Download or read book Studying the Interactions Between Tau Amyloid and Alpha Synuclein in Alzheimer s Disease Animal and Human Cell Models written by Wesley W. L. Chen and published by . This book was released on 2016 with total page 210 pages. Available in PDF, EPUB and Kindle. Book excerpt: Alzheimer's disease (AD) is the leading cause of age related dementia and involves a progressive loss of neurons and synapses, leading to anxiety, cognitive impairment and a diminished quality of life. Pathologically, AD is characterized by extracellular amyloid beta (Abeta) plaque accumulation and the intraneuronal formation of tau-laden neurofibrillary tangles. In up to 70% of AD patients, these two hallmark pathologies are accompanied by a third proteinopathy; the aggregation of ??synuclein into intraneuronal Lewy bodies. The aggregate stress caused by these proteinopathies interacts with the immune system to produce a chronic neuroinflammatory condition that can further exacerbate disease progression.The goal of my dissertation is investigate how beta-amyloid, tau and alpha-synuclein pathologies interact with each other and to examine the role of the immune system in these interactions. To study how these proteinapathies interact in later stages of AD, I developed a new mouse model of AD termed 'T5x' mice, by crossing two existing transgenic lines; 5xFAD and Tau22 mice---aggressive lines that exhibit robust amyloidosis and tauopathy respectively. During my studies I found that T5x mice exhibit dramatically increased tau hyperphosphorylation, neuroinflammatory response, and microgliosis. However, quite surprisingly I also found that T5x mice exhibit increased microglial Abeta phagocytosis leading to decreased amyloid plaque burden and insoluble Abeta. In subsequent studies I further determine that T5x mice also develop inclusions composed of murine alpha-synuclein (alpha-syn) and form Lewy-body like pathologies---the first transgenic AD model to our knowledge to be found to develop Lewy body-like inclusions without an alpha-synuclein transgene.To further study the specific effects that the immune system has on the development of tau pathology, I also developed a mouse model of tau pathology lacking the adaptive immune. Thy1-Tau22 mice were crossed with Rag2 -/-/Il2rgamma-/- double knockout mice over multiple generations to create 'RagTau' mice. RagTau mice lack T-, B- and NK-cells, yet exhibit significant accumulation and hyperphosphorylation of human tau. Although RagTau mice exhibit increases microglial activation relative to immune-intact Tau22 transgenics, no significant increases in tau pathology were detected in RagTau mice. To further validate the minimal influence of the adaptive immune system on the development of tau pathology, I performed adoptive transfer experiments, transplanting bone marrow cells from strain-matched GFP donors into RagTau mice. Using this approach I examined the potential effects of bone marrow reconstitution on tau pathology and the infiltration of GFP-labeled cells into the brain of tau mice. Unlike recent equivalent studies performed in our lab with Abeta-producing mice, I detected no changes in tau pathology in response to bone marrow transplantation. However, I did find that tau pathology induces a significant increase in T-cell infiltration into the brain parenchyma in comparison to Rag-wild type recipients. Lastly, I was the first in our lab to establish the paradigm of generating human induced pluripotent stem cells (iPSCs). Using this approach I differentiated iPSCs into neural stem cells (NSCs) and transplanted into RagTau mice to examine potential questions about tau propagation. Interestingly, while iPSC-derived NSCs survived for at least 3 months post-transplantation I found no evidence that tau pathology could spread to these transplanted human cells. Taken together, my thesis research has helped to improve our understanding of the interactions between AD pathologies and the immune system.
