Please use this identifier to cite or link to this item: http://hdl.handle.net/2445/113862
Title: Altered blood gene expression of tumor-related genes (PRKCB, BECN1 and CDKN2A) in Alzheimer's disease
Author: Antonell, Anna
Lladó Plarrumaní, Albert
Sánchez del Valle Díaz, Raquel
Sanfeliu i Pujol, Coral
Casserras, Teresa
Rami, Lorena
Muñoz-García, Cristina
Dangla-Valls, Adrià
Balasa, Mircea
Boya, Patricia
Kalko, Susana
Molinuevo, José L.
Keywords: Malalties neurodegeneratives
Malaltia d'Alzheimer
Expressió gènica
Autofàgia
Mitocondris
Sang
Neurodegenerative Diseases
Alzheimer's disease
Gene expression
Autophagy
Mitochondria
Blood
Issue Date: 28-Oct-2015
Publisher: Humana Press.
Abstract: Alzheimer's disease (AD) is the most common of the neurodegenerative diseases. Recent diagnostic criteria have defined a preclinical disease phase during which neuropathological substrates are thought to be present in the brain. There is an urgent need to find measurable alterations in this phase as well as a good peripheral biomarker in the blood. We selected a cohort of 100 subjects (controls = 47; preclinical AD = 11; patients with AD = 42) and analyzed whole blood expression of 20 genes by quantitative polymerase chain reaction. The selected genes belonged to calcium-signaling, senescence and autophagy, and mitochondria/oxidative stress pathways. Additionally, two genes associated with an increased risk of developing AD (CLU and BIN1) were also analyzed. We detected significantly different gene expressions of BECN1 and PRKCB between the control and the AD groups; and, of CDKN2A between the control and the preclinical AD groups. Notably, these three genes are also considered tumor suppressor (CDKN2A and BECN1) or tumor promoter (PRKCB) genes. Gene-gene expression Pearson correlations were computed separately for controls and patients with AD. The significant correlations (p<0.001) were represented in a network analysis with Cytoscape tool, which suggested an uncoupling of mitochondriarelated genes in AD group. Whole blood is emerging as a valuable tissue in the study of the physiopathology of AD.
Note: Versió postprint del document publicat a: https://doi.org/10.1007/s12035-015-9483-9
It is part of: Molecular Neurobiology, 2015, vol. 53, num. 9, p. 5902-5911
Related resource: https://doi.org/10.1007/s12035-015-9483-9
URI: http://hdl.handle.net/2445/113862
ISSN: 0893-7648
Appears in Collections:Articles publicats en revistes (Biomedicina)
Articles publicats en revistes (IDIBAPS: Institut d'investigacions Biomèdiques August Pi i Sunyer)

Files in This Item:
File Description SizeFormat 
659719.pdf784.44 kBAdobe PDFView/Open


Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.