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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 neighbor...

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Detalles Bibliográficos
Clasificación:Libro Electrónico
Autor principal: D'Andrea, Michael R. (Michael Robert) (Autor)
Formato: Electrónico eBook
Idioma:Inglés
Publicado: London : Elsevier, [2015]
Temas:
Acceso en línea:Texto completo

MARC

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100 1 |a D'Andrea, Michael R.  |q (Michael Robert),  |e author. 
245 1 0 |a Bursting neurons and fading memories :  |b an alternative hypothesis of the pathogenesis of Alzheimer's disease /  |c Michael R. D'Andrea. 
264 1 |a London :  |b Elsevier,  |c [2015] 
264 4 |c �2015 
300 |a 1 online resource (170 pages) :  |b illustrations (some color) 
336 |a text  |b txt  |2 rdacontent 
337 |a computer  |b c  |2 rdamedia 
338 |a online resource  |b cr  |2 rdacarrier 
504 |a Includes bibliographical references. 
588 0 |a Online resource; title from PDF title page (ebrary, viewed October 22, 2014). 
520 |a 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 
505 0 |a Cover; Title Page; Copyright Page; Dedication; Table of contents; About the Author; Preface; Acknowledgments; Introduction; References; Chapter 1 -- Alzheimer's Disease Today; Neurological factors; Non-neurological factors; The amyloid cascade; Looking ahead; References; Chapter 2 -- Seeds of a New Perspective; Histology; Ready to start; References; Chapter 3 -- Introducing the "Inside-Out" Hypothesis; Presentation time; References; Chapter 4 -- Addressing Technical Concerns; Lipofuscin; Primary antibodies; Heat is the ticket; Antibodies; In situ ELISA; References 
505 8 |a Chapter 5 -- The Good Intentions of Formic AcidFormic acid is the problem; Running like mascara; Reference; Chapter 6 -- Connecting MAP-2 and Cell Lysis; Reverse logic; Diffuse plaques are benign; Troublesome end point; Reference; Chapter 7 -- Classifying Plaques; Three dimensions; Multiple colors; Inflammation; Triple IHC; Microglia's unanticipated location; The diffuse amyloid plaque; Diffuse-vascular amyloid plaques; Dense-vascular amyloid plaques and others; Call for a nomenclature; References; Chapter 8 -- When Is a Star Like a Plaque?; Similar initial hypotheses; New technology 
505 8 |a Reflections of a discoveryReinforcing evidence; Star nomenclature; Scientific parallels; Composition; Closing comment; References; Chapter 9 -- The Inflammation Cascade; References; Chapter 10 -- Innocent Ab42; References; Chapter 11 -- The Alpha 7 Nicotinic Acetylcholine Receptor; References; Chapter 12 -- Immunoglobulin: Another Perpetrator; Immunoglobulin neurons; Degenerating Ig-positive neurons; References; Chapter 13 -- Add AD to the List of Autoimmune Diseases; References; Chapter 14 -- The BBB and BRB in AD; BRB, a vascular harbinger; In vivo BBB support; References 
505 8 |a Chapter 15 -- "Inside-Out" in the FieldNeuronal death by amyloid (via vascular issues); Neuronal death by ApoE4; Neuronal death by inflammation; Neuronal death by tau; Neuronal death by autoantibodies; Miscellaneous notes; References; Chapter 16 -- Alzheimer's Disease Tomorrow; State of the AD nation; Targeting the a7 receptor; Targeting Ab42: not plaques; Targeting the BBB; Targeting inflammation; Biomarker discovery; Assessing BBB integrity via BRB; New work; Closing statement; References; Glossary 
650 0 |a Alzheimer's disease  |x Pathogenesis. 
650 2 |a Alzheimer Disease  |x etiology  |0 (DNLM)D000544Q000209 
650 6 |a Maladie d'Alzheimer  |0 (CaQQLa)201-0114128  |x Pathogen�ese.  |0 (CaQQLa)201-0377536 
650 7 |a Alzheimer's disease  |x Pathogenesis  |2 fast  |0 (OCoLC)fst00806555 
776 0 8 |i Print version:  |a D'Andrea, Michael R.  |t Bursting neurons and fading memories : an alternative hypothesis of the pathogenesis of Alzheimer's disease.  |d London : Elsevier, [2015]  |z 9780128019795  |w (OCoLC)903315326 
856 4 0 |u https://sciencedirect.uam.elogim.com/science/book/9780128019795  |z Texto completo