Abstract
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.
Highlights
In the recent years, much attention has been directed to the roles of the choroid plexus in the central nervous system (CNS) under both normal and pathological conditions
The deficits in mitochondrial activity, increase in oxidative stress together with above mentioned morphological changes which are observed in Alzheimer’s disease (AD), are likely to lead to abnormal brain Aβ clearance at the blood–CSF barrier (BCSFB), and increased or defective Aβ processing from amyloid precursor protein (APP), which has been described in choroid plexus (Kalaria et al, 1996; Premkumar and Kalaria, 1996) and would contribute to the development of Aβ accumulation in this tissue
We have shown that mitochondrial dysfunction in choroid plexus from AD subjects occurs through a down-regulation of mitochondrial proteins and activity (Vargas et al, 2010b)
Summary
Much attention has been directed to the roles of the choroid plexus in the central nervous system (CNS) under both normal and pathological conditions. This specialized ventricular structure has recently emerged as a key player in a variety of processes that monitor and maintain the biochemical and cellular homeostasis of the CNS. Epithelial cells acquire numerous lipofuscin vacuoles and Biondi bodies increase significantly in AD patients (Miklossy et al, 1998; Wen et al, 1999; Alvira-Botero and Carro, 2010) These modifications could alter choroid plexus functions, including synthesis, secretion, and transport of proteins and other molecules. In the authors’ view, altered choroid plexus functions may be, at least, one of the primary pathogenic events in late-onset AD www.frontiersin.org
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