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Download Alzheimer's Disease by Philippe Derreumaux (ed.) PDF

By Philippe Derreumaux (ed.)

ISBN-10: 1848167547

ISBN-13: 9781848167544

Alzheimer's ailment is the most typical type of senile dementia, affecting greater than 24 million humans world wide. it really is characterized pathologically through abnormally excessive degrees of neurofibrillary tangles caused by the buildup of tau protein in useless and death neurons, and by way of increased numbers of senile plaques within the cortex and hippocampus of the mind. the main portion of senile plaques is a small protein of 39-43 amino acids known as amyloid- (A ). to date, no remedy has been proven to gradual the development of sporadic and familial Alzheimer's disorder.

a wide physique of proof issues, besides the fact that, to the early A -formed oligomers because the fundamental poisonous species in Alzheimer's sickness. a strong technique for constructing pharmaceutical remedies opposed to Alzheimer's is to clarify the pathways of oligomer formation and be sure the constructions of the poisonous aggregates.

This e-book offers a breathtaking view throughout fresh in vitro and in vivo reviews in addition to cutting-edge desktop simulations, designed to extend the readers' knowing of A oligomerisation and fibril formation. whilst, the booklet delves into the pathogenesis of familial and sporadic Alzheimer's affliction on the atomic point of aspect.

Written by means of top authors of their respective fields, this e-book might be worthy to all scientists engaged on Alzheimer's ailment.

Readership: common public, PhD scholars, postdocs, in addition to all scientists operating within the following fields: Alzheimer's sickness, amyloids, neuroscience, oligomers, protofibrils, fibrils, toxicity, constructions, dynamics, kinetics, thermodynamics, all-atom and coarse grained simulations, biophysics, reminiscence, studying, transgenic mouse types, steel ions, membrane, nanoparticles, computational chemistry, drug layout and bioinformatics.

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Extra resources for Alzheimer's Disease

Sample text

L. E. (1994). Expression of the low-affinity nerve growth factor receptor enhances beta-amyloid peptide toxicity, Proc. Natl. Acad. Sci. , 91, 10703–10706. M. J. (2006). Androgens regulate the development of neuropathology in a triple transgenic mouse model of Alzheimer’s disease, J. , 26, 13384–13389. A. A. (2005). Opinion: What is the role of protein aggregation in neurodegeneration? Nat. Rev. Mol. Cell. , 6, 891–898. , Takeuchi, M. and Makita, Z. (2001). Immunohistochemical distribution of the receptor for advanced glycation end products in neurons and astrocytes in Alzheimer’s disease.

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And Stefani, M. (2006). Prefibrillar amyloid aggregates could be generic toxins in higher organisms, J. , 26, 8160–8167. G. and Lynch, G. (1998). Amyloid beta protein is internalized selectively by hippocampal field CA1 and causes neurons to accumulate amyloidogenic carboxyterminal fragments of the amyloid precursor protein, J. Comp. , 397, 139–147. Bechinger, B. (1997). Structure and functions of channel-forming peptides: magainins, cecropins, melittin and alamethicin, J. Membr. , 156, 197–211.

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