Keywords:
Mitochondria - Formation.
;
Electronic books.
Type of Medium:
Online Resource
Pages:
1 online resource (526 pages)
Edition:
1st ed.
ISBN:
9781119017103
Series Statement:
Wiley Series on Neuropharmacology Series
URL:
https://ebookcentral.proquest.com/lib/geomar/detail.action?docID=4045097
DDC:
572.8/69
Language:
English
Note:
Intro -- TITLE PAGE -- TABLE OF CONTENTS -- CONTRIBUTORS -- PREFACE -- SECTION I: MITOCHONDRIAL STRUCTURE AND ION CHANNELS -- 1 MITOCHONDRIAL PERMEABILITY TRANSITION: A LOOK FROM A DIFFERENT ANGLE -- 1.1 REGULATION OF INTRACELLULAR CALCIUM IN NEURONS -- 1.2 CALCIUM OVERLOAD AND MITOCHONDRIAL PERMEABILITY TRANSITION -- 1.3 THE MITOCHONDRIAL TRANSITION PORE -- ACKNOWLEDGMENTS -- REFERENCES -- 2 THE MITOCHONDRIAL PERMEABILITY TRANSITION PORE, THE c-SUBUNIT OF THE F1Fo ATP SYNTHASE, CELLULAR DEVELOPMENT, AND SYNAPTIC EFFICIENCY -- 2.1 INTRODUCTION -- 2.2 MITOCHONDRIA AT THE CENTER OF CELL METABOLISM AND CELL DEATH -- 2.3 MITOCHONDRIAL INNER MEMBRANE LEAK: REGULATOR OF METABOLIC RATE AND UNCOUPLING -- 2.4 MITOCHONDRIAL INNER MEMBRANE CHANNELS AND EXCHANGERS ARE NECESSARY FOR Ca2+ CYCLING AND CELLULAR Ca2+ DYNAMICS -- 2.5 MITOCHONDRIAL INNER AND OUTER MEMBRANE CHANNEL ACTIVITY REGULATES Ca2+ RE-RELEASE FROM MITOCHONDRIA AFTER BUFFERING -- 2.6 BCL-2 FAMILY PROTEINS REGULATE PATHOLOGICAL OUTER MITOCHONDRIAL MEMBRANE PERMEABILIZATION (MOMP) -- 2.7 PATHOLOGICAL INNER MEMBRANE DEPOLARIZATION: MITOCHONDRIAL PERMEABILITY TRANSITION -- 2.8 THE QUEST FOR AN INNER MEMBRANE Ca2+-SENSITIVE UNCOUPLING CHANNEL: THE PT PORE -- 2.9 THE mPTP: A MOLECULAR DEFINITION -- 2.10 CLOSING OF THE mPTP MAY ENHANCE MITOCHONDRIAL METABOLIC PLASTICITY AND REGULATE SYNAPTIC PROPERTIES IN HIPPOCAMPAL NEURONS -- 2.11 mPTP OPENING CORRELATES WITH CELL DEATH IN ACUTE ISCHEMIA, ROS DAMAGE, OR GLUTAMATE EXCITOTOXICITY -- 2.12 PRO-APOPTOTIC PROTEOLYTIC CLEAVAGE FRAGMENT OF Bcl-xL CAUSES LARGE CONDUCTANCE MITOCHONDRIAL ION CHANNEL ACTIVITY CORRELATED WITH HYPOXIC SYNAPTIC FAILURE: OUTER MITOCHONDRIAL CHANNEL MEMBRANE ACTIVITY ALONE OR mPTP? -- 2.13 SYNAPTIC RESPONSES DECLINE DURING LONG-TERM DEPRESSION IN AsSOCIATION WITH BCL-2 FAMILY-REGULATED MITOCHONDRIAL CHANNEL ACTIVITY.
