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Type 2 Diabetes and Dementia details the relationship between diabetes, dementia and the future of medicine and therapeutics. Chapters range from epidemiology, clinical features, neuroimaging biomarkers, neuropathology, macrostructural and molecular mechanisms, risk assessment and prevention strategies, and the application of therapeutics. The book reflects the translational aspects of the current science in the field, with an emphasis on the display of neuroimaging and neuropathology. It contains contributions from world experts, and is ideal for clinicians and researchers in the fields of neurology, neuroscience, geriatric medicine and endocrinology. - Presents a comprehensive overview that details the relationship between diabetes, dementia and the future of medicine and therapeutics - Written for researchers and clinicians in neurology, neuroscience, geriatric medicine and endocrinology - Includes topics ranging from epidemiology, clinical features, neuroimaging biomarkers, neuropathology, macrostructural and molecular mechanisms, risk assessment, prevention strategies and therapeutic applications
Neuroinflammation in Vascular Dementia describes the molecular mechanisms that drive this transition to mixed pathology, along with the newer lifestyle and pharmacological approaches that can reduce the incidence of dementia. The book describes the practical aspects of neuroimaging methods, along with novel neuroimaging methods, using MRI, that are becoming important clinically. The author also discusses how the diagnosis of dementias will be greatly aided by biomarkers from neuroimaging, blood and CSF biochemistry and neuropsychological testing in the future. This information will be used in precision medicine to design treatment strategies based on the most likely causes of the disease. Dementia research has undergone dramatic growth driven by current and projected increases in the aging of the population, and thus leading to a larger number of patients with dementia by 2050. Hence, advances in neuroimaging, brain chemistry, and genetics have accelerated our understanding of diseases that lead to cognitive decline. - Reviews the clinical aspects and subtypes of dementia - Explains molecular pathways involved in brain inflammation - Includes the role of CSF and blood in diagnosis - Covers established and novel neuroimaging methods - Discusses established and developing treatment strategies - Identifies future directions, such as machine learning and precision medicine
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”.
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.
This e-book will review special features of the cerebral circulation and how they contribute to the physiology of the brain. It describes structural and functional properties of the cerebral circulation that are unique to the brain, an organ with high metabolic demands and the need for tight water and ion homeostasis. Autoregulation is pronounced in the brain, with myogenic, metabolic and neurogenic mechanisms contributing to maintain relatively constant blood flow during both increases and decreases in pressure. In addition, unlike peripheral organs where the majority of vascular resistance resides in small arteries and arterioles, large extracranial and intracranial arteries contribute significantly to vascular resistance in the brain. The prominent role of large arteries in cerebrovascular resistance helps maintain blood flow and protect downstream vessels during changes in perfusion pressure. The cerebral endothelium is also unique in that its barrier properties are in some way more like epithelium than endothelium in the periphery. The cerebral endothelium, known as the blood-brain barrier, has specialized tight junctions that do not allow ions to pass freely and has very low hydraulic conductivity and transcellular transport. This special configuration modifies Starling's forces in the brain microcirculation such that ions retained in the vascular lumen oppose water movement due to hydrostatic pressure. Tight water regulation is necessary in the brain because it has limited capacity for expansion within the skull. Increased intracranial pressure due to vasogenic edema can cause severe neurologic complications and death.
Presenting the novel concept of white matter dementia, this unique book offers hope for a better understanding and treatment of dementia.
The hippocampus is one of the most intriguing structures of the human brain. Damage to this part causes symptoms ranging from transient disorders accompanied by tiny lesions to severely debilitating cognitive disorders with marked tissue loss. This publication provides a predominantly clinical approach to the complex workings of the hippocampus from different perspectives, ranging from basic principles to specific diseases. The first part of the book summarizes current knowledge regarding the structure and physiology of the hippocampus and establishes the ties to basic neuroscience. The second part deals with the function and assessment of the human hippocampus, including memory function, neuropsychological measures, and conventional and functional imaging studies. The chapters of the third part are devoted to the hippocampus in neurological disorders, e.g. the interaction between stress and memory function, and the pathological conditions of common as well as selected rare neurological diseases affecting the hippocampus. The book is highly recommended to clinical neurologists who wish to gain a broad understanding of this complex and fascinating organ in terms of basic principles, modern imaging findings, and specific diseases.
This innovative, comprehensive book covers the key elements of perioperative management of older patients. The book's chapter structure coincides with the clinical path patients tread during their treatment, from preoperative evaluation to post-hospital care. Epidemiological aspects and aging processes are illustrated, providing keys to understanding the quick expansion of geriatric surgery and defining the clinical profile of older surgical patients in a cybernetic perspective. Preoperative evaluation and preparation for surgery, including medication reconciliation and pre-habilitation, are developed in the light of supporting decision-making about surgery in an evidence-based and patient-focused way. Intra- and postoperative management are discussed, aiming to tailor anesthetic, surgical and nursing approaches to specific patients' needs, in order to prevent both general and age-related complications. This volume also addresses issues relevant to geriatric surgery, from different organizational models to clinical risk management and systems engineering applied to hospital organization.
Brain dysfunction is a major clinical problem in intensive care, with potentially debilitating long-term consequences for post-ICU patients of any age. The resulting extended length of stay in the ICU and post-discharge cognitive dysfunction are now recognized as major healthcare burdens. This comprehensive clinical text provides intensivists and neurologists with a practical review of the pathophysiology of brain dysfunction and a thorough account of the diagnostic and therapeutic options available. Initial sections review the epidemiology, outcomes, relevant behavioral neurology and biological mechanisms of brain dysfunction. Subsequent sections evaluate the available diagnostic options and preventative and therapeutic interventions, with a final section on clinical encephalopathy syndromes encountered in the ICU. Each chapter is rich in illustrations, with an executive summary and a helpful glossary of terms. Brain Disorders in Critical Illness is a seminal reference for all physicians and neuroscientists interested in the care and outcome of severely ill patients.
This monograph offers the reader an integrated point-of-view about the inflammatory response related to injury, infections and tumors. This integration is based on the hypothesis that the multiple pathophysiological mechanisms making up inflammation represent the re-expression of ontogenic mechanisms during early embryo development as well as the recapitulation of ancestral phylogenetic mechanisms. The relevance of the anti-inflammatory treatments is also highlighted with respect to polytraumatic patients, advances in stem cell research, embryology and the wound healing mechanism. Readers of this book will have the chance of gaining a unique perspective about of the pathophysiological mechanisms involved in the multiple inflammatory conditions. This integrative concept about inflammation can be applied in biological investigation, as well as in clinical research and translational medicine.