NG2 cells, a new trail for Alzheimer’s disease mechanisms?
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- 作者：Henrietta M Nielsen (1) (2)
Danyal Ek (1)
Una Avdic (1)
Camilla Orbj?rn (1)
Oskar Hansson (3)
Robert Veerhuis (5)
Annemieke JM Rozemuller (6)
Arne Brun (7)
Lennart Minthon (1) (3)
Malin Wennstr?m (1) - 关键词：NG2 cells ; Alzheimer’s disease ; Amyloid beta ; Cerebrospinal fluid ; Brain tissue ; Cell culture
- 刊名：Acta Neuropathologica Communications
- 出版年：2013
- 出版时间：December 2013
- 年：2013
- 卷：1
- 期：1
- 全文大小：659KB
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72. Folstein MF, Folstein SE, McHugh PR: - 作者单位：Henrietta M Nielsen (1) (2)
Danyal Ek (1)
Una Avdic (1)
Camilla Orbj?rn (1)
Oskar Hansson (3)
Robert Veerhuis (5)
Annemieke JM Rozemuller (6)
Arne Brun (7)
Lennart Minthon (1) (3)
Malin Wennstr?m (1)
1. Department of Clinical Sciences Malm?, Molecular Memory Research Unit, Lund University, The Wallenberg Laboratory 2nd floor, Inga Marie Nilssons gata, entrance 53, Sk?ne University Hospital, Malm?, 205 02, Sweden
2. Department of Neuroscience, Mayo Clinic College of Medicine, 4500 San Pablo Road, Jacksonville, FL, 32224, USA
3. Department of Clinical Sciences Malm?, Clinical Memory Research Unit, The Memory Clinic at Sk?ne University Hospital (SUS), Lund University, Malm?, 205 02, Sweden
5. Department of Clinical Chemistry, Neuroscience Campus Amsterdam, VU University Medical Center, Amsterdam, The Netherlands
6. Department of Pathology, Neuroscience Campus Amsterdam, VU University Medical Center, Amsterdam, The Netherlands
7. Department of Pathology, Lund University, Lund, 22224, Sweden - ISSN：2051-5960
文摘
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 A?1-42, 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.