A Common Biological Mechanism in Cancer and Alzheimer's Disease?

被引:138
作者
Behrens, M. I. [1 ,2 ]
Lendon, C. [3 ]
Roe, C. M. [4 ,5 ]
机构
[1] Univ Chile, Hosp Clin, Dept Neurol & Neurocirugia, Santiago, Chile
[2] Clin Alemana Santiago, Santiago, Chile
[3] Queensland Inst Med Res, Brisbane, Qld 4006, Australia
[4] Washington Univ, Sch Med, Alzheimers Dis Res Ctr, St Louis, MO USA
[5] Washington Univ, Sch Med, Dept Neurol, St Louis, MO 63110 USA
关键词
Alzheimer; cancer; tumor suppressors; Pin1; Wnt signaling pathway; PROLYL ISOMERASE PIN1; WNT SIGNALING PATHWAY; NF-KAPPA-B; FRONTOTEMPORAL LOBAR DEGENERATION; BETA-CATENIN; TAU-PHOSPHORYLATION; PARKINSONS-DISEASE; TUMOR-SUPPRESSOR; CELL-DEATH; OXIDATIVE MODIFICATION;
D O I
10.2174/156720509788486608
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
Cancer and Alzheimer's disease (AD) are two common disorders for which the final pathophysiological mechanism is not yet clearly defined. In a prospective longitudinal study we have previously shown an inverse association between AD and cancer, such that the rate of developing cancer in general with time was significantly slower in participants with AD, while participants with a history of cancer had a slower rate 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, either caused by, or concomitant with, beta amyloid (A beta) and tau deposition. The possibility that perturbations of mechanisms involved in cell survival/death regulation could be involved in both disorders is discussed. Genetic polymorphisms, DNA methylation or other mechanisms that induce changes in activity of molecules with key roles in determining the decision to "repair and live" -or "die" could be involved in the pathogenesis of the two disorders. As examples, the role of p53, Pin1 and the Wnt signaling pathway are discussed as potential candidates that, speculatively, may explain inverse associations between AD and cancer.
引用
收藏
页码:196 / 204
页数:9
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