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Lim, Mi Hee
MetalloNeuroChemistry Lab (MNCL)
Research Interests
  • Neurodegenerative disease, small molecule design, network between metal, proteins, and ROS

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Untangling Amyloid-beta, Tau, and Metals in Alzheimer's Disease

Cited 34 times inthomson ciCited 19 times inthomson ci
Title
Untangling Amyloid-beta, Tau, and Metals in Alzheimer's Disease
Author
Lee, SanghyunLiu, YuzhongLiu, Y.Lim, Mi Hee
Keywords
A-BETA; NEUROFIBRILLARY TANGLES; OXIDATIVE STRESS; IN-VITRO; NEURODEGENERATIVE DISORDERS; STRUCTURAL-CHARACTERIZATION; PROTEIN OLIGOMERIZATION; TRANSGENIC MICE; MOUSE MODEL; PHF-TAU
Issue Date
2013-05
Publisher
AMER CHEMICAL SOC
Citation
ACS CHEMICAL BIOLOGY, v.8, no.5, pp.856 - 865
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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DOI
10.1021/cb400080f
ISSN
1554-8929
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PHY_Journal Papers
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