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[Alzheimer's disease and fragile X syndrome: the Wnt/ß-catenin pathway as a common biological mechanism].

INTRODUCTION
Various disorders affecting the canonical Wnt/ß-catenin signalling pathway have been related to the activation or inactivation of oncogenes and tumour suppressor genes that give rise to a number of well-defined neoplasias, as well as several genes involved in a growing group of complaints, including Alzheimer's disease (AD) and fragile X syndrome (FXS).


AIM
To examine the Wnt/ß-catenin signalling pathway as a possible common biological mechanism involved in the origin and development of neurodegenerative conditions and its relationship with cancer.


DEVELOPMENT
We review the most recent biomedical literature dealing with the Wnt/ß-catenin signalling pathway and its participation in the genesis of complaints such as AD and FXS. An analysis is also conducted to determine the role that this metabolic pathway might play in explaining the lowered risk of developing cancer displayed by these patients.


CONCLUSIONS
The evidence found suggests that the Wnt/ß-catenin pathway could be regulating a set of genes linked with the control of the cell cycle and apoptosis. This would give rise to a metabolic state in which, in conditions such as AD and FXS, the cells would be more likely to undergo apoptosis than initiate mitosis, which would in turn account for the reduced risk of developing cancer.