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This book reviews the functions and roles of DJ-1 in various oxidative stress-related diseases and applications of DJ-1 and its binding compounds to the diseases. The DJ-1 gene was first found to be a novel oncogene in 1997 and later, in 2003, also found to be a causative gene for a familial form of Parkinson’s disease (PD), park7. The DJ-1 gene is therefore the first gene discovered that is known to cause cancer and neurodenegerative diseases, including PD. The research field has expanded as the research has developed. Thus this volume begins with a general introduction of DJ-1, and explains the history and research development to understand the following chapters. Those chapters present the roles of DJ-1 in various oxidative stress-related diseases such as neurodegenerative diseases, as well as cancer, diabetes, and fertility. Moreover, several chapters present evidence that DJ-1 is useful for therapeutic strategies against these diseases. The reader will discover that DJ-1 is a promising protein both for basic cell biology and for the mechanism and therapy for oxidative stress-related diseases.
Oxidative stress is the result of an imbalance in pro-oxidant/antioxidant homeostasis that leads to the generation of toxic reactive oxygen species. Brain cells are continuously exposed to reactive oxygen species generated by oxidative metabolism, and in certain pathological conditions defense mechanisms against oxygen radicals may be weakened and/or overwhelmed. DNA is a potential target for oxidative damage, and genomic damage can contribute to neuropathogenesis. It is important therefore to identify tools for the quantitative analysis of DNA damage in models on neurological disorders. This book presents detailed information on various neurodegenerative disorders and their connection with oxidative stress. This information will provide clinicians with directions to treat these disorders with appropriate therapy and is also of vital importance for the drug industries for the design of new drugs for treatment of degenerative disorders.* Contains the latest information on the subject of neurodegenerative disorders* Reflects on various factors involved in degeneration and gives suggestions for how to tackle these problems
Most proteins undergo post-translational modifications altering physical and chemical properties, folding, conformation distribution, stability, activity and function. Ubiquitin and SUMOs are related small proteins that are members of the large ubiquitin superfamily of post-translational modifiers. Written by highly respected leaders in their fields under the expert guidance of the editor, this volume covers the principles of ubiquitination and SUMOylation, presents detailed reviews of current and emerging concepts and highlights new advances in all areas of SUMOylation and ubiquitination. Topics of note include: the ubiquitin superfamily, the ubiquitin toolbox, onco viral exploitation of the SUMO system, small molecule modulators of desumoylation, mass spectrometry, global proteomic profiling of SUMO and ubiquitin, biotin-based approaches, genetic screening, SUMOylation networks in humans, targets for ubiquitin ligases, regulation of p53, protein homeostasis, miRNAs, DNA replication, DNA damage response, telomere biology, intracellular trafficking, regulation of angiogenesis, brain ischemia, autophagy, assembly and activity, antiviral defense, HIV infection, amyloid and amyloid-like proteins, plant immunity. This comprehensive and up-to-date book is the definitive reference volume on all aspects of SUMOylation and ubiquitination and is an essential acquisition for anyone involved in this area of biology.
There is a widespread consensus that use of antioxidants as a therapeutic approach may counteract free radical mediated pathologies. However, the role of antioxidants in normal physiology and redox signaling is still in its infancy. Since oxidative stress is related to various diseases and pathologies, scientists are eager to study the disease in humans, but it is not always ethical to study all the aspects of the disease in humans. Thus, it becomes mandatory to study the disease process and the mechanisms behind it through experimental models which generally involve animals, in vitro/cell culture studies, primates and even humans to a certain extent. Studies on Experimental Models contains data on the experimental models or review of such models of oxidative stress in various diseases. It is structured into six sections, which are as follows: diabetes, cardiovascular, neurology, ocular diseases, toxicology/environmental and in vitro/tissue culture. Each section presents a sketch of models in humans, animals and in vitro methods. Taken together, they comprise a valuable reference for basic and clinical scientists, one aimed at contributing to the advancement of oxidative stress research using appropriate animal models.
