The Molecular Basis of Programmed Cell Death and Neuroinflammation in Neurodegenerative Diseases


Book Description

Age-related neurodegenerative diseases such as Alzheimer's disease and Parkinson's disease are characterized by progressive neuroinflammation as well as neuronal degeneration. Apoptosis, necrosis, and autophagy are all types of programmed cell death that are morphologically distinct from one another. Over the last decade, extensive research has been conducted on necroptosis, resulting in a better understanding of its molecular underpinnings and role in neurodegenerative diseases. A later study investigates the processes of apoptosis and necroptosis, as well as their roles in the activation of inflammatory immune responses. Although there is a distinct mode of cell death with distinct morphological characteristics, its identification and implications in neurological diseases are still unknown. Interestingly, emerging evidence has established a direct link between epigenetic and posttranslational modifications and neurodegenerative disease. Using epigenetic and proteomic methods, researchers uncovered genes and proteins that may play a function in the area of neuroinflammation, a role that has hitherto been overlooked. New pharmacological targets and therapeutic options for neurodegenerative diseases are being investigated in order to gain a better understanding of the disease's origins and progression by using neuronal death and neuroinflammation models that are associated with epigenetic changes.




The Aging Mind


Book Description

Possible new breakthroughs in understanding the aging mind that can be used to benefit older people are now emerging from research. This volume identifies the key scientific advances and the opportunities they bring. For example, science has learned that among older adults who do not suffer from Alzheimer's disease or other dementias, cognitive decline may depend less on loss of brain cells than on changes in the health of neurons and neural networks. Research on the processes that maintain neural health shows promise of revealing new ways to promote cognitive functioning in older people. Research is also showing how cognitive functioning depends on the conjunction of biology and culture. The ways older people adapt to changes in their nervous systems, and perhaps the changes themselves, are shaped by past life experiences, present living situations, changing motives, cultural expectations, and emerging technology, as well as by their physical health status and sensory-motor capabilities. Improved understanding of how physical and contextual factors interact can help explain why some cognitive functions are impaired in aging while others are spared and why cognitive capability is impaired in some older adults and spared in others. On the basis of these exciting findings, the report makes specific recommends that the U.S. government support three major new initiatives as the next steps for research.




The Molecular and Cellular Basis of Neurodegenerative Diseases


Book Description

The Molecular and Cellular Basis of Neurodegenerative Diseases: Underlying Mechanisms presents the pathology, genetics, biochemistry and cell biology of the major human neurodegenerative diseases, including Alzheimer's, Parkinson's, frontotemporal dementia, ALS, Huntington's, and prion diseases. Edited and authored by internationally recognized leaders in the field, the book's chapters explore their pathogenic commonalities and differences, also including discussions of animal models and prospects for therapeutics. Diseases are presented first, with common mechanisms later. Individual chapters discuss each major neurodegenerative disease, integrating this information to offer multiple molecular and cellular mechanisms that diseases may have in common. This book provides readers with a timely update on this rapidly advancing area of investigation, presenting an invaluable resource for researchers in the field. - Covers the spectrum of neurodegenerative diseases and their complex genetic, pathological, biochemical and cellular features - Focuses on leading hypotheses regarding the biochemical and cellular dysfunctions that cause neurodegeneration - Details features, advantages and limitations of animal models, as well as prospects for therapeutic development - Authored by internationally recognized leaders in the field - Includes illustrations that help clarify and consolidate complex concepts




Neurodegenerative Diseases


Book Description

This reference book provides a comprehensive overview of models and therapeutic approaches against neurodegenerative diseases, including Parkinson’s disease, Alzheimer’s disease, Huntington’s disease, and amyotrophic lateral sclerosis. It explores models based on the chemical, induced, cellular, genetic, transgenic, and 3D organoid approaches in neurodegenerative diseases. The book also reviews advantages and limitations of these models in designing the treatment strategies. Additionally, the book covers the emerging field of bioinformatics and its application in modeling various neurodegenerative diseases. Towards the end, the book highlights the role of holistic management, precision medicine, OMICS, and gene therapy against neurodegenerative disorders. It examines the implications and significance of stem cells therapy in translational models of neurodegenerative diseases. This book is an invaluable resource for researchers, neuroscientists, and neurosurgeons for getting in-depth information on the neurodegenerative models and therapeutic approaches. Key Features: Provides a comprehensive overview of neurodegenerative diseases and their models Examines the limitations associated with modeling neurodegenerative diseases Presents novel treatment strategies for Alzheimer's disease using cellular models Reviews importance of 3D organoid models for therapeutic approaches in Parkinson's disease Covers modeling techniques in understanding prion diseases Explores the role of genetic models in understanding Huntington's disease




