International Journal of Alzheimer’s Disease

The Contribution of the Amyloid Hypothesis to the Understanding of Alzheimer’s Disease: A Critical Overview

Publishing date
15 May 2012
Submission deadline
15 Nov 2011

Lead Editor

1Laboratory of Amyloidosis and Neurodegeneration, Leloir Institute. IIBBA-CONICET, Ciudad de Buenos Aires, Argentina

2University of Texas at San Antonio, San Antonio, TX, USA

3Department of Neurodegenerative Diseases, Carlo Besta Neurological Institute (CBNI), Milan, Italy

The Contribution of the Amyloid Hypothesis to the Understanding of Alzheimer’s Disease: A Critical Overview


Alzheimer's disease (AD) was first described over a century ago; however, at the present its precise etiology remains unknown. Several hypotheses have been postulated to explain the pathogenesis of sporadic AD. Among these, the “amyloid cascade hypothesis” (ACH) has gained enormous relevance based on genetic and biochemical evidence. One of its major predictions is that the interference with Aß aggregation may be therapeutically useful. Interestingly, the outcome of recent clinical trials including vaccination and targeted therapy aimed at reducing extracellular Aß levels suggests that such strategy may not have the expected impact on AD progression and, in some cases, it may even cause life-threatening side effects. Thus, we think it is timely and highly relevant to the AD research community to revisit this subject in a thorough, objective, and open-minded way.

In addition to papers tackling the ACH, we are interested in articles that explore advances in molecular genetics and molecular diagnostics, new insights into neuropathology using animal models, and current concepts in the treatment of AD. Potential topics include, but are not limited to:

  • Biomarkers to diagnose AD
  • Genetic polymorphisms as risk factors for AD
  • New cellular and animal models to understand AD pathogenesis
  • Alterations in the metabolism of APP, Aß, and tau protein and their impact on cell membrane, ion-exchange, and key metabolic functions of the cell
  • Compensatory processes of the brain to overcome changing conditions in normal and pathologic aging
  • Mitochondrial function and biochemical pathways in normal aging and AD brains

Before submission authors should carefully read over the journal's Author Guidelines, which are located at Prospective authors should submit an electronic copy of their complete manuscript through the journal Manuscript Tracking System at according to the following timetable:


  • Special Issue
  • - Volume 2012
  • - Article ID 709613
  • - Editorial

The Contribution of the Amyloid Hypothesis to the Understanding of Alzheimer's Disease: A Critical Overview

Laura Morelli | George Perry | Fabrizio Tagliavini
  • Special Issue
  • - Volume 2012
  • - Article ID 383796
  • - Review Article

The Alzheimer's Amyloid-Degrading Peptidase, Neprilysin: Can We Control It?

N. N. Nalivaeva | N. D. Belyaev | ... | A. J. Turner
  • Special Issue
  • - Volume 2012
  • - Article ID 489428
  • - Review Article

Apolipoprotein E: Essential Catalyst of the Alzheimer Amyloid Cascade

Huntington Potter | Thomas Wisniewski
  • Special Issue
  • - Volume 2012
  • - Article ID 321280
  • - Research Article

Insulin Receptor Expression and Activity in the Brains of Nondiabetic Sporadic Alzheimer’s Disease Cases

Lap Ho | Shrishailam Yemul | ... | Giulio Maria Pasinetti
  • Special Issue
  • - Volume 2012
  • - Article ID 369808
  • - Review Article

Alzheimer's Disease and the Amyloid Cascade Hypothesis: A Critical Review

Christiane Reitz
  • Special Issue
  • - Volume 2012
  • - Article ID 353145
  • - Review Article

The Amyloid Precursor Protein Intracellular Domain-Fe65 Multiprotein Complexes: A Challenge to the Amyloid Hypothesis for Alzheimer's Disease?

Daniel A. Bórquez | Christian González-Billault
International Journal of Alzheimer’s Disease
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