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Journal of Biomedicine and Biotechnology
Volume 2010 (2010), Article ID 805405, 7 pages
Research Article

Gelsolin Restores A 𝛽 -Induced Alterations in Choroid Plexus Epithelium

1Neuroscience Laboratory, Research Center, Hospital 12 de Octubre, Avenida de Córdoba, 28041 Madrid, Spain
2Neurodegenerative Diseases Biomedical Research Center (CIBERNED), Madrid, Spain
3Mitochondrial Diseases Laboratory, Research Center, Hospital 12 de Octubre, 28041 Madrid, Spain
4Rare Disorders Biomedical Research Center (CIBERER), Madrid, Spain

Received 30 June 2009; Accepted 19 January 2010

Academic Editor: Amanda McCann

Copyright © 2010 Teo Vargas et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Histologically, Alzheimer's disease (AD) is characterized by senile plaques and cerebrovascular amyloid deposits. In previous studies we demonstrated that in AD patients, amyloid- 𝛽 (A 𝛽 ) peptide also accumulates in choroid plexus, and that this process is associated with mitochondrial dysfunction and epithelial cell death. However, the molecular mechanisms underlying A 𝛽 accumulation at the choroid plexus epithelium remain unclear. A 𝛽 clearance, from the brain to the blood, involves A 𝛽 carrier proteins that bind to megalin, including gelsolin, a protein produced specifically by the choroid plexus epithelial cells. In this study, we show that treatment with gelsolin reduces A 𝛽 -induced cytoskeletal disruption of blood-cerebrospinal fluid (CSF) barrier at the choroid plexus. Additionally, our results demonstrate that gelsolin plays an important role in decreasing A 𝛽 -induced cytotoxicity by inhibiting nitric oxide production and apoptotic mitochondrial changes. Taken together, these findings make gelsolin an appealing tool for the prophylactic treatment of AD.