Neuronal Cell Death


Book Description

This volume represents a valuable and readily reproducible collection of established and emerging techniques for neuronal cell death research. Conveniently divided into four parts, sections cover a series of techniques for the molecular, structural, functional and genomic characterization of dying neurons, a number of protocols that are of primary interest in neuropathology and in experimental neuropathology, a series of gene engineering techniques to obtain and manipulate neuronal stem cells and progenitors, to prepare HSV-1 vectors for the gene therapy, and to CNS transplantation of bone marrow stem cells, and finally, some very interesting protocols for the study of cell death in non-mammalian models. Written in the successful Methods in Molecular Biology series format, chapters include introductions to their respective topics, lists of the necessary materials and reagents, step-by-step, readily reproducible protocols, and notes on troubleshooting and avoiding known pitfalls. Authoritative and easily accessible, Neuronal Cell Death: Methods and Protocols seeks to serve a large audience of scientists that are currently active in the field or are willing to enter such an exciting and still expanding area of neurobiology.




The Prion Protein


Book Description

A conformational transition of the cellular prion protein (PrPC) into an aberrantly folded isoform designated scrapie prion protein (PrPSc) is the hallmark of a variety of neurodegenerative disorders collectively called prion diseases. They include Creutzfeldt-Jakob disease and Gerstmann-Stäussler-Scheinker syndrome in humans, scrapie in sheep, bovine spongiform encephalopathy (BSE) in cattle and chronic wasting disease (CWD) in free-ranging deer. In contrast to the deadly properties of misfolded PrP, PrPC seems to possess a neuroprotective activity. More-over, animal models indicated that the stress-protective activity of PrPC and the neurotoxic effects of PrPSc are somehow interconnected. In this timely book, leading scientists in the field have come together to highlight the apparently incongruous activities of different PrP conformers. The articles outline current research on celluar pathways implicated in the formation and signaling of neurotoxic and physiological PrP isoforms and delineate future research direction. Topics covered include the physiologcial activity of PrPC and its possible role as a neurotrophic factor, the finding that aberrant PrP conformers can cause neurodegeneration in the absence of infectious prion propagation, the requirement of the GPI anchor of PrPC for the neurotoxic effects of scrapie prions, the pathways implicated in the formation and neurotoxic properties of cytosolically localized PrP, the impact of metal ions on the processing of PrP, and the role of autophagy in the propagation and clearance of PrPSc. The book is fully illustrated and chapters include comprehensive reference sections. Essential reading for scientists involved in prion research.




Oxidative Stress and Neurodegenerative Disorders


Book Description

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







Drug Delivery to the Brain


Book Description

The development of new CNS drugs is notoriously difficult. Drugs must reach CNS target sites for action and these sites are protected by a number of barriers, the most important being the blood –brain barrier (BBB). Many factors are therefore critical to consider for CNS drug delivery, e.g. active/passive transport across the BBB, intra-brain distribution, and central/systemic pharmacokinetics, to name a few. Neurological disease and trauma conditions add further complexity because CNS barriers, drug distribution and pharmacokinetics are dynamic and often changed by disease/trauma. Knowledge of all these factors and their interplay in different conditions is of utmost importance for proper CNS drug development and disease treatment. In recent years much information has become available for a better understanding of the many factors important for CNS drug delivery and how they interact to affect drug action. This book describes small and large drug delivery to the brain with an emphasis on the physiology of the BBB and the principles and concepts for drug delivery across the BBB and distribution within the brain. It contains methods descriptions for studying drug delivery, routes and approaches of administering drugs into the brain, the influence of disease, and drug industry perspectives. Therewith, it contributes to an in-depth understanding of the interplay between brain (patho)-physiology and drug characteristics. Furthermore, the content is designed to be both cutting-edge and educational, so that the book can be used in high-level training of academic and industry scientists with full references to original publications. ​




Ocular Neuroprotection


Book Description

Ocular neuroprotection is aimed at protecting the death of photoreceptors, retinal ganglion, or other important neurons in cases of disease or trauma. Levin (ophthalmology and neurology, U. of Wisconsin at Madison, US) and Di Polo (pathology and cell biology, U. of Montreal, Canada) present 18 chapt.