Alzheimer’s Disease

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Guest Editor
Dr. Khue Vu Nguyen
1. Department of Medicine, Biochemical Genetics and Metabolism, The Mitochondrial and Metabolic Disease Center, School of Medicine, University of California, San Diego, Building CTF, Room C-103, 214 Dickinson Street, San Diego, CA 92103-8467, USA
2. Department of Pediatrics, University of California, San Diego, School of Medicine, San Diego, La Jolla, CA 92093, USA
Tel: +1 619 543 2105
Fax: +1 619 543 7868

Research Interests: Molecular Biology, Genetic Diseases, Enzymology, Biosensors, Biopolymers,
Neurodevelopmental and Neurodegenerative Disorders, and Cancer.

It is with great pleasure to introduce a special issue, namely “Alzheimer’s disease”, which is scheduled to appear this year in AIMS Neuroscience.  I cordially invite authors to contribute their excellent works to this exciting forum.  Submissions are now open and will be fully considered for publication.

More than 45 million people worldwide have Alzheimer’s disease (AD), a deterioration of memory and other cognitive domains that leads to death within 3 to 9 years after diagnosis.  The principal risk factor for AD is age.  As the aging population increases, the prevalence will approach 131 million cases worldwide in 2050.  AD is therefore a global problem creating a rapidly growing epidemic and becoming a major threat to healthcare in our societies.  It has been more than 20 years since it was first proposed the amyloid hypothesis in which the neurodegeneration in AD may be caused by deposition of amyloid-β (Aβ) peptides in plaques in brain tissue.  Current available medications appear to be able to produce moderate symptomatic benefits but not to stop disease progression.  The search for biomarkers as well as novel therapeutic approaches for AD has been a major focus of research.  Recent findings, however, show that neuronal-injury biomarkers are independent of Aβ suggesting epigenetic modifications, gene-gene and/or gene-environment interactions in the disease etiology, and calling for reconsideration of the pathological cascade and assessment of alternative therapeutic strategies.  As such, greater insights into the physiological function of the β-amyloid precursor protein (APP) are required.  In addition, recent research results regarding the expression APP gene resulting in the presence of various APP-mRNA isoforms and their quantification, especially for identifying the most abundant one that may decisive for the normal status or disease risk, have been described.  These findings may provide new directions for the research in neurodevelopmental and neurodegenerative disorders in which the APP gene is involved in the pathogenesis of diseases and may pave the way for new strategies applicable to rational antisense drugs design. 

Paper submission
All manuscripts will be peer-reviewed before their acceptance for publication.
The deadline for manuscript submission is 30th October 2019.

Instructions for authors
Please submit your manuscript to online submission system

Mohammad Azizur Rahman, Shahdat Hossain, Noorlidah Abdullah, Norhaniza Aminudin
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Khue Vu Nguyen
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Danton H. O’Day
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Khue Vu Nguyen
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