Download or read book Tau oligomers written by Jesus Avila and published by Frontiers E-books. This book was released on 2014-08-18 with total page 114 pages. Available in PDF, EPUB and Kindle. Book excerpt: Neurofibrillary tangles (NFTs) composed of intracellular aggregates of tau protein are a key neuropathological feature of Alzheimer’s Disease (AD) and other neurodegenerative diseases, collectively termed tauopathies. The abundance of NFTs has been reported to correlate positively with the severity of cognitive impairment in AD. However, accumulating evidences derived from studies of experimental models have identified that NFTs themselves may not be neurotoxic. Now, many of tau researchers are seeking a “toxic” form of tau protein. Moreover, it was suggested that a “toxic” tau was capable to seed aggregation of native tau protein and to propagate in a prion-like manner. However, the exact neurotoxic tau species remain unclear. Because mature tangles seem to be non-toxic component, “tau oligomers” as the candidate of “toxic” tau have been investigated for more than one decade. In this topic, we will discuss our consensus of “tau oligomers” because the term of “tau oligomers” [e.g. dimer (disulfide bond-dependent or independent), multimer (more than dimer), granular (definition by EM or AFM) and maybe small filamentous aggregates] has been used by each researchers definition. From a biochemical point of view, tau protein has several unique characteristics such as natively unfolded conformation, thermo-stability, acid-stability, and capability of post-translational modifications. Although tau protein research has been continued for a long time, we are still missing the mechanisms of NFT formation. It is unclear how the conversion is occurred from natively unfolded protein to abnormally mis-folded protein. It remains unknown how tau protein can be formed filaments [e.g. paired helical filament (PHF), straight filament and twisted filament] in cells albeit in vitro studies confirmed tau self-assembly by several inducing factors. Researchers are still debating whether tau oligomerization is primary event rather than tau phosphorylation in the tau pathogenesis. Inhibition of either tau phosphorylation or aggregation has been investigated for the prevention of tauopathies, however, it will make an irrelevant result if we don’t know an exact target of neurotoxicity. It is a time to have a consensus of definition, terminology and methodology for the identification of “tau oligomers”.
Download or read book Animal Models for the Study of Human Disease written by Mengqi Chen and published by Elsevier Inc. Chapters. This book was released on 2013-05-29 with total page 100 pages. Available in PDF, EPUB and Kindle. Book excerpt: Alzheimer’s disease (AD) is a major and increasing burden on families, communities, and national health budgets. Despite intensive and extended research, there is still widespread debate about its cause(s), and no effective treatments exist. Familial (inherited, mainly early onset) and sporadic (mainly late onset) forms of the disease exist, and it is uncertain to what extent they are related. Transgenic mouse models have dominated the investigation of this disease, but their validity can be questioned. Numerous alternative models exist that can provide valuable information on the molecular and cellular basis of AD. In this chapter, we review the various invertebrate, nonmammalian vertebrate, and mammalian models and how these have been used to investigate this disease. We examine the strengths and weaknesses of these various model systems. Of course, animal models never completely reflect the true nature of a human disease, but progress in understanding and finding preventative and ameliorative treatments for AD is hindered by the lack of a convincing hypothesis for the cause of this complex condition.
Download or read book Apolipoprotein E and Alzheimer s Disease written by A.D. Roses and published by Springer Science & Business Media. This book was released on 2012-12-06 with total page 208 pages. Available in PDF, EPUB and Kindle. Book excerpt: There is now considerable genetic evidence that the type 4 allele of the apolipoprotein E gene is a major susceptibility factor associated with late-onset Alzheimer's disease, the common form of the disease defined as starting after sixty years of age. The role of apolipoprotein E in normal brain metabolism and in the pathogenesis of Alzheimer's disease are new and exciting avenues of research. This book, written by the most outstanding scientists in this new filed, is the first presentation of results concerning the implications of apolipoprotein E on the genetics, cell biology, neuropathology, biochemistry, and therapeutic management of Alzheimer's disease.
Download or read book Neurodegenerative Diseases written by Shamim I. Ahmad and published by Springer Science & Business Media. This book was released on 2012-03-12 with total page 421 pages. Available in PDF, EPUB and Kindle. Book excerpt: The editor of this volume, having research interests in the field of ROS production and the damage to cellular systems, has identified a number of enzymes showing ·OH scavenging activities details of which are anticipated to be published in the near future as confirmatory experiments are awaited. It is hoped that the information presented in this book on NDs will stimulate both expert and novice researchers in the field with excellent overviews of the current status of research and pointers to future research goals. Clinicians, nurses as well as families and caregivers should also benefit from the material presented in handling and treating their specialised cases. Also the insights gained should be valuable for further understanding of the diseases at molecular levels and should lead to development of new biomarkers, novel diagnostic tools and more effective therapeutic drugs to treat the clinical problems raised by these devastating diseases.
