Oligomerization of amyloid beta and tau in Alzheimer’s disease

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Guest Editor
Dr. Yongquan Zhang
Program of Cellular Neuroscience, Neurodegeneration and repair, Department of Neurology, Yale School of Medicine, USA.

Manuscript Topics
Alzheimer’s disease (AD) is the most common dementia affecting the health of the aging population. So far there is no cure or prevention for this devastating disease. Postmortem brains of AD patients are featured by intracellular neurofibrillary tangles composed of hyperphosphorylated tau and extracellular amyloid plaques comprising amyloid beta peptides. Recent advance in AD research has demonstrated that oligomers of abeta and tau, rather than the fibrils, are neurotoxic and causal for neurodegeneration. However, the dynamic change of the conformation from monomers to oligomers and the regulation of this process during the progress of AD are not well defined. Moreover, it is still elusive whether toxic oligomers are single species or the mixture of variable isoforms. In this special issue ‘Oligomerization of amyloid beta and tau in Alzheimer’s disease’ we emphasize on the identification, characterization and modulation of the oligomerization of abeta and tau using a variety of biophysical approaches. The ultimate goal of this special issue is to provide an up-to-date view for the frontier research on the pathogenesis of Alzheimer’s disease.

In this context, we would like to invite authors to submit original research and review articles. Submitted papers should not have been previously published nor be currently under consideration for publication elsewhere. All manuscripts will be peer-reviewed before their acceptance for publication. AIMS Biophysics charges 300 USD Article Processing Charge (APC) for accepted paper after peer review. AIMS Biophysics waive the charges for these article types: Review, Editorial, Letter, Conference Reports, Commentary, Corrections, and Erratum.
The deadline for manuscript submission is November 15, 2018.

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