Common Biological Mechanisms in Alzheimer's Disease and Cancer
- Authors: Maria I. Behrens1, Daniela P. Ponce2, Catherine M. Roe3, Felipe Salech4
-
View Affiliations Hide Affiliations1 Departamento de Neurología y Neurocirugía, Hospital Clínico Universidad de Chile, Chile 2 Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile, Chile 3 Department of Neurology and the Charles F. and Joanne Knight Alzheimer Disease Center, Washington, University School of Medicine in St Louis and 4Clínica Alemana de Santiago, Chile 4 Instituto de Ciencias Biomédicas, Facultad de Medicina, Universidad de Chile, Chile
- Source: Advances in Alzheimer's Research Volume 2 , pp 33-57
- Publication Date: September 2014
- Language: English
Common Biological Mechanisms in Alzheimer's Disease and Cancer, Page 1 of 1
< Previous page | Next page > /docserver/preview/fulltext/9781608058525/chapter-2-1.gif
Epidemiological studies show an inverse association between Alzheimer's disease (AD) and cancer, such that the risk of developing cancer is significantly lower in patients with AD, while participants with a history of cancer in the past have a lower risk of developing AD. In cancer, cell regulation mechanisms are disrupted with augmentation of cell survival and/or proliferation, whereas conversely, AD is associated with increased neuronal death. Here we discuss the possibility that perturbations of mechanisms involved in cell survival/death regulation could be involved in both disorders. Mechanisms that induce changes in the activity of molecules with key roles in determining the decision to "repair and live"- or "die" could play a role in the pathogenesis of the two disorders. As examples, the roles of p53, PARP-1, the Wnt signaling pathway, and the process of adult neurogenesis are discussed as potential candidates that, speculatively, may explain an inverse association between AD and cancer.
-
From This Site
/content/books/9781608058525.chapter-2dcterms_subject,pub_keyword-contentType:Journal -contentType:Figure -contentType:Table -contentType:SupplementaryData105