Current Hypotheses And Research Milestones In Alzheimer S Disease

Almost four decades of innovative and intensive research on Alzheimer’s disease (AD) have brought major advances in our understanding of its pathogenesis, improved tools for diagnosis, and strategies for its treatment. This research has helped build a solid foundation of knowledge in the neurosciences and biological basis of AD and AD-related neurological disorders. Scientific background and insightful hypotheses are of major relevance in order to approach to an effective therapy for this devastating disease. Current Hypotheses and Research Milestones in Alzheimer's Disease contains 20 seminal chapters by authors with varying views on the neuroanatomical, neuropathological, neuropsychological, neurological, and molecular aspects of AD. These chapters grew out of “Current Hypothesis on Alzheimer’s Disease”, held in Viña del Mar, Chile, in November of 2007. Participants included the world’s leading Alzheimer’s researchers, whose work has illuminated AD investigations during the past few decades. Students, academics and medical professionals will find this text an invaluable addition to the study of this important subject.

Addresses in roughly equal measure the science and management behind several recent marketable biomedical innovations.

The End of Alzheimer’s: The Brain and Beyond, Second Edition is the first comprehensive overview on the molecular basis of Alzheimer’s outside of the brain, merging the most recent findings within the field into a single book. It aims to educate the reader on the many overlooked aspects of Alzheimer’s disease that occur outside the brain. This book uniquely provides step-by-step, peer-reviewed evidence that the current research model may be misguided and that a new and emerging model is more accurate. It carefully outlines the molecular research in Alzheimer’s outside the brain and argues that a more thorough, whole-body diagnosis will provide better answers about its causes and lead to new treatments. It is beneficial to researchers who need to be apprised of the emerging science on the causes of Alzheimer’s, and will hopefully redirect many into new avenues of cellular research and discovery. Comprehensive literature-based summary of the current state of molecular Alzheimer’s disease research Details the shortcomings of the prevailing model and therapeutics in development Reviews blood-based biomarkers for Alzheimer’s and their link to amyloid- and Tau-independent causes outside the brain Describes the tissues outside the brain impacted by Alzheimer’s and the underlying molecular causes Explains the whole-body risks associated with Alzheimer’s, along with concomitant measures to slow or prevent the disease Provides a protocol to properly research, evaluate, measure, diagnose, and potentially treat Alzheimer’s patients

The Neuronal Doctrine recently reached its 100th year and together with the development of psychopharmacology by the middle of 20th century promoted spectacular developments in the knowledge of the biological bases of behavior. The overwhelming amount of data accumulated, forced the division of neuroscience into several subdisciplines, but this division needs to dissolve in the 21st century and focus on specific processes that involve diverse methodological and theoretical approaches. The chapters contained in this book illustrate that neuroscience converges in the search for sound answers to several questions, including the pathways followed by cells, how individuals communicate with each other, inflammation, learning and memory, the development of drug dependence, and approaches to explaining the processes that underlie two highly incapacitating chronic degenerative illnesses.

The dementia challenge is the largest health effort of the times we live in. The whole society has to move to a realization of the significance of prioritization to make an attempt in the direction of mental health promotion and dementia risk reduction. New priorities for research are needed to go far beyond the usual goal of constructing a disease course-modifying medication. Moreover, a full empowerment and engagement of men and women living with dementia and their caregivers, overcoming stigma and discrimination should be promoted. The common efforts and the final aim will have to be the progress of a ''dementia-constructive'' world, where people with dementia can take advantage of equal opportunities.

Amyloid-forming proteins are implicated in over 30 human diseases. The proteins involved in each disease have unrelated sequences and dissimilar native structures, but they all undergo conformational alterations to form fibrillar polymers. The fibrillar assemblies accumulate progressively into disease-specific lesions in vivo. Substantial evidence suggests these lesions are the end state of aberrant protein folding whereas the actual disease-causing culprits likely are soluble, non-fibrillar assemblies preceding the aggregates. The non-fibrillar protein assemblies range from small, low-order oligomers to spherical, annular, and protofibrillar species. Oligomeric species are believed to mediate various pathogenic mechanisms that lead to cellular dysfunction, cytotoxicity, and cell loss, eventuating in disease-specific degeneration and systemic morbidity. The particular pathologies thus are determined by the afflicted cell types, organs, systems, and the proteins involved. Evidence suggests that the oligomeric species may share structural features and possibly common mechanisms of action. In many cases, the structure–function interrelationships amongst the various protein assemblies described in vitro are still elusive. Deciphering these intricate structure–function correlations will help understanding a complex array of pathogenic mechanisms, some of which may be common across different diseases albeit affecting different cell types and systems.

Herpesviruses are unique among viruses as they encode for a complex self-regulatory system, aggressively invade and persist in the host, evade immune defense, alter all regulatory mechanisms of the macroorganism and modify the replication of heterologous viruses. Environmental factors influence these unconventional relationships. Consequently, a single herpesvirus species can be attributed to a wide range of diseases as etiological agents or cofactors. This book is intended to give an overview on selected clinical hot topics: herpes simplex virus encephalitis, persistent infection in the gingiva, thymidine kinase gene expression causing male infertility, and pharmaceutical reactivation of Epstein-Barr virus for oncolysis. Immune evasion mechanisms and new ways to formulate vaccines are exhaustively reviewed. Finally, a surprise: bovine herpesviruses could serve as models to study the pathomechanism of herpesviruses.

The fifth edition of this comprehensive text explains the key issues, concepts and clinical applications of cognitive neuroscience.