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2.14 SYNAPSE LOSS DURING NEURODEGENERATIVE DISEASE MAY REQUIRE MITOCHONDRIAL CHANNEL ACTIVITY -- 2.15 CONCLUSIONS -- ACKNOWLEDGMENTS -- REFERENCES -- 3 MITOCHONDRIAL CHANNELS IN NEURODEGENERATION -- 3.1 INTRODUCTION -- 3.2 Mitochondrial Channels in the Healthy Neuron -- 3.3 MITOCHONDRIAL CHANNELS IN THE DYING CELL -- 3.4 MITOCHONDRIAL CHANNELS IN NEURODEGENERATIVE DISEASES -- 3.5 CONCLUSIONS -- REFERENCES -- SECTION II: CONTROL OF MITOCHONDRIAL SIGNALING NETWORKS -- 4 MITOCHONDRIAL Ca2+ TRANSPORT IN THE CONTROL OF NEURONAL FUNCTIONS: MOLECULAR AND CELLULAR MECHANISMS -- 4.1 INTRODUCTION -- 4.2 PHYSIOLOGICAL AND PHARMACOLOGICAL CHARACTERISTICS OF MITOCHONDRIAL Ca2+ TRANSPORT IN NEURONS -- 4.3 MOLECULAR COMPONENTS OF MITOCHONDRIAL Ca2+ TRANSPORT IN NEURONS -- 4.4 MITOCHONDRIAL Ca2+ SIGNALING AND NEURONAL EXCITABILITY -- 4.5 MITOCHONDRIAL Ca2+ CYCLING IN THE REGULATION OF SYNAPTIC TRANSMISSION -- 4.6 MITOCHONDRIAL Ca2+ TRANSPORT AND THE REGULATION OF GENE EXPRESSION IN NEURONS -- 4.7 FUTURE DIRECTIONS -- ACKNOWLEDGMENTS -- REFERENCES -- 5 AMP-ACTIVATED PROTEIN KINASE (AMPK) AS A CELLULAR ENERGY SENSOR AND THERAPEUTIC TARGET FOR NEUROPROTECTION -- 5.1 INTRODUCTION -- 5.2 CONCLUSION AND FUTURE PERSPECTIVES -- REFERENCES -- 6 HDAC6: A MOLECULE WITH MULTIPLE FUNCTIONS IN NEURODEGENERATIVE DISEASES -- 6.1 INTRODUCTION -- 6.2 MOLECULAR PROPERTIES OF HDAC6 -- 6.3 HDAC6 AND NEURODEGENERATIVE DISEASES -- 6.4 PERSPECTIVES -- REFERENCES -- 7 NEURONAL MITOCHONDRIAL TRANSPORT -- 7.1 INTRODUCTION -- 7.2 COMPLEX MOTILITY PATTERNS OF AXONAL MITOCHONDRIA -- 7.3 MECHANISMS OF MITOCHONDRIAL TRANSPORT -- 7.4 MECHANISMS OF AXONAL MITOCHONDRIAL ANCHORING -- 7.5 REGULATION OF MITOCHONDRIAL TRANSPORT BY SYNAPTIC ACTIVITY -- 7.6 MITOCHONDRIAL TRANSPORT AND SYNAPTIC TRANSMISSION -- 7.7 MITOCHONDRIAL TRANSPORT AND PRESYNAPTIC VARIABILITY.
