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Trends Pharmacol Sci. 2018 Dec;39(12):1049-1063. doi: 10.1016/j.tips.2018.10.001. Epub 2018 Oct 20.

Copper and Zinc Dysregulation in Alzheimer's Disease.

Author information

1
Center of Excellence on Aging and Translational Medicine, CeSI-MeT, Chieti, Italy; Department of Neuroscience, Imaging, and Clinical Sciences, University G. d'Annunzio of Chieti-Pescara, Chieti-Pescara, Italy; Departments of Neurology and Pharmacology, Institute for Mind Impairments and Neurological Disorders, University of California, Irvine, Irvine, USA. Electronic address: ssensi@uci.edu.
2
Center of Excellence on Aging and Translational Medicine, CeSI-MeT, Chieti, Italy; Department of Neuroscience, Imaging, and Clinical Sciences, University G. d'Annunzio of Chieti-Pescara, Chieti-Pescara, Italy.
3
IRCSS Fondazione Don Carlo Gnocchi, Milan, Italy.
4
IRCCS Istituto Centro San Giovanni di Dio Fatebenefratelli, Brescia, Italy. Electronic address: rosanna.squitti@afar.it.

Abstract

Alzheimer's disease (AD) is one of the most common forms of dementia. Despite a wealth of knowledge on the molecular mechanisms involved in AD, current treatments have mainly focused on targeting amyloid β (Aβ) production, but have failed to show significant effects and efficacy. Therefore, a critical reconsideration of the multifactorial nature of the disease is needed. AD is a complex multifactorial disorder in which, along with Aβ and tau, the convergence of polygenic, epigenetic, environmental, vascular, and metabolic factors increases the global susceptibility to the disease and shapes its course. One of the cofactors converging on AD is the dysregulation of brain metals. In this review, we focus on the role of AD-related neurodegeneration and cognitive decline triggered by the imbalance of two endogenous metals: copper and zinc.

KEYWORDS:

BDNF; Wilson’s disease; amyloid; ceruloplasmin; excitotoxicity; synaptic plasticity

PMID:
30352697
DOI:
10.1016/j.tips.2018.10.001
[Indexed for MEDLINE]

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