent disassembly of Mfn2 complexes from the outer mitochondrial membrane. Mitofusin-mediated ER stress elicited neurodegeneration in Pink1/Parkin models of PD. α-Synuclein, a presynaptic protein, can bind to the ER-mitochondria tethering protein vesicle-associated membrane protein-associated protein B (VAPB) to disrupt Ca2+ homeostasis and mitochondrial ATP production. It has been reported that ER stress and mitochondrial cell death pathways might mediate A53T mutant α-synuclein-induced toxicity. Mitochondria-ER signaling mechanism is poorly characterized in neurons and its association in neuronal pathophysiology remains uncertain. The presence of mitochondria-ER contacts in neurons, preferentially at synapses, suggests a potential role in regulating synaptic activity. Alterations in mitochondria-ER associations are expected to be potentially detrimental to neurons, especially to SN DA neurons. Compounds from an unbiased chemical screen reverse both ER-to-Golgi trafficking defects and associated mitochondrial dysfunction in different PD models. In addition, a dibenzoylmethane derivative protects DA neurons against ER stress. Thus, mitochondria-ER signaling may represent a possible upstream drug target as potential therapeutic strategy for PD. In this Research Topic, we bring together knowledge that emphasizes the importance of mitochondria-ER communication and its impact to further dissect the pathogenic mechanisms in PD.
Author: Sandeep Kumar Barodia
Publisher:
ISBN:
Category :
Languages : en
Pages : 0
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Book Description
This eBook is a collection of articles from a Frontiers Research Topic. Frontiers Research Topics are very popular trademarks of the Frontiers Journals Series: they are collections of at least ten articles, all centered on a particular subject. With their unique mix of varied contributions from Original Research to Review Articles, Frontiers Research Topics unify the most influential researchers, the latest key findings and historical advances in a hot research area! Find out more on how to host your own Frontiers Research Topic or contribute to one as an author by contacting the Frontiers Editorial Office: frontiersin.org/about/contact.
Author: Lawrence H. Lash
Publisher: Elsevier
ISBN: 1483218619
Category : Science
Languages : en
Pages : 527
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Book Description
Methods in Toxicology, Volume 2: Mitochondrial Dysfunction provides a source of methods, techniques, and experimental approaches for studying the role of abnormal mitochondrial function in cell injury. The book discusses the methods for the preparation and basic functional assessment of mitochondria from liver, kidney, muscle, and brain; the methods for assessing mitochondrial dysfunction in vivo and in intact organs; and the structural aspects of mitochondrial dysfunction are addressed. The text also describes chemical detoxification and metabolism as well as specific metabolic reactions that are especially important targets or indicators of damage. The methods for measurement of alterations in fatty acid and phospholipid metabolism and for the analysis and manipulation of oxidative injury and antioxidant systems are also considered. The book further tackles additional methods on mitochondrial energetics and transport processes; approaches for assessing impaired function of mitochondria; and genetic and developmental aspects of mitochondrial disease and toxicology. The text also looks into mitochondrial DNA synthesis, covalent binding to mitochondrial DNA, DNA repair, and mitochondrial dysfunction in the context of developing individuals and cellular differentiation. Microbiologists, toxicologists, biochemists, and molecular pharmacologists will find the book invaluable.
Author: Yuzuru Imai
Publisher: Frontiers Media SA
ISBN: 2889713911
Category : Science
Languages : en
Pages : 165
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Book Description
Author: Amy K. Reeve
Publisher: Springer
ISBN: 3319286374
Category : Medical
Languages : en
Pages : 379
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Book Description
This second edition brings together up-to-date contributions from leaders in the field internationally on the various ways in which mitochondrial dysfunction contributes to the pathogenesis of neurodegenerative diseases, including Parkinson’s disease, Alzheimer’s disease and multiple sclerosis. The reader is guided through the basic functions of mitochondria and the mechanisms that lead to their dysfunction, and on to the consequences of this dysfunction for neuronal function before finishing with the modelling of these disorders and discussion of new potential therapeutic targets. Additional chapters have been added to the book to reflect advances in the field and there are many new contributors and topics, including how mitochondria are degraded and the interaction of the mitochondria with pathologically relevant proteins. Mitochondrial Dysfunction in Neurodegenerative Disorders provides an accessible, authoritative guide to this important area for neurologists; research and clinical neuroscientists; neuropathologists; and residents with an interest in clinical research.
