Bursting Neurons and Fading Memories: An Alternative Hypothesis of the Pathogenesis of Alzheimer's Disease

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9780128019795: Bursting Neurons and Fading Memories: An Alternative Hypothesis of the Pathogenesis of Alzheimer's Disease

Advances in Alzheimer's disease (AD) research have been challenging and without major breakthroughs in understanding its pathological basis. The reigning hypothesis suggests AD is the result of extracellular amyloid deposition that seed to form amyloid plaques, which then grow and kill neighboring neurons. However, there are several inconsistencies with this hypothesis, not to mention the inability to show clinical benefit in several failed clinical trials by pharmaceuticals (i.e., from Pfizer, Eli Lilly, etc.), and it is in the field's best interest to explore and test multiple hypotheses for pathology rather than drive the majority of research on this single amyloid theory. Reviewing many scientifically peer-reviewed publications, this book describes the "Inside-Out" hypothesis on how amyloid escapes the circulatory system through a dysfunctional blood-brain barrier to bind to the alpha 7 nicotinic acetylcholine receptor on pyramidal neurons. Over time, excessive amounts of amyloid appear to be internalized, resulting in neuron death and lysis. This simple mechanism readily explains plaque composition, size, shape, and location. Based on the current direction of research in the field, this hypothesis appears years from any research and development. * The clear, compelling, and unifying "Inside-Out" hypothesis of AD is brought to life through a string of scientific publications, synthesizing many known features of disease pathology* A high-level text on AD pathology, and suggestions for progress in a stagnating field* Point-by-point discussion on the issues surrounding the current amyloid cascade, and possible reasons why current clinical trials have failed* Contains high-quality photomicrographs in support of the "Inside-Out" hypothesis using single, double, and triple immunohistochemistry on human AD CNS tissues* Chapters address the need for a unifying plaque nomenclature, the importance of intracellular amyloid, the blood-brain barrier, inflammation, and autoimmunity

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About the Author:

Michael R. D'Andrea received his PhD in Cell and Developmental Biology and his MS in Molecular Biology at Rutger's University, New Brunswick, NJ, and his BA in Psycho-Biology at Western Maryland College, Westminster, MD. His dissertation work utilized molecular and histological assays to study the regulation of DNA topoisomerases in human cancers. His earlier career concerned the use of the high magnification electron microscopy to support oncogenesis in preclinical models, and then moved into a new field where he and his peers co-invented the chorionic villus sampling method at Thomas Jefferson for clinical chromosomal analysis. In the late 1980s and early 1990s, he mastered immunohistochemical methods at the light and electron microscopy levels when he began publishing his work in scientific journals. However, it wasn't until the mid-1990s, while working at Johnson & Johnson's Pharmaceutical Research & Development as the Target Validation Team Leader, did he become engaged in Alzheimer's disease (AD) research. His Team was responsible for supporting target discovery and validation, while supporting biomarker discovery in preclinical and experimental models using genomic, proteomic, and histopathological methods across many therapeutic areas and was honored with over a dozen Leadership and Scientific awards. Currently, he has over 100 scientifically peer-reviewed scientific publications and invited reviews, about a third of which concern the neuropathology of AD, and holds 11 scientific patents. He has reviewed hundreds of papers for many scientific journals, reviewed international grants in the AD field, and is currently on the editorial board of the journal, Biotechnic & Histochemistry. He has been invited to speak at numerous International, National, and Regional meetings, as well as at Universities and other companies to discuss his novel observations concerning the origin of amyloid plaques, the existence of various plaque types, and most recently that AD is also an autoimmune disease; all of which is presented in this book. Recently, Michael established a contract research company, Slidomics, LLC (www.slidomics.com) to apply his histopathological and target validation expertise by providing high quality data and analysis much like what you see in this book.

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D'Andrea, Michael R.
Published by Elsevier Science Publishing Co Inc, United States (2015)
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Book Description Elsevier Science Publishing Co Inc, United States, 2015. Paperback. Book Condition: New. 228 x 152 mm. Language: English . Brand New Book. Advances in Alzheimer s disease (AD) research have been challenging and without major breakthroughs in understanding its pathological basis. The reigning hypothesis suggests AD is the result of extracellular amyloid deposition that seed to form amyloid plaques, which then grow and kill neighboring neurons. However, there are several inconsistencies with this hypothesis, not to mention the inability to show clinical benefit in several failed clinical trials by pharmaceuticals (i.e., from Pfizer, Eli Lilly, etc.), and it is in the field s best interest to explore and test multiple hypotheses for pathology rather than drive the majority of research on this single amyloid theory. Reviewing many scientifically peer-reviewed publications, this book describes the Inside-Out hypothesis on how amyloid escapes the circulatory system through a dysfunctional blood-brain barrier to bind to the alpha 7 nicotinic acetylcholine receptor on pyramidal neurons. Over time, excessive amounts of amyloid appear to be internalized, resulting in neuron death and lysis. This simple mechanism readily explains plaque composition, size, shape, and location. Based on the current direction of research in the field, this hypothesis appears years from any research and development. Bookseller Inventory # AA59780128019795

