International Journal of Alzheimer’s Disease

Genetics and Genomics of Late-Onset Alzheimer's Disease and Its Endophenotypes


Publishing date
01 Mar 2011
Status
Published
Submission deadline
01 Sep 2010

1G.H. Sergievsky Center, Taub Institute for Research on the Aging Brain and the Department of Neurology, Columbia University, New York, NY 10032, USA

2Centre for Research in Neurodegenerative Diseases, University of Toronto, Toronto, ON, Canada M551A8

3Department of Medical and Molecular Genetics, Indiana University, Indianapolis, IN, USA

4Departments of Medicine, Neurology, Genetics & Genomics, Epidemiology, and Biostatistics, Boston University Schools of Medicine and Public Health, Boston, MA, USA


Genetics and Genomics of Late-Onset Alzheimer's Disease and Its Endophenotypes

Description

Late-onset Alzheimer's disease (AD) is the most common cause of dementia in western societies. Despite remarkable advances in the past few years in the technologies available for human genetic studies, only a small proportion of the genetic contribution to AD has been identified. This leaves many remaining genetic risk factors still to be identified. There are several possible reasons for our failure to rapidly advance the field of AD genetics. First, AD is a multifactorial complex disorder with both genetic and environmental components. Second, multiple genes, each with small effects, are likely to contribute not only to AD susceptibility, but also to the quantitative traits associated with the disease (i.e., endophenotypes), including memory performance, amyloid/tau pathology, or hippocampal atrophy. Identifying the genetics underlying the variation in these endophenotypes could shed light on disease pathogenesis and would provide potential targets for effective treatment, screening, and prevention.

We invite investigators to submit original research and review articles that seek to elucidate the genetic factors contributing to the molecular pathologies underlying AD and its endophenotypes. We are particularly interested in articles that explore these factors in either humans or animal models of AD. We would also encourage manuscripts that focus on genetic, functional, translational, or bioinformatic approaches to gene identification.

Potential topics include, but are not limited to:

  • Genetic linkage and association studies of AD
  • Genetic studies employing CSF and blood biomarkers, imaging markers, or neuropsychological measures
  • Meta-analyses of existing genetic data
  • Gene-environment and gene-gene interactions in AD
  • Studies employing sequence analysis, structure analysis, or gene expression analysis
  • Studies employing bioinformatic and computational methods to identify genetic networks in AD
  • Epigenetics in AD
  • Pharmacogenomic or pharmacogenetic studies in AD
  • Results of animal models designed to identify novel genes contributing to AD or its related endophenotypes.

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
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Acceptance rate17%
Submission to final decision100 days
Acceptance to publication36 days
CiteScore4.900
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