Author: Jorge S. Valadas (Doctor in Biomedical Sciences)
Publisher:
ISBN:
Category :
Languages : en
Pages : 0
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Book Description
Author: Luis A. del Río
Publisher: Springer Science & Business Media
ISBN: 9400768893
Category : Medical
Languages : en
Pages : 353
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Book Description
Peroxisomes are a class of ubiquitous and dynamic single membrane-bounded cell organelles, devoid of DNA, with an essentially oxidative type of metabolism. In recent years it has become increasingly clear that peroxisomes are involved in a range of important cellular functions in almost all eukaryotic cells. In higher eukaryotes, including humans, peroxisomes catalyze ether phospholipids biosynthesis, fatty acid alpha-oxidation, glyoxylate detoxification, etc, and in humans peroxisomes are associated with several important genetic diseases. In plants, peroxisomes carry out the fatty acid beta-oxidation, photorespiration, metabolism of ROS, RNS and RSS, photomorphogenesis, biosynthesis of phytohormones, senescence, and defence against pathogens and herbivores. In recent years it has been postulated a possible contribution of peroxisomes to cellular signaling. In this volume an updated view of the capacity and function of peroxisomes from human, animal, fungal and plant origin as cell generators of different signal molecules involved in distinct processes of high physiological importance is presented.
Author: Victor Tapias
Publisher: Frontiers Media SA
ISBN: 2889634507
Category :
Languages : en
Pages : 209
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Book Description
Author: J.W. Langston
Publisher: IOS Press
ISBN: 1614993327
Category : Medical
Languages : en
Pages : 264
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Book Description
In the summer of 1982, hospital emergency rooms in the San Francisco Bay Area were suddenly confronted with mysteriously “frozen” patients – young men and women who, though conscious, could neither move nor speak. Doctors were baffled, until neurologist J. William Langston, recognizing the symptoms of advanced Parkinson’s disease, administered L-dopa – the only known effective treatment – and “unfroze” his patient. Dr. Langston determined that this patient and five others had all used the same tainted batch of synthetic heroin, inadvertently laced with a toxin that had destroyed an area of their brains essential to normal movement. This same area, the substantia nigra, slowly deteriorates in Parkinson’s disease. As scientists raced to capitalize on this breakthrough, Dr. Langston struggled to salvage the lives of his frozen patients, for whom L-dopa provided only short-term relief. The solution he found lay in the most daring area of research: fetal-tissue transplants. The astonishing recovery of two of his patients garnered worldwide press coverage, helped overturn federal restrictions on fetal-tissue research, and offered hope to millions suffering from Parkinson’s, Alzheimer’s, and other degenerative brain disorders. This is the story behind the headline – a spellbinding account that brings to life the intellectual excitement, ethical dilemmas, and fierce competitiveness of medical research. This new updated edition of the classic neurological mystery tale, “The Case of the Frozen Addicts,” illuminates how the solution to a baffling mystery of the brain’s chemistry opened a new frontier in medicine and restored life to people without hope. “It begins with a series of quixotic discoveries, escalates to providing possible solutions for one of humanity’s most intractable medical problems, and then catapults the reader into the center of America’s hottest political arena – abortion and fetal sanctity. Bravo! A brilliant read.” – Laurie Garrett, author of The Coming Plague “[Langston and Palfreman] weave a highly readable and spellbinding medical detective tale... It is as absorbing as a good mystery, as entertaining as an exciting novel, and as enlightening as a good biography.” – Stanley Fahn, New England Journal of Medicine “I could not put it down... it is the lives of the ‘frozen addicts’ themselves – and the fullness with which this is presented – which makes the whole thing overwhelming.” – Oliver Sacks
Author: Paul C. Guest
Publisher: Springer Nature
ISBN: 3030550354
Category : Science
Languages : en
Pages : 274
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Book Description
Aging is an inevitable part of life, and is becoming a worldwide social, economic and health problem due to the fact that an increasing proportion of individuals in the advanced age category have a higher probability of developing age-related disorders. New therapeutic approaches are still in need to decrease or slow the effects of such diseases in this aging society. Advances in ‘omic technologies such as genomics, transcriptomics, proteomics and metabolomics have significantly advanced our understanding of diseases in multiple medical areas. It is hoped that emerging hits from these analyses might be prioritized for further screening as potential novel drug targets for increasing the human healthspan in line with the lifespan, which will in turn lead to new therapeutic strategies and drug development projects by the pharmaceutical industry. This new book presents a series of reviews describing studies which have resulted in the identification of potential new drug targets for age-related disorders. Much of this information has come from ‘omic comparisons of healthy and disease states or from testing the effects of potential new therapeutic approaches. Each chapter will be presented in the context of specific chronic diseases or different therapeutic strategies, providing important information on disease mechanisms related to the aging process. This book will be of interest to researchers in the areas of aging and chronic disease, as well as clinical scientists, physicians, and major drug companies. With contributors from Australia, Brazil, Canada, France, Germany, India, Iran, Iraq, South Africa, South Korea, Thailand, Ukraine, United Kingdom, United States of America, Uruguay and Vietnam, this is a timely follow up to Guest’s previous book Reviews on New Drug Targets in Age-Related Disorders.
