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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Bibliographic Details
Main Author: D'Andrea, Michael R. (Author)
Format: Book
Language:English
Published: Amsterdam Elsevier Academic Press [2015]
Subjects:
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Call Number :med WT 155 .D17 2015

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100 1 |a D'Andrea, Michael R.  |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 Amsterdam  |b Elsevier Academic Press  |c [2015] 
264 4 |c © 2015 
300 |a xxi, 147 pages  |b illustrations (some color)  |c 23 cm 
336 |a text  |2 rdacontent 
337 |a unmediated  |2 rdamedia 
338 |a volume  |2 rdacarrier 
504 |a Includes bibliographical references 
505 0 |a Alzheimer's disease today -- Seeds of a new perspective -- Introducing the "inside-out" hypothesis -- Addressing technical concerns -- The good intentions of formic acid -- Connecting MAP-2 and cell lysis -- Classifying plaques -- When is a star like a plaque -- The inflammation cascade-- Innocent A[beta]42 -- The Alpha 7 nicotinic acetylcholine receptor -- Immunoglobulin: another perpetrator -- Add AD to the list of autoimmune diseases - - The BBB and BRB in AD -- "Inside-out" in the field --Alzheimer's disease tomorrow 
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 
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650 0 |a Alzheimer's disease  |x Pathogenesis 
650 1 2 |a Alzheimer Disease  |x etiology 
650 2 2 |a Alzheimer Disease  |x physiopathology 
650 2 2 |a Neurons  |x pathology 
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