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The Neuroscience of Dementia brings together different fields of dementia research into a single book, covering a wide range of subjects, including Alzheimer's disease, Lewy body dementia, mixed dementia, vascular dementia, physical activity, risk factors, mortality, biomarkers, SPECT, CT, MRI, questionnaires, nutrition, sleep, delirium, hearing loss, agitation, aggression, delusions, anxiety, depression, hallucinations, psychosis, senile plaques, tau and amyloid-beta, neuroinflammation, molecular biology, and more. This foundational, comprehensive book compiles the latest understanding on all forms of dementia and their common features in a single source. It is an invaluable resource for neuroscientists, neurologists, and anyone in the field. - Offers comprehensive coverage of a broad range of topics related to dementia - Contains in each chapter an abstract, key facts, mini dictionary of terms, and summary points to aid in understanding - Provides unique sections on specific subareas, intellectual components, and knowledge-based niches that will help readers navigate key areas for research and further clinical recommendations - Features preclinical and clinical studies to help researchers map out key areas for research and further clinical recommendations - Serves as a "one-stop" source for everything you need to know about dementia
The Shriver Report: A Woman’s Nation Takes on Alzheimer’s will be the first comprehensive multi-disciplinary look at these questions at this transformational moment. The Report will digest the current trends in thinking about Alzheimer’s, examine cutting-edge medical research, look at societal impacts, and include a groundbreaking and comprehensive national poll. It will feature original photography and personal essays by men and women – some from the public arena with names you know, some from everyday America – sharing their personal struggles with the disease as patients, caregivers and family members.
Provides a definitive overview of the complex ecosystem facilitating Alzheimer's Disease drug research and development. Demonstrates a drug's journey from in the lab, clinical trial testing, regulatory review, and marketing by pharmaceutical companies. Details the use of artificial intelligence, clinical trial management, and financing models.
Presents a thorough examination of the unifying principles from the subcellular to the systems and clinical levels; Identifies common themes among molecular biology, genetics, physiology, pathology, biomarkers, behavior, and treatment strategies that are shared between neurodegenerative diseases; Enables better care of patients and help build collaboration across researchers in multiple specializations that could help advance future insights and facilitate novel therapies and enhancing basic scientific understanding of these diseases to a new generation.
New edition, completely rewritten, with new chapters on endovascular surgery and mitochrondrial and ion channel disorders.
Book 9 focuses on a new dementia type, LATE, mistaken as Alzheimer's disease until now.LATE stands for Limbic-predominant age-related TDP-43 encephalopathy, the protein buildup responsible for this dementia. This book is organic, like the series, meaning we never consider our books as finished. Science evolves, which is why our books go through continuous updates. Since LATE is a new dementia classification, we expect continuous further information to emerge. Watch Amazon alerts for potential digital updates. We provide free digital copies on all paperback purchases, so everybody receives free updates.
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”.