Copper and Zinc Dysregulation in Alzheimer's Disease

被引:264
作者
Sensi, Stefano L. [1 ,2 ,3 ,4 ]
Granzotto, Alberto [1 ,2 ]
Siotto, Mariacristina [5 ]
Squitti, Rosanna [6 ]
机构
[1] CeSI MeT, Ctr Excellence Aging & Translat Med, Chieti, Italy
[2] Univ G dAnnunzio, Dept Neurosci Imaging & Clin Sci, Chieti, Italy
[3] Univ Calif Irvine, Inst Mind Impairments & Neurol Disorders, Dept Neurol, Irvine, CA USA
[4] Univ Calif Irvine, Inst Mind Impairments & Neurol Disorders, Dept Pharmacol, Irvine, CA USA
[5] IRCSS Fdn Don Carlo Gnocchi, Milan, Italy
[6] IRCCS Ist Ctr San Giovanni Dio Fatebenefratelli, Brescia, Italy
关键词
MILD COGNITIVE IMPAIRMENT; CERULOPLASMIN-BOUND COPPER; TARGETING A-BETA; WILSON-DISEASE; AMYLOID-BETA; NEUROTROPHIC FACTOR; PRECURSOR PROTEIN; OXIDATIVE STRESS; MEMORY DEFICITS; SERUM IRON;
D O I
10.1016/j.tips.2018.10.001
中图分类号
R9 [药学];
学科分类号
100702 [药剂学];
摘要
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 beta (A beta) 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 A beta 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.
引用
收藏
页码:1049 / 1063
页数:15
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