Download or read book Alzheimer s Disease Research Guide written by Takaomi C. Saido and published by Elsevier. This book was released on 2024-07-25 with total page 284 pages. Available in PDF, EPUB and Kindle. Book excerpt: Alzheimer's Disease Research Guide: Animal Models for Understanding Mechanisms and Medications provides researchers with a comprehensive guide, detailing every aspect of Alzheimer's Disease research, including chapters on neuroinflammation, immunotherapy, biomarkers, and animal modeling. This book begins with historical perspectives of both pathological chronology and pathological biochemistry in relation to Alzheimer’s disease. Other chapters review Amyloidogenic AB and Non-Amyloidogenic tau and Metabolism of AB major components to the research and understanding of Alzheimer’s research. The book concludes with specific treatment chapters including how to develop safe, effective, and inexpensive medications and the application of genome editing to the treatment of Familial Alzheimer's Disease. Written by world renowned expert in Alzheimer’s research, this book is a valuable resource for all researchers. Reviews why familial Alzheimer’s disease is vital to understanding sporadic Alzheimer’s disease Describes the latest “game changer” animal models of Alzheimer's disease and frontotemporal dementia in detail Explains how various Alzheimer’s disease medications have failed clinical trials Discusses pros and cons of therapeutic antibodies, lecanemab and donanemab, that were recently found to be effective in recent clinical trials Details the application of genome editing as a treatment for familial Alzheimer’s disease Proposes publishing “Journal of Negative Data” for the days of generative AI-assisted publication, AI being unable to distinguish between reproducible and unreproducible data, particularly important in Alzheimer’s research
Download or read book Handbook of Animal Models in Alzheimer s Disease written by G. Casadesus and published by IOS Press. This book was released on 2011-07-05 with total page 352 pages. Available in PDF, EPUB and Kindle. Book excerpt: Animals have been used to model diseases or test new treatments since around 300 BC, and undoubtedly our ability to model disease in animals – including transgenic animals – has provided major breakthroughs in all fields of biomedical research. Due to their complexity and plurality of pathology and symptomatology, the study of neurodegenerative diseases relies heavily on animal models. These models have been developed in many species in the attempt to undercover the complex nature of the disease mechanisms involved. The ultimate goal is to test promising therapies and to manage, prevent or cure neurodegenerative disease. But because most animal models in this area do not reproduce the full phenotypical disease spectrum and the etiology and clinical presentation of neurodegenerative diseases differ from one patient to the next, the testing of these diseases in animal models often translates poorly to indices of efficacy when applied to the clinical population. Written by experts in the field with these advances and challenges in mind, this handbook provides an updated overview of the animal models being developed and used to study complex disease dynamics. The first part of the book presents an overview of animal models of various species and includes a review of new invertebrate animal models to study neurodegeneration. The second section presents the use of animal models to pinpoint disease mechanisms, and the last part of the handbook examines the various therapeutic interventions being used in models of neurodegenerative disease.
Download or read book Dementia with Lewy Bodies written by John O'Brien and published by CRC Press. This book was released on 2005-11-29 with total page 286 pages. Available in PDF, EPUB and Kindle. Book excerpt: Filling a noticeable gap in the market for a new text solely focused on Dementia with Lewy Bodies, this book discusses cutting-edge topics covering the condition from diagnosis to management, as well as what is known about the neurobiological changes involved. With huge progress having been made over the last decade in terms of the disorder
Download or read book Animal Models for Neurodegenerative Disease written by Jesús Avila and published by Royal Society of Chemistry. This book was released on 2011 with total page 307 pages. Available in PDF, EPUB and Kindle. Book excerpt: In recent years, medical developments have resulted in an increase in human life expectancy. The editors have extensive knowledge and experience in this field and the book is aimed at undergraduates, postgraduates, and academics. The chapters cover Alzheimer's disease, Parkinson's disease, Huntington's, and other neurodegenerative disorders.
