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Metal Ion Effects on Aβ and Tau Aggregation

Amyloid and tau aggregation are implicated in manifold neurodegenerative diseases and serve as two signature pathological hallmarks in Alzheimer’s disease (AD). Though aging is considered as a prominent risk factor for AD pathogenesis, substantial evidence suggests that an imbalance of essential bio...

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Detalles Bibliográficos
Autores principales: Kim, Anne Claire, Lim, Sungsu, Kim, Yun Kyung
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5796077/
https://www.ncbi.nlm.nih.gov/pubmed/29301328
http://dx.doi.org/10.3390/ijms19010128
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author Kim, Anne Claire
Lim, Sungsu
Kim, Yun Kyung
author_facet Kim, Anne Claire
Lim, Sungsu
Kim, Yun Kyung
author_sort Kim, Anne Claire
collection PubMed
description Amyloid and tau aggregation are implicated in manifold neurodegenerative diseases and serve as two signature pathological hallmarks in Alzheimer’s disease (AD). Though aging is considered as a prominent risk factor for AD pathogenesis, substantial evidence suggests that an imbalance of essential biometal ions in the body and exposure to certain metal ions in the environment can potentially induce alterations to AD pathology. Despite their physiological importance in various intracellular processes, biometal ions, when present in excessive or deficient amounts, can serve as a mediating factor for neurotoxicity. Recent studies have also demonstrated the contribution of metal ions found in the environment on mediating AD pathogenesis. In this regard, the neuropathological features associated with biometal ion dyshomeostasis and environmental metal ion exposure have prompted widespread interest by multiple research groups. In this review, we discuss and elaborate on findings from previous studies detailing the possible role of both endogenous and exogenous metal ions specifically on amyloid and tau pathology in AD.
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spelling pubmed-57960772018-02-09 Metal Ion Effects on Aβ and Tau Aggregation Kim, Anne Claire Lim, Sungsu Kim, Yun Kyung Int J Mol Sci Review Amyloid and tau aggregation are implicated in manifold neurodegenerative diseases and serve as two signature pathological hallmarks in Alzheimer’s disease (AD). Though aging is considered as a prominent risk factor for AD pathogenesis, substantial evidence suggests that an imbalance of essential biometal ions in the body and exposure to certain metal ions in the environment can potentially induce alterations to AD pathology. Despite their physiological importance in various intracellular processes, biometal ions, when present in excessive or deficient amounts, can serve as a mediating factor for neurotoxicity. Recent studies have also demonstrated the contribution of metal ions found in the environment on mediating AD pathogenesis. In this regard, the neuropathological features associated with biometal ion dyshomeostasis and environmental metal ion exposure have prompted widespread interest by multiple research groups. In this review, we discuss and elaborate on findings from previous studies detailing the possible role of both endogenous and exogenous metal ions specifically on amyloid and tau pathology in AD. MDPI 2018-01-02 /pmc/articles/PMC5796077/ /pubmed/29301328 http://dx.doi.org/10.3390/ijms19010128 Text en © 2018 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Review
Kim, Anne Claire
Lim, Sungsu
Kim, Yun Kyung
Metal Ion Effects on Aβ and Tau Aggregation
title Metal Ion Effects on Aβ and Tau Aggregation
title_full Metal Ion Effects on Aβ and Tau Aggregation
title_fullStr Metal Ion Effects on Aβ and Tau Aggregation
title_full_unstemmed Metal Ion Effects on Aβ and Tau Aggregation
title_short Metal Ion Effects on Aβ and Tau Aggregation
title_sort metal ion effects on aβ and tau aggregation
topic Review
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5796077/
https://www.ncbi.nlm.nih.gov/pubmed/29301328
http://dx.doi.org/10.3390/ijms19010128
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