ADAM10 Gene Expression Does Not Differ In Alzheimer?s Disease | 21987
Journal of Alzheimers Disease & Parkinsonism
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Dementia from Alzheimer?s disease (AD) is the most common type of dementia, accounting for approximately 60% of the
cases. Regarding the immense financial, physical and emotional burden of AD, there is a pursuit to find sensitive and
specific biomarkers for this disease. Since the brain histological hallmarks of the disease are amyloid-?1-42 (A?1-42), total Tau
(T-Tau) and Tau phosphorylated (P-Tau), these molecules have been extensively studied. A? peptide is proteolytic fragment
of APP released by sequential cleavages via ? and ?-secretases. In healthy subjects the predominant route of APP processing
consists of successive cleavages by ? and ?-secretase. ADAM10 is the most important ?-secretase involved in cleavage of APP.
Previous studies have demonstrated that protein levels of platelet ADAM10 are reduced in AD patients.In this context, the aim
of this study was to verify the total blood and platelet ADAM10 gene expression in elderly patients with AD dementia and
to compare with mild cognitive impartment (MCI) and healthy elderly subjects. Blood from AD patients, MCI and normal
controls was collected and analyzed by RT-qPCR techniques, using standardized primers for ADAM10 and to endogenous
controls. One-way analysis of variance followed by Bonferroni as a post hoc comparison and Mann-Whitney U followed
by multiple comparison (Kruskal-Wallis and Dunn?s Multiple Comparison Tests) tests were performed. It was observed no
differences between total blood and platelets ADAM10 gene expression in AD patients compared with MCI or controls
patients. Samples for total blood were divided according to CDR and the results were similar, with no difference in ADAM10
gene expression between patients (CDR1, CDR2 or CDR3) and controls (CDR0). In this way, the decrease of ADAM10 protein
levels in platelets from AD patients is not caused by a reduction in platelets or total blood ADAM10 mRNA levels. Further
studies must be performed in order to investigate the influence of other molecules in this pathway, as micro RNAs, for instance.
This would contribute to understand the pathophysiological mechanisms of AD.
Marcia Regina Cominetti completed degree in Biological Sciences (BSc and BA) from the Federal University of Santa Catarina (1993-1997) and Doctor of Science,
Area of Concentration: Physiology, Federal University of Santa Catarina (2000-2004). She completed doctoral internship (2002) at the Department of Microbiology,
University of Virginia Health System, Charlottesville, VA, USA and post-doctorate (2005-2006) at the Institute of Health and RechercheMedicale (INSERM Unite
553) in Paris, France. She is currently a lecturer at the Federal University of Santa Catarina. she has experience in Cell Biology and Biochemistry, Molecular Biology
with an emphasis in acting on the following subjects: integrins, extracellular matrix, cell adhesion, ADAM, Alzheimer?s disease, cancer, angiogenesis, disintegrins,
culture of mammalian cells and expression of recombinant proteins.
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