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Role of metal ions in the cognitive decline of Down syndrome
Down syndrome (DS), caused by trisomy of whole or part of chromosome 21 is the most common mental impairment. All people with DS suffer from cognitive decline and develop Alzheimer’s disease (AD) by the age of 40. The appearance of enlarged early endosomes, followed by Amyloid βpeptide deposition, t...
Autores principales: | , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4066992/ https://www.ncbi.nlm.nih.gov/pubmed/25002847 http://dx.doi.org/10.3389/fnagi.2014.00136 |
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author | Malakooti, Nakisa Pritchard, Melanie A. Adlard, Paul A. Finkelstein, David I. |
author_facet | Malakooti, Nakisa Pritchard, Melanie A. Adlard, Paul A. Finkelstein, David I. |
author_sort | Malakooti, Nakisa |
collection | PubMed |
description | Down syndrome (DS), caused by trisomy of whole or part of chromosome 21 is the most common mental impairment. All people with DS suffer from cognitive decline and develop Alzheimer’s disease (AD) by the age of 40. The appearance of enlarged early endosomes, followed by Amyloid βpeptide deposition, the appearance of tau-containing neurofibrillary tangles and basal forebrain cholinergic neuron (BFCN) degeneration are the neuropathological characteristics of this disease. In this review we will examine the role of metal ion dyshomeostasis and the genes which may be involved in these processes, and relate these back to the manifestation of age-dependent cognitive decline in DS. |
format | Online Article Text |
id | pubmed-4066992 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-40669922014-07-07 Role of metal ions in the cognitive decline of Down syndrome Malakooti, Nakisa Pritchard, Melanie A. Adlard, Paul A. Finkelstein, David I. Front Aging Neurosci Neuroscience Down syndrome (DS), caused by trisomy of whole or part of chromosome 21 is the most common mental impairment. All people with DS suffer from cognitive decline and develop Alzheimer’s disease (AD) by the age of 40. The appearance of enlarged early endosomes, followed by Amyloid βpeptide deposition, the appearance of tau-containing neurofibrillary tangles and basal forebrain cholinergic neuron (BFCN) degeneration are the neuropathological characteristics of this disease. In this review we will examine the role of metal ion dyshomeostasis and the genes which may be involved in these processes, and relate these back to the manifestation of age-dependent cognitive decline in DS. Frontiers Media S.A. 2014-06-23 /pmc/articles/PMC4066992/ /pubmed/25002847 http://dx.doi.org/10.3389/fnagi.2014.00136 Text en Copyright © 2014 Malakooti, Pritchard, Adlard and Finkelstein. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) or licensor are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Neuroscience Malakooti, Nakisa Pritchard, Melanie A. Adlard, Paul A. Finkelstein, David I. Role of metal ions in the cognitive decline of Down syndrome |
title | Role of metal ions in the cognitive decline of Down syndrome |
title_full | Role of metal ions in the cognitive decline of Down syndrome |
title_fullStr | Role of metal ions in the cognitive decline of Down syndrome |
title_full_unstemmed | Role of metal ions in the cognitive decline of Down syndrome |
title_short | Role of metal ions in the cognitive decline of Down syndrome |
title_sort | role of metal ions in the cognitive decline of down syndrome |
topic | Neuroscience |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4066992/ https://www.ncbi.nlm.nih.gov/pubmed/25002847 http://dx.doi.org/10.3389/fnagi.2014.00136 |
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