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Alzheimer’s Disease Physiopathology
Call for Papers
Alzheimer’s disease (AD) is a growing epidemic disorder with a debatable physiopathology. The amyloid cascade hypothesis of AD was formulated in 1992. This hypothesis supports the deposition of amyloid beta-peptide (Abeta) in plaques in brain tissue as the cardinal point in the development of AD. In the last 20 years, there exists the best AD physiopathological explanation, which is in agreement with data from monogenetic forms (very rare) of this disease, with some experimental facts from transgenic mice overexpressing amyloid precursor protein (APP). But there are many points from this hypothesis that do not explain AD physiopathology mainly in sporadic AD. And the AD trials in which there is a clearance of the Abeta had disappointing results.
Perhaps the main problem of AD physiopathology is that the other hypotheses (the two hit is the most known) that pretend to explain the physiopathology of AD do not have success (hypothesis related to tau included). In general, these theories put up that the AD physiopathology is much more complicated than the linearity described by the amyloid cascade. Many of them stress the importance of previous derangements of the neuronal metabolism to the appearance of the amyloid cascade, which could be a secondary phenomenon, toxic or protector of several cellular stresses. There is now a credible physiopathological hypothesis for Alzheimer disease. Potential topics include, but are not limited to:
- Is Abeta (or its oligomeric Abeta residuals) a toxic compound precluding the neuronal death or a protective phenomenon?
- Are the vaccine and Abeta antibodies trials result an experimental finding against the cascade hypothesis?
- Is removing Abeta (or stopping neurofibrillary tangle) the way to cure AD?
- Will the like-prion transmission of Abeta change the current understanding of AD?
- Alternative hypothesis to amyloid cascade in AD.
Before submission authors should carefully read over the journal's Author Guidelines which are located at http://www.hindawi.com/journals/bmri/guidelines/. Prospective authors should submit an electronic copy of their complete manuscript through the journal Manuscript Tracking System at http://mts.hindawi.com/submit/journals/bmri/neuroscience/adp/ according to the following timetable:
|Manuscript Due||Friday, 13 December 2013|
|First Round of Reviews||Friday, 7 March 2014|
|Publication Date||Friday, 2 May 2014|
Lead Guest Editor
- Félix Bermejo-Pareja, Neurology Department and Research Institute, University Hospital “12 de Octubre,” Madrid, Spain