Download or read book Mitochondrial Mechanisms of Degeneration and Repair in Parkinson s Disease written by Lori M. Buhlman and published by Springer. This book was released on 2016-09-13 with total page 279 pages. Available in PDF, EPUB and Kindle. Book excerpt: This volume brings together various theories of how aberrations in mitochondrial function and morphology contribute to neurodegeneration in idiopathic and familial forms of Parkinson’s disease. Moreover, it comprehensively reviews the current search for therapies, and proposes how molecules are involved in specific functions as attractive therapeutic targets. It is expected to facilitate critical thought and discussion about the fundamental aspects of neurodegeneration in Parkinson’s disease and foster the development of therapeutic strategies among researchers and graduate students. Theories of idiopathic Parkinson’s etiology support roles for chronic inflammation and exposure to heavy metals or pesticides. Interestingly, as this project proposes, a case can be made that abnormalities in mitochondrial morphology and function are at the core of each of these theories. In fact, the most common approach to the generation of animal and cell-culture models of idiopathic Parkinson’s disease involves exposure to mitochondrial toxins. Even more compelling is the fact that most familial patients harbor genetic mutations that cause disruptions in normal mitochondrial morphology and function. While there remains to be no effective treatment for Parkinson’s disease, efforts to postpone, prevent and “cure” onset mitochondrial aberrations and neurodegeneration associated with Parkinson’s disease in various models are encouraging. While only about ten percent of Parkinson’s patients inherit disease-causing mutations, discovering common mechanisms by which familial forms of Parkinson’s disease manifest will likely shed light on the pathophysiology of the more common idiopathic form and provide insight to the general process of neurodegeneration, thus revealing therapeutic targets that will become more and more accessible as technology improves.

Download or read book Mitochondria and Endoplasmic Reticulum Dysfunction in Parkinson s Disease written by Sandeep Kumar Barodia and published by Frontiers Media SA. This book was released on 2020-01-23 with total page 132 pages. Available in PDF, EPUB and Kindle. Book excerpt: 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.

Download or read book Mitochondrial Dysfunction in Neurodegenerative Disorders written by Amy Katherine Reeve and published by Springer Science & Business Media. This book was released on 2011-11-15 with total page 252 pages. Available in PDF, EPUB and Kindle. Book excerpt: As age related diseases increase in prevalence and impact more significantly on medical resources it is imperative to understand these diseases and the mechanisms behind their progression. New research has stimulated a growing interest in mitochondrial involvement in neurodegenerative disorders such as Parkinson’s disease, Alzheimer’s disease and multiple sclerosis and the mechanisms which lead from mitochondrial dysfunction to neurodegeneration. Mitochondrial Dysfunction in Neurodegenerative Disorders brings together contributions from leaders in the field internationally on the various ways in which mitochondrial dysfunction contributes to the pathogenesis of these diseases, guiding the reader through the basic functions of mitochondria and the mechanisms that lead to their dysfunction, to the consequences of this dysfunction on neuronal function before finishing with the modelling of these disorders and discussion of new potential therapeutic targets. 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.

Download or read book Mitochondrial Dysfunction written by Lawrence H. Lash and published by Elsevier. This book was released on 2013-10-22 with total page 527 pages. Available in PDF, EPUB and Kindle. Book excerpt: 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.

Download or read book Etiology of Parkinson s Disease written by Jonas H. Ellenberg and published by CRC Press. This book was released on 1995-03-01 with total page 600 pages. Available in PDF, EPUB and Kindle. Book excerpt: This comprehensive reference provides a detailed overview of current concepts regarding the cause of Parkinson's disease-emphasizing the issues involved in the design, implementation, and analysis of epidemiological studies of parkinsonism.

Download or read book Molecular Links Between Mitochondrial Damage and Parkinson s Disease and Related Disorders written by Yuzuru Imai and published by Frontiers Media SA. This book was released on 2021-09-28 with total page 165 pages. Available in PDF, EPUB and Kindle. Book excerpt:

Download or read book Mitochondrial Dynamics and Neurodegeneration written by Bingwei Lu and published by Springer Science & Business Media. This book was released on 2011-05-16 with total page 271 pages. Available in PDF, EPUB and Kindle. Book excerpt: Mitochondria are essential organelles in eukaryotic cells that control such diverse processes as energy metabolism, calcium buffering, and cell death. Recent studies have revealed that changes in mitochondrial morphology by fission and fusion, a process known as mitochondrial dynamics, is particularly important for neuronal function and survival. Defects in this process are commonly found in neurodegenerative diseases, offering a new paradigm for investigating mechanisms of neurodegeneration. To provide researchers working on neurodegenerative diseases and mitochondria with updated information on this rapidly progressing field, we have invited experts in the field to critically review recent progresses and identify future research directions. The topics include genetics of mitochondrial dynamics, mitochondrial dynamics and bioenergetics, autophagy, apoptosis, and axonal transport, and its role in neurological diseases, including Alzheimer’s, Parkinson’s, and Huntington’s diseases.