Protein carbonylation has attracted the interest of a great number of laboratories since the pioneering studies at the Earl Stadtman’s lab at NIH started in early 1980s. Since then, detecting protein carbonyls in oxidative stress situations became a highly efficient tool to uncover biomarkers of oxidative damage in normal and altered cell physiology. In this book, research groups from several areas of interest have contributed to update the knowledge regarding detection, analyses and identification of carbonylated proteins and the sites where these modifications occur. The scientific community will benefit from these reviews since they deal with specific, detailed technical approaches to study formation and detection of protein carbonyls. Moreover, the biological impact of such modifications in metabolic, physiologic and structural functions and, how these alterations can help understanding the downstream effects on cell function are discussed. Oxidative stress occurs in all living organisms and affects proteins and other macromolecules: Protein carbonylation is a measure of oxidative stress in biological systems Mass spectrometry, fluorescent labelling, antibody based detection, biotinylated protein selection and other methods for detecting protein carbonyls and modification sites in proteins are described Aging, neurodegenerative diseases, obstructive pulmonary diseases, malaria, cigarette smoke, adipose tissue and its relationship with protein carbonylation Direct oxidation, glycoxidation and modifications by lipid peroxidation products as protein carbonylation pathways Emerging methods for characterizing carbonylated protein networks and affected metabolic pathways
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.
Rosenberg’s Molecular and Genetic Basis of Neurologic and Psychiatric Disease, Fifth Edition provides a comprehensive introduction and reference to the foundations and key practical aspects relevant to the majority of neurologic and psychiatric disease. A favorite of over three generations of students, clinicians and scholars, this new edition retains and expands the informative, concise and critical tone of the first edition. This is an essential reference for general medical practitioners, neurologists, psychiatrists, geneticists, and related professionals, and for the neuroscience and neurology research community. The content covers all aspects essential to the practice of neurogenetics to inform clinical diagnosis, treatment and genetic counseling. Every chapter has been thoroughly revised or newly commissioned to reflect the latest scientific and medical advances by an international team of leading scientists and clinicians. The contents have been expanded to include disorders for which a genetic basis has been recently identified, together with abundant original illustrations that convey and clarify the key points of the text in an attractive, didactic format. Previous editions have established this book as the leading tutorial reference on neurogenetics. Researchers will find great value in the coverage of genomics, animal models and diagnostic methods along with a better understanding of the clinical implications. Clinicians will rely on the coverage of the basic science of neurogenetics and the methods for evaluating patients with biochemical abnormalities or gene mutations, including links to genetic testing for specific diseases. Comprehensive coverage of the neurogenetic foundation of neurological and psychiatric disease Detailed introduction to both clinical and basic research implications of molecular and genetic understanding of the brain Detailed coverage of genomics, animal models and diagnostic methods with new coverage of evaluating patients with biochemical abnormalities or gene mutations
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.
The Encyclopedia of Movement Disorders is a comprehensive reference work on movement disorders, encompassing a wide variety of topics in neurology, neurosurgery, psychiatry and pharmacology. This compilation will feature more than 300 focused entries, including sections on different disease states, pathophysiology, epidemiology, genetics, clinical presentation, diagnostic tools, as well as discussions on relevant basic science topics. This Encyclopedia is an essential addition to any collection, written to be accessible for both the clinical and non-clinical reader. Academic clinicians, translational researchers and basic scientists are brought together to connect experimental findings made in the laboratory to the clinical features, pathophysiology and treatment of movement disorders. The Encyclopedia targets a broad readership, ranging from students to general physicians, basic scientists and Movement Disorder specialists. Published both in print and via Elsevier’s online platform of Science Direct, this Encyclopedia will have the enhanced option of integrating traditional print with online multimedia. Connects experimental findings made in the laboratory to the clinical features, pathophysiology, and treatment of movement disorders Encompasses a wide variety of topics in neurology neurosurgery, psychiatry, and pharmacology Written for a broad readership ranging from students to general physicians, basic scientists, and movement disorder specialists
This is the first book to assemble the leading researchers in the field of LRRK2 biology and neurology and provide a snapshot of the current state of knowledge, encompassing all major aspects of its function and dysfunction. The contributors are experts in cell biology and physiology, neurobiology, and medicinal chemistry, bringing a multidisciplinary perspective on the gene and its role in disease. The book covers the identification of LRRK2 as a major contributor to the pathogenesis of Parkinson's Disease. It also discusses the current state of the field after a decade of research, putative normal physiological roles of LRRK2, and the various pathways that have been identified in the search for the mechanism(s) of its induction of neurodegeneration.