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Alzheimer's disease : insights into low molecular weight and cytotoxic aggregates from in vitro and computer experiments - molecular basis of amyloid-beta protein aggregation and fibril formation / Philippe Derreumaux, University of Paris 7, France, editor.

Contributor(s): Material type: TextTextSeries: Molecular medicine and medicinal chemistryPublisher: Singapore : World Scientific Publishing Company, [2013]Copyright date: ©2013Description: 1 online resource (xix, 444 pages) : illustrationsContent type:
  • text
Media type:
  • computer
Carrier type:
  • online resource
ISBN:
  • 9781848167551
  • 1848167555
Subject(s): Genre/Form: Additional physical formats: Print version:: Alzheimer's disease.DDC classification:
  • 616.831
LOC classification:
  • RC523
NLM classification:
  • WT 155
Online resources: Summary: Alzheimer's disease is the most common form of senile dementia, affecting more than 24 million people worldwide. It is characterised pathologically by abnormally high levels of neurofibrillary tangles resulting from the accumulation of tau protein in dead and dying neurons, and by elevated numbers of senile plaques in the cortex and hippocampus of the brain. The major component of senile plaques is a small protein of 39-43 amino acids called amyloid-? (A?). Thus far, no treatment has been shown to slow the progression of sporadic and familial Alzheimer's disease. A large body of evidence points.
Holdings
Item type Current library Collection Call number Status Date due Barcode Item holds
eBook eBook e-Library EBSCO Medical Available
Total holds: 0

Includes bibliographical references and index.

Description based on print version record.

Alzheimer's disease is the most common form of senile dementia, affecting more than 24 million people worldwide. It is characterised pathologically by abnormally high levels of neurofibrillary tangles resulting from the accumulation of tau protein in dead and dying neurons, and by elevated numbers of senile plaques in the cortex and hippocampus of the brain. The major component of senile plaques is a small protein of 39-43 amino acids called amyloid-? (A?). Thus far, no treatment has been shown to slow the progression of sporadic and familial Alzheimer's disease. A large body of evidence points.

WorldCat record variable field(s) change: 650

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