Abstract
Oxidative damage is involved in the pathophysiology of age-related ailments, including Alzheimer’s disease (AD). Studies have shown that the brain tissue and also lymphocytes from AD patients present increased oxidative stress compared to healthy controls (HCs). Here, we use lymphoblastoid cell lines (LCLs) from AD patients and HCs to investigate the role of resveratrol (RV) and selenium (Se) in the reduction of reactive oxygen species (ROS) generated after an oxidative injury. We also studied whether these compounds elicited expression changes in genes involved in the antioxidant cell response and other aging-related mechanisms. AD LCLs showed higher ROS levels than those from HCs in response to H2O2 and FeSO4 oxidative insults. RV triggered a protective response against ROS under control and oxidizing conditions, whereas Se exerted antioxidant effects only in AD LCLs under oxidizing conditions. RV increased the expression of genes encoding known antioxidants (catalase, copper chaperone for superoxide dismutase 1, glutathione S-transferase zeta 1) and anti-aging factors (sirtuin 1 and sirtuin 3) in both AD and HC LCLs. Our findings support RV as a candidate for inducing resilience and protection against AD, and reinforce the value of LCLs as a feasible peripheral cell model for understanding the protective mechanisms of nutraceuticals against oxidative stress in aging and AD.
Highlights
Alzheimer’s disease (AD) is a neurodegenerative disease which is the main cause of dementia worldwide, and it is currently incurable
The two hallmarks of AD are the accumulation of extracellular senile plaques formed by amyloid beta (Aβ) peptides, and the accumulation of hyperphosphorylated tau aggregates that form neurofibrillary tangles (NFTs) inside neurons [3]
Treatment with H2 O2 became significant at 500 μM and 1000 μM H2 O2 in AD and healthy controls (HCs) lymphoblasts, respectively, indicating that AD lymphoblasts are more sensitive to oxidative stress insults
Summary
Alzheimer’s disease (AD) is a neurodegenerative disease which is the main cause of dementia worldwide, and it is currently incurable. It is characterized by a loss of memory and progressive. Understanding the mechanisms that lead to the progression of the disease is essential to establish an early diagnosis and slow or prevent its progression. The two hallmarks of AD are the accumulation of extracellular senile plaques formed by amyloid beta (Aβ) peptides, and the accumulation of hyperphosphorylated tau aggregates that form neurofibrillary tangles (NFTs) inside neurons [3]. In addition to plaques and NFTs, oxidative damage to proteins, nucleic acids, and lipids plays a key role in the pathophysiology of the disease, as in most age-related ailments [4]. It has been reported that Aβ promotes the generation of reactive oxygen species (ROS), either directly or indirectly, by triggering N-methyl-D-aspartate receptor-dependent
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
