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Untangling amyloid-β, tau, and metals in Alzheimer's disease.
ACS Chem Biol. 2013 May 17; 8(5):856-65.AC

Abstract

Protein misfolding and metal ion dyshomeostasis are believed to underlie numerous neurodegenerative diseases, including Alzheimer's disease (AD). The pathological hallmark of AD is accumulation of misfolded amyloid-β (Aβ) peptides and hyperphosphorylated tau (ptau) proteins in the brain. Since AD etiology remains unclear, several hypotheses have emerged to elucidate its pathological pathways. The amyloid cascade hypothesis, a leading hypothesis for AD development, advocates Aβ as the principal culprit. Additionally, evidence suggests that tau may contribute to AD pathology. Aβ and tau have also been shown to impact each other's pathology either directly or indirectly. Furthermore, metal ion dyshomeostasis is associated with these misfolded proteins. Metal interactions with Aβ and tau/ptau also influence their aggregation properties and neurotoxicity. Herein, we present current understanding on the roles of Aβ, tau, and metal ions, placing equal emphasis on each of these proposed features, as well as their inter-relationships in AD pathogenesis.

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Publisher Full Text (DOI)

Authors+Show Affiliations

Savelieff MG
Life Sciences Institute, University of Michigan, Ann Arbor, MI 48109, USA.
Lee S
No affiliation info available
Liu Y
No affiliation info available
Lim MH
No affiliation info available

MeSH

Alzheimer DiseaseAmyloid beta-PeptidesAmyloid beta-Protein PrecursorBrainHomeostasisHumansMetalsOxidative StressPhosphorylationtau Proteins

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, Non-P.H.S.
Review

Language

eng

PubMed ID

23506614

Citation

Savelieff, Masha G., et al. "Untangling Amyloid-β, Tau, and Metals in Alzheimer's Disease." ACS Chemical Biology, vol. 8, no. 5, 2013, pp. 856-65.
Savelieff MG, Lee S, Liu Y, et al. Untangling amyloid-β, tau, and metals in Alzheimer's disease. ACS Chem Biol. 2013;8(5):856-65.
Savelieff, M. G., Lee, S., Liu, Y., & Lim, M. H. (2013). Untangling amyloid-β, tau, and metals in Alzheimer's disease. ACS Chemical Biology, 8(5), 856-65. https://doi.org/10.1021/cb400080f
Savelieff MG, et al. Untangling Amyloid-β, Tau, and Metals in Alzheimer's Disease. ACS Chem Biol. 2013 May 17;8(5):856-65. PubMed PMID: 23506614.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Untangling amyloid-β, tau, and metals in Alzheimer's disease. AU - Savelieff,Masha G, AU - Lee,Sanghyun, AU - Liu,Yuzhong, AU - Lim,Mi Hee, Y1 - 2013/03/18/ PY - 2013/3/20/entrez PY - 2013/3/20/pubmed PY - 2014/1/30/medline SP - 856 EP - 65 JF - ACS chemical biology JO - ACS Chem Biol VL - 8 IS - 5 N2 - Protein misfolding and metal ion dyshomeostasis are believed to underlie numerous neurodegenerative diseases, including Alzheimer's disease (AD). The pathological hallmark of AD is accumulation of misfolded amyloid-β (Aβ) peptides and hyperphosphorylated tau (ptau) proteins in the brain. Since AD etiology remains unclear, several hypotheses have emerged to elucidate its pathological pathways. The amyloid cascade hypothesis, a leading hypothesis for AD development, advocates Aβ as the principal culprit. Additionally, evidence suggests that tau may contribute to AD pathology. Aβ and tau have also been shown to impact each other's pathology either directly or indirectly. Furthermore, metal ion dyshomeostasis is associated with these misfolded proteins. Metal interactions with Aβ and tau/ptau also influence their aggregation properties and neurotoxicity. Herein, we present current understanding on the roles of Aβ, tau, and metal ions, placing equal emphasis on each of these proposed features, as well as their inter-relationships in AD pathogenesis. SN - 1554-8937 UR - https://www.unboundmedicine.com/medline/citation/23506614/Untangling_amyloid_��_tau_and_metals_in_Alzheimer's_disease_ L2 - https://doi.org/10.1021/cb400080f DB - PRIME DP - Unbound Medicine ER -