Mini Review ARTICLE

Front. Pharmacol., 03 May 2012 | doi: 10.3389/fphar.2012.00075

Pathological alteration in the choroid plexus of Alzheimer’s disease: implication for new therapy approaches

  • 1 Neuroscience Group, Instituto de Investigacion Hospital 12 de Octubre (i+12), Madrid, Spain
  • 2 Biomedical Research Networking Center in Neurodegenerative Diseases, Madrid, Spain

Morphological alterations of choroid plexus in Alzheimer’s disease (AD) have been extensively investigated. These changes include epithelial atrophy, thickening of the basement membrane, and stroma fibrosis. As a result, synthesis, secretory, and transportation functions are significantly altered resulting in decreased cerebrospinal fluid (CSF) turnover. Recent studies discuss the potential impacts of these changes, including the possibility of reduced resistance to stress insults and slow clearance of toxic compounds from CSF with specific reference to the amyloid peptide. Here, we review new evidences for AD-related changes in the choroid plexus. The data suggest that the significantly altered functions of the choroid plexus contribute to the multiparametric pathogenesis of late-onset AD.

Keywords: choroid plexus, Alzheimer’s disease, amyloid, mitochondria, cell death, oxidative stress

Citation: Krzyzanowska A and Carro E (2012) Pathological alteration in the choroid plexus of Alzheimer’s disease: implication for new therapy approaches. Front. Pharmacol. 3:75. doi: 10.3389/fphar.2012.00075

Received: 10 January 2012; Accepted: 10 April 2012;
Published online: 03 May 2012.

Edited by:

Joana A. Palha, University of Minho, Portugal

Reviewed by:

Jason B. Wu, Cedars-Sinai Medical Center, USA
Catarina Oliveira, CNC-Center for Neuroscience, Portugal

Copyright: © 2012 Krzyzanowska and Carro. This is an open-access article distributed under the terms of the Creative Commons Attribution Non Commercial License, which permits non-commercial use, distribution, and reproduction in other forums, provided the original authors and source are credited.

*Correspondence: Eva Carro, Neuroscience Group, Instituto de Investigacion Hospital 12 de Octubre (i+12), Avenue de Córdoba s/n, 28041 Madrid, Spain. e-mail: carroeva@h120.es

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