Artículos de revistas
Cancer imprints an increased PARP-1 and p53-dependent resistance to oxidative stress on lymphocytes of patients that later develop Alzheimer's disease
Fecha
2018Registro en:
Frontiers in Neuroscience, Volumen 12, Issue FEB, 2018,
1662453X
16624548
10.3389/fnins.2018.00058
Autor
Salech Morales, Felipe
Ponce, Daniela P.
San Martín Rovirosa, Carol
Rogers, Nicole K.
Henríquez, Mauricio
Behrens Pellegrino, María Isabel
Institución
Resumen
© 2018 Salech, Ponce, SanMartín, Rogers, Henríquez and Behrens.We have proposed that a common biological mechanism deregulated in opposite directions might explain the inverse epidemiological association observed between Alzheimer's disease (AD) and cancer. Accordingly, we showed that lymphocytes from AD patients have an increased susceptibility, whereas those from survivors of a skin cancer, an increased resistance to oxidative death induced by hydrogen peroxide (H2O2), compared to healthy controls (HC). We investigated the susceptibility to H2O2-induced death of lymphocytes in survivors of any type of cancer and in cancer survivors who later developed AD (Ca & AD). We also explored the involvement of Poly [ADP-ribose] polymerase-1 (PARP-1) and p53 pathways in the process, since both are involved in the increased susceptibility to death of AD lymphocytes. Lymphocytes from 11 cancer and 13 Ca & AD patients, and 12 HC were submitted to increasing concentrations of H2O2 for 20 h. Cell de