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Hippocampal expression of cell‐adhesion glycoprotein neuroplastin is altered in Alzheimer's disease
Cell‐adhesion glycoprotein neuroplastin (Np) is involved in the regulation of synaptic plasticity and balancing hippocampal excitatory/inhibitory inputs which aids in the process of associative memory formation and learning. Our recent findings show that neuroplastin expression in the adult human hi...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6349345/ https://www.ncbi.nlm.nih.gov/pubmed/30488668 http://dx.doi.org/10.1111/jcmm.13998 |
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author | Ilic, Katarina Mlinac‐Jerkovic, Kristina Jovanov‐Milosevic, Natasa Simic, Goran Habek, Nikola Bogdanovic, Nenad Kalanj‐Bognar, Svjetlana |
author_facet | Ilic, Katarina Mlinac‐Jerkovic, Kristina Jovanov‐Milosevic, Natasa Simic, Goran Habek, Nikola Bogdanovic, Nenad Kalanj‐Bognar, Svjetlana |
author_sort | Ilic, Katarina |
collection | PubMed |
description | Cell‐adhesion glycoprotein neuroplastin (Np) is involved in the regulation of synaptic plasticity and balancing hippocampal excitatory/inhibitory inputs which aids in the process of associative memory formation and learning. Our recent findings show that neuroplastin expression in the adult human hippocampus is specifically associated with major hippocampal excitatory pathways and is related to neuronal calcium regulation. Here, we investigated the hippocampal expression of brain‐specific neuroplastin isoform (Np65), its relationship with amyloid and tau pathology in Alzheimer's disease (AD), and potential involvement of neuroplastin in tissue response during the disease progression. Np65 expression and localization was analysed in six human hippocampi with confirmed AD neuropathology, and six age‐/gender‐matched control hippocampi by imunohistochemistry. In AD cases with shorter disease duration, the Np65 immunoreactivity was significantly increased in the dentate gyrus (DG), Cornu Ammonis 2/3 (CA2/3), and subiculum, with the highest level of Np expression being located on the dendrites of granule cells and subicular pyramidal neurons. Changes in the expression of neuroplastin in AD hippocampal areas seem to be related to the progression of disease. Our study suggests that cell‐adhesion protein neuroplastin is involved in tissue reorganization and is a potential molecular marker of plasticity response in the early neurodegeneration process of AD. |
format | Online Article Text |
id | pubmed-6349345 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-63493452019-02-01 Hippocampal expression of cell‐adhesion glycoprotein neuroplastin is altered in Alzheimer's disease Ilic, Katarina Mlinac‐Jerkovic, Kristina Jovanov‐Milosevic, Natasa Simic, Goran Habek, Nikola Bogdanovic, Nenad Kalanj‐Bognar, Svjetlana J Cell Mol Med Short Communications Cell‐adhesion glycoprotein neuroplastin (Np) is involved in the regulation of synaptic plasticity and balancing hippocampal excitatory/inhibitory inputs which aids in the process of associative memory formation and learning. Our recent findings show that neuroplastin expression in the adult human hippocampus is specifically associated with major hippocampal excitatory pathways and is related to neuronal calcium regulation. Here, we investigated the hippocampal expression of brain‐specific neuroplastin isoform (Np65), its relationship with amyloid and tau pathology in Alzheimer's disease (AD), and potential involvement of neuroplastin in tissue response during the disease progression. Np65 expression and localization was analysed in six human hippocampi with confirmed AD neuropathology, and six age‐/gender‐matched control hippocampi by imunohistochemistry. In AD cases with shorter disease duration, the Np65 immunoreactivity was significantly increased in the dentate gyrus (DG), Cornu Ammonis 2/3 (CA2/3), and subiculum, with the highest level of Np expression being located on the dendrites of granule cells and subicular pyramidal neurons. Changes in the expression of neuroplastin in AD hippocampal areas seem to be related to the progression of disease. Our study suggests that cell‐adhesion protein neuroplastin is involved in tissue reorganization and is a potential molecular marker of plasticity response in the early neurodegeneration process of AD. John Wiley and Sons Inc. 2018-11-28 2019-02 /pmc/articles/PMC6349345/ /pubmed/30488668 http://dx.doi.org/10.1111/jcmm.13998 Text en © 2018 The Authors. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine. This is an open access article under the terms of the http://creativecommons.org/licenses/by/4.0/ License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Short Communications Ilic, Katarina Mlinac‐Jerkovic, Kristina Jovanov‐Milosevic, Natasa Simic, Goran Habek, Nikola Bogdanovic, Nenad Kalanj‐Bognar, Svjetlana Hippocampal expression of cell‐adhesion glycoprotein neuroplastin is altered in Alzheimer's disease |
title | Hippocampal expression of cell‐adhesion glycoprotein neuroplastin is altered in Alzheimer's disease |
title_full | Hippocampal expression of cell‐adhesion glycoprotein neuroplastin is altered in Alzheimer's disease |
title_fullStr | Hippocampal expression of cell‐adhesion glycoprotein neuroplastin is altered in Alzheimer's disease |
title_full_unstemmed | Hippocampal expression of cell‐adhesion glycoprotein neuroplastin is altered in Alzheimer's disease |
title_short | Hippocampal expression of cell‐adhesion glycoprotein neuroplastin is altered in Alzheimer's disease |
title_sort | hippocampal expression of cell‐adhesion glycoprotein neuroplastin is altered in alzheimer's disease |
topic | Short Communications |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6349345/ https://www.ncbi.nlm.nih.gov/pubmed/30488668 http://dx.doi.org/10.1111/jcmm.13998 |
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