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NG2 cells, a new trail for Alzheimer’s disease mechanisms?

BACKGROUND: Neuron Glial 2 (NG2) cells are glial cells known to serve as oligodendrocyte progenitors as well as modulators of the neuronal network. Altered NG2 cell morphology and up-regulation as well as increased shedding of the proteoglycan NG2 expressed on the cell surface have been described in...

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Autores principales: Nielsen, Henrietta M, Ek, Danyal, Avdic, Una, Orbjörn, Camilla, Hansson, Oskar, Veerhuis, Robert, Rozemuller, Annemieke JM, Brun, Arne, Minthon, Lennart, Wennström, Malin
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2013
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4046664/
https://www.ncbi.nlm.nih.gov/pubmed/24252600
http://dx.doi.org/10.1186/2051-5960-1-7
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author Nielsen, Henrietta M
Ek, Danyal
Avdic, Una
Orbjörn, Camilla
Hansson, Oskar
Veerhuis, Robert
Rozemuller, Annemieke JM
Brun, Arne
Minthon, Lennart
Wennström, Malin
author_facet Nielsen, Henrietta M
Ek, Danyal
Avdic, Una
Orbjörn, Camilla
Hansson, Oskar
Veerhuis, Robert
Rozemuller, Annemieke JM
Brun, Arne
Minthon, Lennart
Wennström, Malin
author_sort Nielsen, Henrietta M
collection PubMed
description BACKGROUND: Neuron Glial 2 (NG2) cells are glial cells known to serve as oligodendrocyte progenitors as well as modulators of the neuronal network. Altered NG2 cell morphology and up-regulation as well as increased shedding of the proteoglycan NG2 expressed on the cell surface have been described in rodent models of brain injury. Here we describe alterations in the human NG2 cell population in response to pathological changes characteristic of Alzheimer’s disease (AD). RESULTS: Immunohistological stainings of postmortem brain specimens from clinically diagnosed and postmortem verified AD patients and non-demented controls revealed reduced NG2 immunoreactivity as well as large numbers of NG2 positive astrocytes in individuals with high amyloid beta plaque load. Since fibrillar amyloid beta (Aβ)1-42 is the major component of AD-related senile plaques, we exposed human NG2 cells to oligomer- and fibril enriched preparations of Aβ1-42. We found that both oligomeric and fibrillar Aβ1-42 induced changes in NG2 cell morphology. Further, in vitro exposure to fibrillar Aβ1-42 decreased the NG2 concentrations in both cell lysates and supernatants. Interestingly, we also found significantly decreased levels of soluble NG2 in the cerebrospinal fluid (CSF) from clinically diagnosed AD patients compared to non-demented individuals. Additionally, the CSF NG2 levels were found to significantly correlate with the core AD biomarkers Aß1-42, T-tau and P-tau. CONCLUSION: Our results demonstrate major alterations in the NG2 cell population in relation to AD pathology which highlights the NG2 cell population as a new attractive research target in the search for cellular mechanisms associated with AD pathogenesis. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/2051-5960-1-7) contains supplementary material, which is available to authorized users.
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spelling pubmed-40466642014-06-06 NG2 cells, a new trail for Alzheimer’s disease mechanisms? Nielsen, Henrietta M Ek, Danyal Avdic, Una Orbjörn, Camilla Hansson, Oskar Veerhuis, Robert Rozemuller, Annemieke JM Brun, Arne Minthon, Lennart Wennström, Malin Acta Neuropathol Commun Research BACKGROUND: Neuron Glial 2 (NG2) cells are glial cells known to serve as oligodendrocyte progenitors as well as modulators of the neuronal network. Altered NG2 cell morphology and up-regulation as well as increased shedding of the proteoglycan NG2 expressed on the cell surface have been described in rodent models of brain injury. Here we describe alterations in the human NG2 cell population in response to pathological changes characteristic of Alzheimer’s disease (AD). RESULTS: Immunohistological stainings of postmortem brain specimens from clinically diagnosed and postmortem verified AD patients and non-demented controls revealed reduced NG2 immunoreactivity as well as large numbers of NG2 positive astrocytes in individuals with high amyloid beta plaque load. Since fibrillar amyloid beta (Aβ)1-42 is the major component of AD-related senile plaques, we exposed human NG2 cells to oligomer- and fibril enriched preparations of Aβ1-42. We found that both oligomeric and fibrillar Aβ1-42 induced changes in NG2 cell morphology. Further, in vitro exposure to fibrillar Aβ1-42 decreased the NG2 concentrations in both cell lysates and supernatants. Interestingly, we also found significantly decreased levels of soluble NG2 in the cerebrospinal fluid (CSF) from clinically diagnosed AD patients compared to non-demented individuals. Additionally, the CSF NG2 levels were found to significantly correlate with the core AD biomarkers Aß1-42, T-tau and P-tau. CONCLUSION: Our results demonstrate major alterations in the NG2 cell population in relation to AD pathology which highlights the NG2 cell population as a new attractive research target in the search for cellular mechanisms associated with AD pathogenesis. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1186/2051-5960-1-7) contains supplementary material, which is available to authorized users. BioMed Central 2013-05-09 /pmc/articles/PMC4046664/ /pubmed/24252600 http://dx.doi.org/10.1186/2051-5960-1-7 Text en © Nielsen et al.; licensee BioMed Central Ltd. 2013 This article is published under license to BioMed Central Ltd. 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 Research
Nielsen, Henrietta M
Ek, Danyal
Avdic, Una
Orbjörn, Camilla
Hansson, Oskar
Veerhuis, Robert
Rozemuller, Annemieke JM
Brun, Arne
Minthon, Lennart
Wennström, Malin
NG2 cells, a new trail for Alzheimer’s disease mechanisms?
title NG2 cells, a new trail for Alzheimer’s disease mechanisms?
title_full NG2 cells, a new trail for Alzheimer’s disease mechanisms?
title_fullStr NG2 cells, a new trail for Alzheimer’s disease mechanisms?
title_full_unstemmed NG2 cells, a new trail for Alzheimer’s disease mechanisms?
title_short NG2 cells, a new trail for Alzheimer’s disease mechanisms?
title_sort ng2 cells, a new trail for alzheimer’s disease mechanisms?
topic Research
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4046664/
https://www.ncbi.nlm.nih.gov/pubmed/24252600
http://dx.doi.org/10.1186/2051-5960-1-7
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