Download or read book Human and Animal Models for Translational Research on Neurodegeneration Challenges and Opportunities From South America written by Agustín Ibáñez and published by Frontiers Media SA. This book was released on 2018-06-21 with total page 217 pages. Available in PDF, EPUB and Kindle. Book excerpt: Neurodegenerative diseases are the most frequent cause of dementia, representing a burden for public health systems (especially in middle and middle-high income countries). Although most research on this issue is concentrated in first-world centers, growing efforts in South America are affording important breakthroughs. This emerging agenda poses new challenges for the region but also new opportunities for the field. This book aims to integrate the community of experts across the globe and the region, and to establish new challenges and developments for future investigation. We present research focused on neurodegenerative research in South America. We introduce studies assessing the interplay among genetic, neural, and behavioral dimensions of these diseases, as well as articles on vulnerability factors, comparisons of findings from various countries, and works promoting multicenter and collaborative networking. More generally, our book covers a broad scope of human-research approaches (behavioral assessment, neuroimaging, electromagnetic techniques, brain connectivity, peripheral measures), animal methodologies (genetics, epigenetics, proteomics, metabolomics, other molecular biology tools), species (all human and non-human animals, sporadic, and genetic versions), and article types (original research, review, and opinion papers). Through this wide-ranging proposal, we hope to introduce a fresh approach to the challenges and opportunities of research on neurodegeneration in South America.
Download or read book Data driven Network Models to Characterize the Distribution and Spread of Tau in the Alzheimer s Disease Brain written by Jacob Vogel and published by . This book was released on 2020 with total page pages. Available in PDF, EPUB and Kindle. Book excerpt: "Alzheimer's disease (AD) is a common and debilitating late-life illness comprising progressive brain damage and slow deterioration of cognitive and functional abilities. The primary neuropathological signature of AD involves accumulation of the beta-amyloid (A-beta) and tau proteins into cortical plaques and tangles. While A-beta plaques present diffusely throughout the brain before AD symptoms manifest, fibrillar tau pathology is initially distributed in a very specific part of the brain. As AD symptoms evolve, tau pathology advances through the cerebral cortex in a specific and highly reproducible pattern, perhaps driven by the brain's intrinsic architecture of neuronal connectivity. Most of what we know about tau comes from post-mortem studies and experimental animal models. However, recent advances allow the imaging of tau pathology in the brains of living humans using positron emission tomography (PET). The content of this thesis involves using tau-PET to validate and expand upon the distribution and spread of tau pathology in humans, with a focus on data-driven methodologies. Chapter 1 reviews known aspects of tau biology and pathophysiology -- particularly as it relates to the specific pattern of tau accumulation and spread in AD -- and critically reviews recent contributions to this literature by tau-PET and other tau biomarkers. Chapter 2 presents a study using hypothesis-free clustering methods to investigate whether regional patterns of tau-PET covariance along the AD spectrum match patterns of tau accumulation expected from postmortem histopathology. These data-driven regions partially matched the expected patterns of tau distribution, but also showed superior performance in tracking variation in cognition, compared to regions derived from post-mortem studies. Chapter 3 tests the hypothesis that the pattern of tau distribution in humans is driven by patterns of neuronal connectivity, by simulating the spread of a pathological agent from an epicenter through the healthy human connectome. This simulated pattern matched well the in vivo spatial distribution of tau. Further, regional model error was associated with the magnitude of regional A-beta, suggesting A-beta influences the topography of tau spread. Chapter 4 challenges the notion that tau spreads in a uniform pattern across individuals, by applying a cutting-edge spatiotemporal event-based clustering algorithm to the largest tau-PET dataset described to date. Four different progression patterns emerged from the data, resembling known subtypes of tau and atypical AD variants, with no single pattern predominating. The subtypes are validated and characterized, and the influence of regional cell-type variation and network spread on subtype expression is explored. The results do not support the notion of a single tau spreading pattern, and suggest atypical AD variants represent early-onset and aggressive variants of typical AD phenotypes. Finally, Chapter 5 considers the novel contributions produced by the original work in this thesis, and discusses how these findings contribute to current dialogues in the field of AD research. Together, the work in this thesis suggests that the in vivo and spatially-unbiased nature of tau-PET can provide novel information about the spread of tau through the human brain during AD. In conclusion, current pathological staging systems should be updated to reflect common variation in AD patterns, and models of tau spreading are likely incomplete without incorporating regional vulnerability information and systematic individual variation"--
Download or read book Unraveling Neuroprotective and Neurodegenerative Signals in Neurodegeneration written by Irving E. Vega and published by Frontiers Media SA. This book was released on 2016-09-15 with total page 133 pages. Available in PDF, EPUB and Kindle. Book excerpt: Proteinopathy is a collective term used to classified neurodegenerative diseases associated with the progressive accumulation of toxic protein molecules in specific brain regions. Alzheimer’s disease (AD) is a well-known proteinopathy characterize by the accumulation of A peptides and tau proteins. The accumulation of these toxic molecules in the brain starts many years before any clinical presentation, being the onset in the range of 65 to 72 years of age. Therefore, age is considered a risk factor due, in part, to the loss of molecular competence to clear the brain from these toxic protein molecules. This fact, supported by years of research, demonstrates that brain cells activate a neuroprotective mechanism upon detection of a pathobiological signal that (if the detrimental conditions persist) precedes the activation of the neurodegeneration pathway. The progressive brain region specific neuronal death in neurodegenerative diseases also indicates that the transition from neuroprotection to neurodegeneration is individually triggered in cells of the affected brain region. Thus, molecular understanding of the pathophysiology associated with proteinopathies needs to take in consideration this intricate transition process, especially when genomics and proteomics approaches are used.
