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Homeostatic capabilities of the choroid plexus epithelium in Alzheimer's disease
As the secretory source of vitamins, peptides and hormones for neurons, the choroid plexus (CP) epithelium critically provides substances for brain homeostasis. This distributive process of cerebrospinal fluid (CSF) volume transmission reaches many cellular targets in the CNS. In ageing and ageing-r...
Autores principales: | , , , , , , |
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Formato: | Texto |
Lenguaje: | English |
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BioMed Central
2004
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC546405/ https://www.ncbi.nlm.nih.gov/pubmed/15679944 http://dx.doi.org/10.1186/1743-8454-1-3 |
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author | Johanson, Conrad McMillan, Paul Tavares, Rosemarie Spangenberger, Anthony Duncan, John Silverberg, Gerald Stopa, Edward |
author_facet | Johanson, Conrad McMillan, Paul Tavares, Rosemarie Spangenberger, Anthony Duncan, John Silverberg, Gerald Stopa, Edward |
author_sort | Johanson, Conrad |
collection | PubMed |
description | As the secretory source of vitamins, peptides and hormones for neurons, the choroid plexus (CP) epithelium critically provides substances for brain homeostasis. This distributive process of cerebrospinal fluid (CSF) volume transmission reaches many cellular targets in the CNS. In ageing and ageing-related dementias, the CP-CSF system is less able to regulate brain interstitial fluid. CP primarily generates CSF bulk flow, and so its malfunctioning exacerbates Alzheimers disease (AD). Considerable attention has been devoted to the blood-brain barrier in AD, but more insight is needed on regulatory systems at the human blood-CSF barrier in order to improve epithelial function in severe disease. Using autopsied CP specimens from AD patients, we immunocytochemically examined expression of heat shock proteins (HSP90 and GRP94), fibroblast growth factor receptors (FGFr) and a fluid-regulatory protein (NaK2Cl cotransporter isoform 1 or NKCC1). CP upregulated HSP90, FGFr and NKCC1, even in end-stage AD. These CP adjustments involve growth factors and neuropeptides that help to buffer perturbations in CNS water balance and metabolism. They shed light on CP-CSF system responses to ventriculomegaly and the altered intracranial pressure that occurs in AD and normal pressure hydrocephalus. The ability of injured CP to express key regulatory proteins even at Braak stage V/VI, points to plasticity and function that may be boosted by drug treatment to expedite CSF dynamics. The enhanced expression of human CP 'homeostatic proteins' in AD dementia is discussed in relation to brain deficits and pharmacology. |
format | Text |
id | pubmed-546405 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2004 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-5464052005-02-02 Homeostatic capabilities of the choroid plexus epithelium in Alzheimer's disease Johanson, Conrad McMillan, Paul Tavares, Rosemarie Spangenberger, Anthony Duncan, John Silverberg, Gerald Stopa, Edward Cerebrospinal Fluid Res Review As the secretory source of vitamins, peptides and hormones for neurons, the choroid plexus (CP) epithelium critically provides substances for brain homeostasis. This distributive process of cerebrospinal fluid (CSF) volume transmission reaches many cellular targets in the CNS. In ageing and ageing-related dementias, the CP-CSF system is less able to regulate brain interstitial fluid. CP primarily generates CSF bulk flow, and so its malfunctioning exacerbates Alzheimers disease (AD). Considerable attention has been devoted to the blood-brain barrier in AD, but more insight is needed on regulatory systems at the human blood-CSF barrier in order to improve epithelial function in severe disease. Using autopsied CP specimens from AD patients, we immunocytochemically examined expression of heat shock proteins (HSP90 and GRP94), fibroblast growth factor receptors (FGFr) and a fluid-regulatory protein (NaK2Cl cotransporter isoform 1 or NKCC1). CP upregulated HSP90, FGFr and NKCC1, even in end-stage AD. These CP adjustments involve growth factors and neuropeptides that help to buffer perturbations in CNS water balance and metabolism. They shed light on CP-CSF system responses to ventriculomegaly and the altered intracranial pressure that occurs in AD and normal pressure hydrocephalus. The ability of injured CP to express key regulatory proteins even at Braak stage V/VI, points to plasticity and function that may be boosted by drug treatment to expedite CSF dynamics. The enhanced expression of human CP 'homeostatic proteins' in AD dementia is discussed in relation to brain deficits and pharmacology. BioMed Central 2004-12-10 /pmc/articles/PMC546405/ /pubmed/15679944 http://dx.doi.org/10.1186/1743-8454-1-3 Text en Copyright © 2004 Johanson et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License ( (http://creativecommons.org/licenses/by/2.0) ), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Review Johanson, Conrad McMillan, Paul Tavares, Rosemarie Spangenberger, Anthony Duncan, John Silverberg, Gerald Stopa, Edward Homeostatic capabilities of the choroid plexus epithelium in Alzheimer's disease |
title | Homeostatic capabilities of the choroid plexus epithelium in Alzheimer's disease |
title_full | Homeostatic capabilities of the choroid plexus epithelium in Alzheimer's disease |
title_fullStr | Homeostatic capabilities of the choroid plexus epithelium in Alzheimer's disease |
title_full_unstemmed | Homeostatic capabilities of the choroid plexus epithelium in Alzheimer's disease |
title_short | Homeostatic capabilities of the choroid plexus epithelium in Alzheimer's disease |
title_sort | homeostatic capabilities of the choroid plexus epithelium in alzheimer's disease |
topic | Review |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC546405/ https://www.ncbi.nlm.nih.gov/pubmed/15679944 http://dx.doi.org/10.1186/1743-8454-1-3 |
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