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D'Andrea, Michael R.
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Book Description Elsevier Science Publishing Co Inc, United States, 2015. Paperback. Book Condition: New. 228 x 152 mm. Language: English . Brand New Book. Advances in Alzheimer s disease (AD) research have been challenging and without major breakthroughs in understanding its pathological basis. The reigning hypothesis suggests AD is the result of extracellular amyloid deposition that seed to form amyloid plaques, which then grow and kill neighboring neurons. However, there are several inconsistencies with this hypothesis, not to mention the inability to show clinical benefit in several failed clinical trials by pharmaceuticals (i.e., from Pfizer, Eli Lilly, etc.), and it is in the field s best interest to explore and test multiple hypotheses for pathology rather than drive the majority of research on this single amyloid theory. Reviewing many scientifically peer-reviewed publications, this book describes the Inside-Out hypothesis on how amyloid escapes the circulatory system through a dysfunctional blood-brain barrier to bind to the alpha 7 nicotinic acetylcholine receptor on pyramidal neurons. Over time, excessive amounts of amyloid appear to be internalized, resulting in neuron death and lysis. This simple mechanism readily explains plaque composition, size, shape, and location. Based on the current direction of research in the field, this hypothesis appears years from any research and development. Bookseller Inventory # AA59780128019795

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Book Description Elsevier Science Publishing Co Inc. Paperback. Book Condition: new. BRAND NEW, Bursting Neurons and Fading Memories: An Alternative Hypothesis of the Pathogenesis of Alzheimer's Disease, Michael R. D'Andrea, Advances in Alzheimer's disease (AD) research have been challenging and without major breakthroughs in understanding its pathological basis. The reigning hypothesis suggests AD is the result of extracellular amyloid deposition that seed to form amyloid plaques, which then grow and kill neighboring neurons. However, there are several inconsistencies with this hypothesis, not to mention the inability to show clinical benefit in several failed clinical trials by pharmaceuticals (i.e., from Pfizer, Eli Lilly, etc.), and it is in the field's best interest to explore and test multiple hypotheses for pathology rather than drive the majority of research on this single amyloid theory. Reviewing many scientifically peer-reviewed publications, this book describes the "Inside-Out" hypothesis on how amyloid escapes the circulatory system through a dysfunctional blood-brain barrier to bind to the alpha 7 nicotinic acetylcholine receptor on pyramidal neurons. Over time, excessive amounts of amyloid appear to be internalized, resulting in neuron death and lysis. This simple mechanism readily explains plaque composition, size, shape, and location. Based on the current direction of research in the field, this hypothesis appears years from any research and development. * The clear, compelling, and unifying "Inside-Out" hypothesis of AD is brought to life through a string of scientific publications, synthesizing many known features of disease pathology* A high-level text on AD pathology, and suggestions for progress in a stagnating field* Point-by-point discussion on the issues surrounding the current amyloid cascade, and possible reasons why current clinical trials have failed* Contains high-quality photomicrographs in support of the "Inside-Out" hypothesis using single, double, and triple immunohistochemistry on human AD CNS tissues* Chapters address the need for a unifying plaque nomenclature, the importance of intracellular amyloid, the blood-brain barrier, inflammation, and autoimmunity. Bookseller Inventory # B9780128019795

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Book Description Oxford Elsevier LTD Dez 2014, 2014. Taschenbuch. Book Condition: Neu. 228x151x10 mm. Neuware - Advances in Alzheimer's disease (AD) research have been challenging and without major breakthroughs in understanding its pathological basis. The reigning hypothesis suggests AD is the result of extracellular amyloid deposition that seed to form amyloid plaques, which then grow and kill neighboring neurons. However, there are several inconsistencies with this hypothesis, not to mention the inability to show clinical benefit in several failed clinical trials by pharmaceuticals (i.e., from Pfizer, Eli Lilly, etc.), and it is in the field's best interest to explore and test multiple hypotheses for pathology rather than drive the majority of research on this single amyloid theory. Reviewing many scientifically peer-reviewed publications, this book describes the 'Inside-Out' hypothesis on how amyloid escapes the circulatory system through a dysfunctional blood-brain barrier to bind to the alpha 7 nicotinic acetylcholine receptor on pyramidal neurons. Over time, excessive amounts of amyloid appear to be internalized, resulting in neuron death and lysis. This simple mechanism readily explains plaque composition, size, shape, and location. Based on the current direction of research in the field, this hypothesis appears years from any research and development. 147 pp. Englisch. Bookseller Inventory # 9780128019795

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Book Description Oxford Elsevier LTD Dez 2014, 2014. Taschenbuch. Book Condition: Neu. 228x151x10 mm. Neuware - Advances in Alzheimer's disease (AD) research have been challenging and without major breakthroughs in understanding its pathological basis. The reigning hypothesis suggests AD is the result of extracellular amyloid deposition that seed to form amyloid plaques, which then grow and kill neighboring neurons. However, there are several inconsistencies with this hypothesis, not to mention the inability to show clinical benefit in several failed clinical trials by pharmaceuticals (i.e., from Pfizer, Eli Lilly, etc.), and it is in the field's best interest to explore and test multiple hypotheses for pathology rather than drive the majority of research on this single amyloid theory. Reviewing many scientifically peer-reviewed publications, this book describes the 'Inside-Out' hypothesis on how amyloid escapes the circulatory system through a dysfunctional blood-brain barrier to bind to the alpha 7 nicotinic acetylcholine receptor on pyramidal neurons. Over time, excessive amounts of amyloid appear to be internalized, resulting in neuron death and lysis. This simple mechanism readily explains plaque composition, size, shape, and location. Based on the current direction of research in the field, this hypothesis appears years from any research and development. 147 pp. Englisch. Bookseller Inventory # 9780128019795

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