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Updated: Aug 3, 2025

Imaging the Intracellular Trafficking of APP with Photoactivatable GFP
Published on: October 17, 2015
Untangle the mystery behind DS-associated AD - Is APP the main protagonist?
Ajay Elangovan1, Harysh Winster Suresh Babu1, Mahalaxmi Iyer2
1Stem Cell and Regenerative Medicine/ Translational Research, Department of Zoology, School of Basic Sciences, Central University of Punjab, Bathinda 151401, Punjab, India; Human Molecular Cytogenetics and Stem Cell Laboratory, Department of Human Genetics and Molecular Biology, Bharathiar University, Coimbatore 641 046, Tamil Nadu, India.
Abstract:
Amyloid precursor protein profusion in Trisomy 21, also called Down Syndrome (DS), is rooted in the genetic determination of Alzheimer's disease (AD). With the recent development in patient care, the life expectancy of DS patients has gradually increased, leading to the high prospect of AD development, consequently leading to the development of plaques of amyloid proteins and neurofibrillary tangles made of tau by the fourth decade of the patient leading to dementia. The altered gene expression resulted in cellular dysfunction due to impairment of autophagy, mitochondrial and lysosomal dysfunction, and copy number variation controlled by the additional genes in Trisomy 21. The cognitive impairment and mechanistic insights underlying DS-AD conditions have been reviewed in this article. Some recent findings regarding biomarkers and therapeutics of DS-AD conditions were highlighted in this review.
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