International Journal of Alzheimer’s Disease

New Thinking on the Etiology and Pathogenesis of Late-Onset Alzheimer’s Disease


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

Lead Editor

1Department of Immunology and Microbiology, School of Medicine, Wayne State University, Detroit, MI 48375, USA

2Department of Pathology, Microbiology, and Immunology, Philadelphia College of Osteopathic Medicine, Philadelphia, PA 19131, USA

3University of Cincinnati, Cincinnati, OH, USA

4School of Psychology and Psychiatry, Monash University, Clayton, VIC 3800, Australia


New Thinking on the Etiology and Pathogenesis of Late-Onset Alzheimer’s Disease

Description

The etiology of early onset Alzheimer's disease (AD) is genetic in nature for the vast majority of patients, with the mutations involved primarily located in pathways dealing with processing of β-amyloid peptide. However, much research over the last two decades has established that, while one or more genetic risk factors have been identified for development of late-onset AD, that disease is not primarily genetic in origin. Research in the field has been strongly influenced by the Amyloid Cascade Hypothesis, which posits that plaques of β-amyloid (neuritic senile plaques, NSP) accumulate in the neuropil, subsequently initiating a neuropathogenic process that engenders insoluble tangles of modified tau protein (neurofibrillary tangles, NFT), and ultimately to progressive cognitive dysfunction. Firm diagnosis of the disease still depends primarily on postmortem examination of the density and character of NSP and NFT in the affected brain. Inflammation in the AD brain has been documented but has not found a major place in the suite of factors playing primary roles in the neuropathogenesis.

Accumulating evidence from animal models and various clinical trials indicates that late-onset AD is not adequately explained solely or primarily by NSP and NFT, even though these are the most obvious and consistent pathological features of this disease. Rather, late-onset AD appears to result from a complex interplay between genetic and environmental factors, both aspects of which remain to be elucidated. We are interested in submissions that present alternate viewpoints regarding the apparently complex etiology and pathogenic processes underlying late-onset AD. Articles in the form of primary research papers, reviews of recent developments focusing on etiology and neuropathogenic mechanisms in AD, or hypothesis-driven but evidence-based arguments all will be appropriate. Potential topics include, but are not limited to:

  • Information from comparative genome sequencing studies that shed new light on the complex genetic background providing increased susceptibility to disease induction
  • Information concerning possible environmental influences for induction of late-onset AD
  • Recent insights related to the origin and role of inflammation in the neuropathogenesis of late-onset AD
  • New research into the biochemistry and molecular genetics of the AD brain
  • Ideas concerning the role of the ε4 gene product from the APOE locus in conferring susceptibility to late-onset AD

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:


Articles

  • Special Issue
  • - Volume 2011
  • - Article ID 848395
  • - Editorial

New Thinking on the Etiology and Pathogenesis of Late-Onset Alzheimer's Disease

Alan P. Hudson | Brian J. Balin | ... | Stephen Robinson
  • Special Issue
  • - Volume 2011
  • - Article ID 929042
  • - Research Article

Knockdown of BACE1-AS Nonprotein-Coding Transcript Modulates Beta-Amyloid-Related Hippocampal Neurogenesis

Farzaneh Modarresi | Mohammad Ali Faghihi | ... | Miguel A. Lopez-Toledano
  • Special Issue
  • - Volume 2011
  • - Article ID 690121
  • - Research Article

Beta-Amyloid Downregulates MDR1-P-Glycoprotein (Abcb1) Expression at the Blood-Brain Barrier in Mice

Anja Brenn | Markus Grube | ... | Silke Vogelgesang
  • Special Issue
  • - Volume 2011
  • - Article ID 484021
  • - Research Article

Adenosine A2A Receptor and IL-10 in Peripheral Blood Mononuclear Cells of Patients with Mild Cognitive Impairment

Beatrice Arosio | Luigina Mastronardi | ... | Luigi Bergamaschini
  • Special Issue
  • - Volume 2011
  • - Article ID 865432
  • - Review Article

Possible Role of the Transglutaminases in the Pathogenesis of Alzheimer's Disease and Other Neurodegenerative Diseases

Antonio Martin | Giulia De Vivo | Vittorio Gentile
  • Special Issue
  • - Volume 2011
  • - Article ID 630865
  • - Research Article

The Pathogenesis of Alzheimer's Disease: A Reevaluation of the “Amyloid Cascade Hypothesis”

R. A. Armstrong
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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