Download or read book Investigating the Role of Fyn and Tau Interactions in Alzheimer s Disease written by Alessia Usardi and published by . This book was released on 2010 with total page 440 pages. Available in PDF, EPUB and Kindle. Book excerpt: Alzheimer's disease (AD) is characterised by the extracellular deposition of 13-amyloid in senile plaques, and by the intraneuronal accumulation of hyperphosphorylated, aggregated tau as neurofibrillary tangles. Tau isolated from AD brain is hyperphosphorylated predominantly on serine and threonine residues, however recent evidence has that it is also phosphorylated on tyrosine residues. The non-receptor tyrosine kinase fyn interacts with and phosphorylates tau, and tau and fyn colocalise in tangle-bearing neurons in AD brain. Fyn is principally located in membrane rafts, sterol- and sphingolipid-enriched domains that compartmentalise cellular processes. Both hyperphosphorylated tau and 13- amyloid accumulate in membrane rafts of AD brain, and their accumulation in neuronal membrane rafts appears to be fyn-dependent. Thus, it is possible that tyrosine phosphorylation of tau by fyn may be an important event during the development of AD. To further elucidate these events, this thesis describes the characterisation of fyn and tau interactions, the importance of these interactions in mediating the relocalisation of tau to membrane rafts, and the roles of fyn and tau in 13-amyloid induced neurotoxicity. -- In transfected Chinese Hamster Ovary cells, a novel interaction between tau and the SH2 domain of fyn was observed, that is increased when tau is tyrosine phosphorylated. The tyrosine phosphorylation status of tau was shown to be important for regulating the localisation of tau in membrane rafts from wild type primary cortical neurons, and the use of fyn deficient mice indicated that fyn plays an important role in this process. Finally, the effect of two synthetic 13-amyloid preparations on neuronal viability was investigated in wild type neurons and those deficient in fyn or tau.
