International Journal of Alzheimer’s Disease

Glycogen Synthase Kinase-3


Publishing date
01 Jul 2011
Status
Published
Submission deadline
01 Jan 2011

Lead Editor

1Department of Pathology, University of Melbourne, Melbourne, VIC 3010, Australia

2Neurosignalling Group, Garvan Institute for Medical Research, 384 Victoria St. Darlinghurst, Sydney, Australia

3Centre for Integrative Physiology, University of Edinburgh, George Square, Edinburgh, Scotland EH8 9XD, UK

4Instituto de Química Médica (CSIC), Juan de la Cierva 3, 28006 Madrid, Spain

5Department of Neurobiology, A. I. Virtanen Institute for Molecular Sciences, University of Kuopio, 70211 Kuopio, Finland


Glycogen Synthase Kinase-3

Description

Research into the biology of Alzheimer's disease (AD) has expanded dramatically over the past few decades, and we now have a greater understanding of the complexity of the pathogenic pathways involved. Multiple pathways contribute to the loss of functional synapses in the AD brain, and it is becoming clear that treatments targeting these pathways in isolation will have limited therapeutic value.

It is for this reason that the inhibition of glycogen synthase kinase-3 (GSK3) as a potential therapeutic strategy for AD has generated considerable excitement. GSK3 is one of several kinases that phosphorylates tau, and numerous research reports implicate active GSK3 as a mediator of amyloid-β toxicity. Further to this, levels of active GSK3 are elevated in the AD brain. It therefore appears that the inhibition of GSK3 has the potential to prevent two important pathways in AD; tau hyperphosphorylation and amyloid-β toxicity.

We invite the submission of original research articles as well as review articles on GSK3. We are interested in articles that describe GSK3 in AD-associated toxic pathways, articles on therapeutic strategies developed to target GSK3, and articles on the fundamental biological function of GSK3. By bringing together a broad range of GSK3 reviews, we hope to present a balanced appraisal of GSK3 inhibition as a valid therapeutic strategy to treat AD. Potential topics include, but are not limited to:

  • GSK3 substrates in the brain
  • The kinases and phosphatases that regulate GSK3 phosphorylation
  • The role of GSK3 in the synapse
  • GSK3-mediated regulation of neurite outgrowth and the cytoskeleton
  • GSK3 and microtubule transport
  • A comparison of GSK3 isoforms in the brain
  • GSK3 in transgenic mouse models of AD
  • The role of GSK3 in AD pathology
  • GSK3 as a potential therapeutic target

Before submission authors should carefully read over the journal's Author Guidelines, which are located at http://www.hindawi.com/journals/ijad/guidelines/. Prospective authors should submit an electronic copy of their complete manuscript through the journal Manuscript Tracking System at http://mts.hindawi.com/ according to the following timetable:

International Journal of Alzheimer’s Disease
 Journal metrics
Acceptance rate17%
Submission to final decision100 days
Acceptance to publication36 days
CiteScore3.800
Impact Factor-
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