Download or read book Oxidative Stress and Redox Signalling in Parkinson s Disease written by Rodrigo Franco and published by Royal Society of Chemistry. This book was released on 2017-07-25 with total page 537 pages. Available in PDF, EPUB and Kindle. Book excerpt: Parkinson's Disease is the second most common neurodegenerative disorder affecting millions of people worldwide. In order to find neuroprotective strategies, a clear understanding of the mechanisms involved in the dopaminergic death of cells that progresses the disease is needed. Oxidative stress can be defined as an imbalance between the production of reactive species and the ability to detoxify them and their intermediates or by-products. Oxidative damage to lipids, proteins, and DNA has been detected in autopsies from individuals with Parkinson’s Disease and so links can be made between oxidative stress and Parkinson’s Disease pathogenesis. This book provides a thorough review of the mechanisms by which oxidative stress and redox signalling mediate Parkinson’s Disease. Opening chapters bring readers up to speed on basic knowledge regarding oxidative stress and redox signalling, Parkinson’s Disease, and neurodegeneration before the latest advances in this field are explored in detail. Topics covered in the following chapters include the role of mitochondria, dopamine metabolism, metal homeostasis, inflammation, DNA-damage and thiol-signalling. The role of genetics and gene-environment interactions are also explored before final chapters discuss the identification of potential biomarkers for diagnosis and disease progression and the future of redox/antioxidant based therapeutics. Written by recognized experts in the field, this book will be a valuable source of information for postgraduate students and academics, clinicians, toxicologists and risk assessment groups. Importantly, it presents the current research that might later lead to redox or antioxidant – based therapeutics for Parkinson’s disease.

Download or read book Mitochondrial Dysfunction and Neurodegeneration written by Victor Tapias and published by Frontiers Media SA. This book was released on 2020-01-30 with total page 209 pages. Available in PDF, EPUB and Kindle. Book excerpt:

Download or read book Mitochondrial Mechanisms of Neuronal Injury written by and published by . This book was released on 2002 with total page 70 pages. Available in PDF, EPUB and Kindle. Book excerpt: This project is focused on understanding the mechanisms of neuronal injury in acute and chronic neurodegenerative diseases. In particular, we are interested in the role that mitochondria play in both the maintenance of neuronal viability and in the execution of neurons following injurious stimuli. Our prior studies have shown that mitochondria are an essential target for calcium overload in excitotoxic neuronal injury. In the experiments described here we are pursuing the study of mitochondria in neurons in additional ways. We are developing a model of neuronal injury in an organotypic slice preparation that should provide insights into mitochondrial events in doparninergic neurons. We hope that this will allow the study of mitochondrial physiology in neurons that are selectively vulnerable in Parkinson's disease. In addition, we are investigating the properties of mitochondrial trafficking in neurons, which, together with an in situ study of mitochondrial DNA replication, will start to provide an unprecedented insight into mitochondrial biogenesis, movement and turnover. We believe that an understanding of the long-term properties of mitochondria in neurons will provide information that is critical to the full appreciation of the mechanisms of neuronal injury in chronic neurodegenerative disease.

Download or read book Mitochondrial Function and Dysfunction written by Anthony Schapira and published by Elsevier. This book was released on 2003-01-10 with total page 581 pages. Available in PDF, EPUB and Kindle. Book excerpt: Mitochondria are critical to the survival of cells, therefore, it is not surprising that abnormalities in mitochondrial function may lead to human disease. This book concentrates on the biology and pathology of mitochondria, covering some ot the important basic science features of the biology of mitochondria. It then moves on to discuss the breadth of human diseases related to mitochondrial dysfunction, including Parkinson's disease, Amyotrophic Lateral Sclerosis (ALS), and Alzheimer's disease.* Provides comprehensive coverage of basic science and clinical features of mitochondrial dysfunction* Presents detailed analysis of "hot" topics in mitochondrial function and neurodegenerative diseases* Includes outstanding list of contributing authors