Download or read book The Molecular and Cellular Basis of Neurodegenerative Diseases written by Michael S. Wolfe and published by Academic Press. This book was released on 2018-03-29 with total page 561 pages. Available in PDF, EPUB and Kindle. Book excerpt: 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
Download or read book Molecular Intervention in Mouse Models of Amyotrophic Lateral Sclerosis and Alzheimer s Disease written by Steven Prescott Bennett and published by . This book was released on 2009 with total page 534 pages. Available in PDF, EPUB and Kindle. Book excerpt: ABSTRACT: Neurodegeneration describes the progressive loss of structure and function of neurons, leading ultimately to cell and organism death. Although the initiating factors of neurodegenerative diseases such as Alzheimer's, Parkinson's, Huntington's, and Amyotrophic Lateral Sclerosis may be different, they share common pathophysiologies. Proteinopathies, as these diseases are now termed, are characterized by atypical deposits of proteins, often due to misfolding. Associated with these deposits are dysfunctional mitochondria, oxidative stress, disrupted axonal transport, inflammation, and apoptotic cell death. If this occurs in motor neurons, as in ALS, ataxia precedes death with little or no change in cognition. On the other hand, if the deposits are found in cortical neurons, as in Alzheimer's disease, the outcome is dementia and motor function remains largely intact. Each disease is selective for particular types of neurons and brain regions. Although research has elucidated much of the molecular biology involved in these diseases, their initiating causes remain largely unknown. Most of our current understanding originated with the identification of gene mutations that cause rare familial forms of these diseases. As a result, numerous strains of transgenic animals have been developed to study neurodegenerative disease phenomena and were central to the studies presented in this body of work. Novel routes of drug and gene delivery are described here as well as characterization of the mouse models studied. In particular, this work demonstrates that the blood brain barrier is disrupted in ALS followed by the formation of autorosettes in ALS mice. In various Alzheimer's disease mouse models, it was demonstrated that the acute phase reactant alpha-1-antichymotrypsin (ACT) not only interacts with amyloid plaques, but also induces tau phosphorylation in vivo; tying together these disease hallmarks. It was also shown that small fragments of amyloid beta (1-11) could disrupt the formation of mature amyloid plaques in these mice. Lastly, it was demonstrated that mature plaques could also be decreased by intracranial delivery of granulocyte-macrophage stimulating factor (GM-CSF). My dissertation research goal was to understand and develop these treatment strategies based on protein disaggregation, neuroprotection, and inflammation, meanwhile developing novel methods for targeted delivery of molecules into the CNS of mice.
Download or read book Disease Modifying Targets in Neurodegenerative Disorders written by Veerle Baekelandt and published by Academic Press. This book was released on 2017-03-31 with total page 324 pages. Available in PDF, EPUB and Kindle. Book excerpt: Disease-Modifying Targets in Neurodegenerative Disorders: Paving the Way for Disease-Modifying Therapies examines specific neurodegenerative disorders in comprehensive chapters written by experts in the respective fields. Each chapter contains a summary of the disease management field, subsequently elaborating on the molecular mechanisms and promising new targets for disease-modifying therapies. This overview is ideal for neuroscientists, biomedical researchers, medical doctors, and caregivers, not only providing readers with a summary of the way patients are treated today, but also offering a glance at the future of neurodegenerative disorder treatment. Provides a comprehensive overview of how key proteins in neurodegenerative disorders can be used as targets to modify disease progress Summarizes how patients are treated today, providing a glance at future disease management Includes intelligible and informative information that is perfect for non-specialists, medical practitioners, and scientists Written and peer reviewed by outstanding scientists in their respective fields
Download or read book Magnesium in the Central Nervous System written by Robert Vink and published by University of Adelaide Press. This book was released on 2011 with total page 354 pages. Available in PDF, EPUB and Kindle. Book excerpt: The brain is the most complex organ in our body. Indeed, it is perhaps the most complex structure we have ever encountered in nature. Both structurally and functionally, there are many peculiarities that differentiate the brain from all other organs. The brain is our connection to the world around us and by governing nervous system and higher function, any disturbance induces severe neurological and psychiatric disorders that can have a devastating effect on quality of life. Our understanding of the physiology and biochemistry of the brain has improved dramatically in the last two decades. In particular, the critical role of cations, including magnesium, has become evident, even if incompletely understood at a mechanistic level. The exact role and regulation of magnesium, in particular, remains elusive, largely because intracellular levels are so difficult to routinely quantify. Nonetheless, the importance of magnesium to normal central nervous system activity is self-evident given the complicated homeostatic mechanisms that maintain the concentration of this cation within strict limits essential for normal physiology and metabolism. There is also considerable accumulating evidence to suggest alterations to some brain functions in both normal and pathological conditions may be linked to alterations in local magnesium concentration. This book, containing chapters written by some of the foremost experts in the field of magnesium research, brings together the latest in experimental and clinical magnesium research as it relates to the central nervous system. It offers a complete and updated view of magnesiums involvement in central nervous system function and in so doing, brings together two main pillars of contemporary neuroscience research, namely providing an explanation for the molecular mechanisms involved in brain function, and emphasizing the connections between the molecular changes and behavior. It is the untiring efforts of those magnesium researchers who have dedicated their lives to unraveling the mysteries of magnesiums role in biological systems that has inspired the collation of this volume of work.
