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Single-Walled Carbon Nanotubes Alleviate Autophagic/Lysosomal Defects in Primary Glia from a Mouse Model of Alzheimer’s Disease
[Image: see text] Defective autophagy in Alzheimer’s disease (AD) promotes disease progression in diverse ways. Here, we demonstrate impaired autophagy flux in primary glial cells derived from CRND8 mice that overexpress mutant amyloid precursor protein (APP). Functionalized single-walled carbon nan...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
American Chemical Society
2014
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Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4160261/ https://www.ncbi.nlm.nih.gov/pubmed/25115676 http://dx.doi.org/10.1021/nl501839q |
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author | Xue, Xue Wang, Li-Rong Sato, Yutaka Jiang, Ying Berg, Martin Yang, Dun-Sheng Nixon, Ralph A. Liang, Xing-Jie |
author_facet | Xue, Xue Wang, Li-Rong Sato, Yutaka Jiang, Ying Berg, Martin Yang, Dun-Sheng Nixon, Ralph A. Liang, Xing-Jie |
author_sort | Xue, Xue |
collection | PubMed |
description | [Image: see text] Defective autophagy in Alzheimer’s disease (AD) promotes disease progression in diverse ways. Here, we demonstrate impaired autophagy flux in primary glial cells derived from CRND8 mice that overexpress mutant amyloid precursor protein (APP). Functionalized single-walled carbon nanotubes (SWNT) restored normal autophagy by reversing abnormal activation of mTOR signaling and deficits in lysosomal proteolysis, thereby facilitating elimination of autophagic substrates. These findings suggest SWNT as a novel neuroprotective approach to AD therapy. |
format | Online Article Text |
id | pubmed-4160261 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | American Chemical Society |
record_format | MEDLINE/PubMed |
spelling | pubmed-41602612015-08-12 Single-Walled Carbon Nanotubes Alleviate Autophagic/Lysosomal Defects in Primary Glia from a Mouse Model of Alzheimer’s Disease Xue, Xue Wang, Li-Rong Sato, Yutaka Jiang, Ying Berg, Martin Yang, Dun-Sheng Nixon, Ralph A. Liang, Xing-Jie Nano Lett [Image: see text] Defective autophagy in Alzheimer’s disease (AD) promotes disease progression in diverse ways. Here, we demonstrate impaired autophagy flux in primary glial cells derived from CRND8 mice that overexpress mutant amyloid precursor protein (APP). Functionalized single-walled carbon nanotubes (SWNT) restored normal autophagy by reversing abnormal activation of mTOR signaling and deficits in lysosomal proteolysis, thereby facilitating elimination of autophagic substrates. These findings suggest SWNT as a novel neuroprotective approach to AD therapy. American Chemical Society 2014-08-12 2014-09-10 /pmc/articles/PMC4160261/ /pubmed/25115676 http://dx.doi.org/10.1021/nl501839q Text en Copyright © 2014 American Chemical Society Terms of Use (http://pubs.acs.org/page/policy/authorchoice_termsofuse.html) |
spellingShingle | Xue, Xue Wang, Li-Rong Sato, Yutaka Jiang, Ying Berg, Martin Yang, Dun-Sheng Nixon, Ralph A. Liang, Xing-Jie Single-Walled Carbon Nanotubes Alleviate Autophagic/Lysosomal Defects in Primary Glia from a Mouse Model of Alzheimer’s Disease |
title | Single-Walled Carbon Nanotubes Alleviate Autophagic/Lysosomal
Defects in Primary Glia from a Mouse Model of Alzheimer’s Disease |
title_full | Single-Walled Carbon Nanotubes Alleviate Autophagic/Lysosomal
Defects in Primary Glia from a Mouse Model of Alzheimer’s Disease |
title_fullStr | Single-Walled Carbon Nanotubes Alleviate Autophagic/Lysosomal
Defects in Primary Glia from a Mouse Model of Alzheimer’s Disease |
title_full_unstemmed | Single-Walled Carbon Nanotubes Alleviate Autophagic/Lysosomal
Defects in Primary Glia from a Mouse Model of Alzheimer’s Disease |
title_short | Single-Walled Carbon Nanotubes Alleviate Autophagic/Lysosomal
Defects in Primary Glia from a Mouse Model of Alzheimer’s Disease |
title_sort | single-walled carbon nanotubes alleviate autophagic/lysosomal
defects in primary glia from a mouse model of alzheimer’s disease |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4160261/ https://www.ncbi.nlm.nih.gov/pubmed/25115676 http://dx.doi.org/10.1021/nl501839q |
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