Download or read book Neuronal and Mitochondrial Protection in Chronic Parkinsonism written by Gaurav Deepak Patki and published by . This book was released on 2010 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt: Among the several plausible neuropathological hypotheses underlying the progression of aging and neurodegenerative diseases such as Parkinson's disease (PD), oxidative stress and mitochondrial damage have emerged as one of the attractive biochemical mechanisms. However, most of the past studies linking mitochondrial dysfunction to neuronal degeneration have been carried out in vitro or in acute in vivo studies. It is not known whether mitochondrial dysfunction is an immediate response to cytotoxic-inducing agents or is sustained as a long-term consequence of neuronal death. The purpose of our research was to first validate the chronic mouse model of Parkinson's disorder (MPD), which has been developed and characterized by our laboratory as a suitable animal model for investigating neuronal and mitochondrial dysfunctions and then to examine the protective effects of endurance exercise and melatonin treatment on this model. Male, C57/BL retired breeder mice at 6-10 months of age were used in the present study. The aged chronic MPD was treated with of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) (15 mg/kg, s.c), twice a week for 5 weeks. MPTP was co-administered with probenecid (250 mg/kg, i.p), an adjuvant that is known to inhibit the peripheral and neuronal clearance of MPTP and potentiate the neurotoxicity of MPTP. The chronic MPD was previously shown to display neurochemical, histological, behavioral and pathological features resembling those of PD-like neurodegeneration lasting for at least 6 months. Six to twelve weeks after chronic MPTP treatment, aged mice showed sustained decrease in striatal mitochondrial respiration as well as loss of antioxidant enzymes, Cu-Zn superoxide dismutase (SOD), Mn SOD and cytochrome c (cyt c) expression. Striatal mitochondrial dysfunction correlated with dopamine neuron and behavioral deficits in the aged chronic MPD. When the chronic MPD was exercise-trained on a motorized treadmill 5 days/week for 18 weeks, the dopamine neuronal, mitochondrial and behavioral deficits as seen in the sedentary chronic MPD were prevented. Melatonin (5 mg/kg, i.p), a known natural antioxidant and free radical scavenger was injected to the chronic MPD 5 days/week for 18 weeks. Melatonin alone did not alter the striatal neuronal, mitochondrial and motor functions in normal mice. However, melatonin was effective to reverse dopaminergic, mitochondrial and motor impairment as exercise did to the chronic MPD. We conclude that endurance exercise training and melatonin treatment are effective neuroprotective and mitochondrial protective measures in the chronic MPD. Exercise and melatonin treatment may have the potential to slow the progression of PD related neurodegeneration.

Download or read book Mitochondrial Dynamics and Neurodegeneration written by Bingwei Lu and published by Springer. This book was released on 2013-01-02 with total page 260 pages. Available in PDF, EPUB and Kindle. Book excerpt: Mitochondria are essential organelles in eukaryotic cells that control such diverse processes as energy metabolism, calcium buffering, and cell death. Recent studies have revealed that changes in mitochondrial morphology by fission and fusion, a process known as mitochondrial dynamics, is particularly important for neuronal function and survival. Defects in this process are commonly found in neurodegenerative diseases, offering a new paradigm for investigating mechanisms of neurodegeneration. To provide researchers working on neurodegenerative diseases and mitochondria with updated information on this rapidly progressing field, we have invited experts in the field to critically review recent progresses and identify future research directions. The topics include genetics of mitochondrial dynamics, mitochondrial dynamics and bioenergetics, autophagy, apoptosis, and axonal transport, and its role in neurological diseases, including Alzheimer’s, Parkinson’s, and Huntington’s diseases.