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7.8 MITOCHONDRIAL TRANSPORT AND AXONAL BRANCHING -- 7.9 MITOCHONDRIAL TRANSPORT AND MITOPHAGY -- 7.10 CONCLUSIONS AND NEW CHALLENGES -- ACKNOWLEDGMENTS -- REFERENCES -- 8 MITOCHONDRIA IN CONTROL OF HYPOTHALAMIC METABOLIC CIRCUITS -- 8.1 INTRODUCTION -- 8.2 YIN-YANG RELATIONSHIP BETWEEN COMPONENTS OF HYPOTHALAMIC FEEDING AND SATIETY CIRCUITS -- 8.3 MITOCHONDRIA AND THEIR DYNAMICS -- 8.4 METABOLIC PRINCIPLES OF HUNGER AND SATIETY PROMOTION: MITOCHONDRIA IN SUPPORT OF FAT VERSUS GLUCOSE UTILIZATION -- 8.5 MITOCHONDRIA DYNAMICS AND CELLULAR ENERGETICS -- 8.6 MITOCHONDRIAL DYSFUNCTION AND METABOLIC DISORDERS -- 8.7 CONCLUSIONS -- REFERENCES -- 9 MITOCHONDRIA ANCHORED AT THE SYNAPSE -- 9.1 INTRODUCTION -- 9.2 CALIBRATED POSITIONING OF MITOCHONDRIA -- 9.3 MITOCHONDRIA AND CRISTA STRUCTURE -- 9.4 ADHERING JUNCTIONS AND LINKAGES TO THE CYTOSKELETON -- 9.5 LINKAGES OF THE OMM TO THE MITOCHONDRIAL PLAQUE AND RETICULATED MEMBRANE -- 9.6 FUNCTIONS OF THE ORGANELLE COMPLEX -- 9.7 MACs AND FILAMENTOUS CONTACTS: A CONTINUUM OF STRUCTURE? -- ACKNOWLEDGMENTS -- REFERENCES -- SECTION III: DEFECTIVE MITOCHONDRIAL DYNAMICS AND MITOPHAGY -- 10 NEURONAL MITOCHONDRIA ARE DIFFERENT: RELEVANCE TO NEURODEGENERATIVE DISEASE -- 10.1 INTRODUCTION -- 10.2 MITOCHONDRIAL DYNAMICS IN NEURONS AND NEURODEGENERATIVE DISEASE -- 10.3 TRIGGERING MITOPHAGY IN NEURONS VERSUS OTHER CELL TYPES -- 10.4 BCL-xL: THE GUARDIAN OF MITOCHONDRIA -- ACKNOWLEDGMENTS -- REFERENCES -- 11 PINK1 AS A SENSOR FOR MITOCHONDRIAL FUNCTION: DUAL ROLES -- 11.1 INTRODUCTION -- 11.2 PINK1 PROMOTES MITOCHONDRIAL FUNCTION -- 11.3 HEALTHY MITOCHONDRIA IMPORT AND PROCESS PINK1 -- 11.4 ACCUMULATION OF FULL LENGTH-PINK1 AS A SENSOR OF MITOCHONDRIAL DYSFUNCTION -- 11.5 CYTOSOLIC PINK1 AS A SENSOR FOR MITOCHONDRIAL FUNCTION -- 11.6 PINK1 AND MITOCHONDRIAL DYNAMICS.
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11.7 DUAL ROLES FOR PINK1 AS A SENSOR OF MITOCHONDRIAL FUNCTION AND DYSFUNCTION -- REFERENCES -- 12 A GET-TOGETHER TO TEAR IT APART: THE MITOCHONDRION MEETS THE CELLULAR TURNOVER MACHINERY -- 12.1 MITOCHONDRIAL QUALITY CONTROL IN NEURODEGENERATION -- 12.2 AN OVERVIEW OF THE UBIQUITIN-PROTEASOME SYSTEM -- 12.3 ACTIVITIES OF THE CYTOSOLIC PROTEASOME AT THE OUTER MITOCHONDRIAL MEMBRANE -- 12.4 THE TURNOVER OF WHOLE MITOCHONDRIA BY MITOPHAGY -- 12.5 PROTEASOMES AND PHAGOPHORES CONVERGE IN THE PINK1/PARKIN PATHWAY -- 