Senescence biomarkers in adults and elderly with Down syndrome

Abstract

AbstractBackgroundThe Down syndrome (DS) is a genetic disturb caused for the trisomy of chromosome 21. It is the most common cause of intellectual disability, in addition DS accelerates aging and others development and health problems. Some pathological aspects, common to DS with dementia and Alzheimer disease (AD) suggest common pathogenic aspects. This study aims to investigate biomarkers related to cellular aging and their interrelationship with pathological markers of AD in adults and elderly individuals with DS by determining the expression of apoptotic pathway proteins: β‐catenin plays a role int the cell adhesion, cell survival and cell proliferation, in addition it is a key factor in the Wnt pathway. The activation of Wnt/β‐catenin pathway can protect against neurotoxic effects caused by accumulation of β‐amyloid peptide and the phosphorylation of Tau protein, two neuropathological hallmarks in the AD. The Bcl‐2 protein prevents cell death a promoting the cell survival. The tumoral protein P53 functions in the conservation and stability of DNA. It is normally activated in response of cellular stress, acting in the cell cycle, apoptosis, DNA repairing and the cell metabolism.MethodProteins expressions were measured in platelets from non‐medicated older adults with DS (n=37), and healthy adults and older adults (n=28) by western blotting. The samples were analyzed in duplicate and normalization was done using β‐actin as control.Resultβ‐catenin and P53 expressions were higher in DS samples (p=0.001 and p=0.04 respectively). We found a higher expression of Bcl‐2 in healthy control samples (p=0.05).ConclusionWe concluded that the increased expression of β‐catenin and P53, in addition with the decrease levels of Bcl‐2 might indicate a deregulation in the mechanisms responsible for the cell survival process. It is possible to speculate that these changes are related to the increase in cellular stress related to DS.