Download or read book Mitochondrial Dysfunction in Ageing and Diseases written by Jaime M. Ross and published by MDPI. This book was released on 2018-09-28 with total page 543 pages. Available in PDF, EPUB and Kindle. Book excerpt: This book is a printed edition of the Special Issue "Mitochondrial Dysfunction in Ageing and Diseases" that was published in IJMS

Download or read book Mechanisms of Cell Death and Approaches to Neuroprotection Disease Modification in Parkinson s Disease written by and published by Academic Press. This book was released on 2021-11-10 with total page 316 pages. Available in PDF, EPUB and Kindle. Book excerpt: Mechanisms of Cell Death and Approaches to Neuroprotection/Disease Modification in Parkinson's Disease explores the results of numerous studies surrounding in vitro and animal model evidence that looks at the impact of a-synucleinopathy on neuronal dysfunction and behavioral impairments, (ii) how research in animal models supports the development of therapeutic strategies, and (iii) how findings in animal models might relate to the disease process in humans. In this book, the author's shed light upon the complex scenario of the mechanisms of cell death and approaches to neuroprotection/disease modification in PD, both in vitro to in vivo. Along with degeneration, the pathological hallmark of PD is the presence of intraneuronal proteinaceous cytoplasmic inclusions, named Lewy Bodies (LB) that invade the whole nervous system as the disease progresses. Several fundamental discoveries have shed light upon the implication of the a-syn protein in the pathogenesis of familial and sporadic forms of PD. Other proteins also accumulate in LB, but a-syn is a major protein component of the pathological landmarks. - Updates on the latest research surrounding Mechanisms of Cell Death in Parkinson's Disease - Includes In vitro and In vivo models of synucleinopathy - Presents therapeutic strategies in Parkinson's Disease

Download or read book Parkinson s Disease Genes Orchestrate Mechanisms of Mitochondrial Quality Control written by Gian-Luca McLelland and published by . This book was released on 2018 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt: "A functional mitochondrial network is cardinal to cellular fitness, and declines in mitochondrial function are linked to neurodegeneration, most notably the motor disorder Parkinson's disease. Two genes mutated in autosomal recessive juvenile parkinsonism, PARKIN and PINK1, work together to maintain mitochondrial health in vivo. Study over the past decade has revealed that PARKIN and PINK1 constitute a molecular system that recognizes and destroys damaged mitochondria via the autophagy pathway, in a process known as mitophagy. By removing dysfunctional organelles from the reticulum via this quality control mechanism, the PARKIN/PINK1 pathway protects the integrity of the mitochondrial network. The work comprised within this thesis delves into the mechanism of PINK1/PARKIN mitochondrial quality control. Firstly, it is shown that, in addition to mitophagy, PARKIN and PINK1 function in a second quality control mechanism that oversees the removal of damaged mitochondrial components, preserving mitochondrial function in the absence of organellar destruction. Selected, damaged mitochondrial cargo are extracted from the organelle via a class of mitochondrial-derived vesicles (MDVs), which are shuttled to the lysosome for turnover in a manner involving classical membrane fusion factors. Secondly, the work here demonstrates that uncoupling of mitochondria from the endoplasmic reticulum via the destruction of a tethering factor represents an important step in the mitophagic cascade. Together, these findings have furthered our understanding regarding the cellular toolkit that maintains mitochondrial health, and how its deterioration can lead to neurodegenerative disease." --

Download or read book Homeostatic Control of Brain Function written by Detlev Boison and published by Oxford University Press. This book was released on 2016 with total page 657 pages. Available in PDF, EPUB and Kindle. Book excerpt: Homeostatic Control of Brain Function offers a broad view of brain health and diverse perspectives for potential treatments, targeting key areas such as mitochondria, the immune system, epigenetic changes, and regulatory molecules such as ions, neuropeptides, and neuromodulators. Loss of homeostasis becomes expressed as a diverse array of neurological disorders. Each disorder has multiple comorbidities - with some crossing over several conditions - and often disease-specific treatments remain elusive. When current pharmacological therapies result in ineffective and inadequate outcomes, therapies to restore and maintain homeostatic functions can help improve brain health, no matter the diagnosis. Employing homeostatic therapies may lead to future cures or treatments that address multiple comorbidities. In an age where brain diseases such as Alzheimer's or Parkinson's are ever present, the incorporation of homeostatic techniques could successfully promote better overall brain health. Key Features include · A focus on the homeostatic controls that significantly depend on the way one lives, eats, and drinks. · Highlights from emerging research in non-pharmaceutical therapies including botanical medications, meditation, diet, and exercise. · Incorporation of homeostatic therapies into existing basic and clinical research paradigms. · Extensive scientific basic and clinical research ranging from molecules to disorders. · Emerging practical information for improving homeostasis. · Examples of homeostatic therapies in preventing and delaying dysfunction. Both editors, Detlev Boison and Susan Masino, bring their unique expertise in homeostatic research to the overall scope of this work. This book is accessible to all with an interest in brain health; scientist, clinician, student, and lay reader alike.