12.6 IMPLICATIONS OF PINK1-/PARKIN-DEPENDENT MITOPHAGY IN THE BRAIN AND IN PD -- 12.7 EMERGING MITOCHONDRIAL QUALITY CONTROL MECHANISMS -- REFERENCES -- 13 MITOCHONDRIAL INVOLVEMENT IN NEURODEGENERATIVE DEMENTIA -- 13.1 INTRODUCTION -- 13.2 MITOCHONDRIAL DYSFUNCTION IN ALZHEIMER DISEASE -- 13.3 MITOCHONDRIAL DYSFUNCTION, BIOENERGETIC DEFICITS, AND OXIDATIVE STRESS IN AD -- 13.4 MITOCHONDRIAL FRAGMENTATION IN AD -- 13.5 SYNAPTIC MITOCHONDRIA IN AD -- 13.6 MITOCHONDRIAL DYSFUNCTION AND CATIONIC DYSHOMEOSTASIS IN AD -- 13.7 MITOCHONDRIAL DYSFUNCTION IN DLB -- 13.8 LRRK2 MUTATIONS, MITOCHONDRIA AND DLB -- 13.9 AKINETIC CRISIS IN SYNUCLEINOPATHIES IS LINKED TO GENETIC MUTATIONS INVOLVING MITOCHONDRIAL PROTEINS -- 13.10 CONCLUSIONS -- REFERENCES -- SECTION IV: MITOCHONDRIA-TARGETED THERAPEUTICS AND MODEL SYSTEMS -- 14 NEURONAL MITOCHONDRIA AS A TARGET FOR THE DISCOVERY AND DEVELOPMENT OF NEW THERAPEUTICS -- 14.1 NEURODEGENERATIVE DISORDERS AND THE STATUS OF DRUG DISCOVERY -- 14.2 MITOCHONDRIA AS TARGETS FOR THE DEVELOPMENT OF NEW NDD THERAPIES -- 14.3 THE EFFECTS OF DEXPRAMIPEXOLE ON MITOCHONDRIAL CONDUCTANCES: AN EXAMPLE OF AN APPROACH FOR ALS AND OTHER NDDs -- 14.4 WHAT IS THE FUTURE OF A MITOCHONDRIAL APPROACH FOR NDD THERAPY? -- ACKNOWLEDGMENTS -- REFERENCES -- 15 MITOCHONDRIA AS A THERAPEUTIC TARGET FOR ALZHEIMER'S DISEASE -- 15.1 INTRODUCTION.
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15.2 MITOCHONDRIAL ABNORMALITIES AND DYSFUNCTION IN ALZHEIMER'S DISEASE -- 15.3 MITOCHONDRIA AS A DRUG TARGET -- 15.4 CONCLUSIONS -- REFERENCES -- 16 MITOCHONDRIA IN PARKINSON'S DISEASE -- 16.1 INTRODUCTION -- 16.2 ROLE OF MITOCHONDRIA IN SPORADIC PD -- 16.3 MITOCHONDRIAL DYSFUNCTION IN MONOGENIC PD -- 16.4 CONCLUSIONS -- REFERENCES -- 17 THERAPEUTIC TARGETING OF NEURONAL MITOCHONDRIA IN BRAIN INJURY -- 17.1 INTRODUCTION -- 17.2 MITOCHONDRIA BIOENERGETICS -- 17.3 TRAUMATIC BRAIN INJURY -- 17.4 PHARMACEUTICAL INTERVENTIONS -- 17.5 CONCLUSION -- REFERENCES -- 18 THE USE OF FIBROBLASTS FROM PATIENTS WITH INHERITED MITOCHONDRIAL DISORDERS FOR PATHOMECHANISTIC STUDIES AND EVALUATION OF THERAPIES -- 18.1 INTRODUCTION -- 18.2 PATHOMECHANISTIC STUDIES OF MITOCHONDRIAL DISORDERS IN PATIENTS' FIBROBLASTS -- 18.3 EVALUATION OF THERAPEUTIC OPTIONS USING PATIENT DERIVED FIBROBLASTS -- 18.4 CONCLUSION -- ACKNOWLEDGMENTS -- REFERENCES -- INDEX -- END USER LICENSE AGREEMENT.
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