Iron in Neurodegeneration - Cause or Consequence?

被引:221
作者
Ndayisaba, Alain [1 ]
Kaindlstorfer, Christine [1 ]
Wenning, Gregor K. [1 ]
机构
[1] Med Univ Innsbruck, Dept Neurol, Innsbruck, Austria
基金
奥地利科学基金会;
关键词
iron; neurodegeneration; neurodegenerative mechanisms; mitochondrial dysfunction; autophagic-lysosomal dysfunction; protein aggregation; neuroinflammation; AMYLOID PRECURSOR PROTEIN; BLOOD-BRAIN-BARRIER; GLUTATHIONE-PEROXIDASE; 4; METAL TRANSPORTER DMT1; CENTRAL-NERVOUS-SYSTEM; APP MESSENGER-RNA; TARGETING A-BETA; ALZHEIMERS-DISEASE; SUBSTANTIA-NIGRA; ALPHA-SYNUCLEIN;
D O I
10.3389/fnins.2019.00180
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Iron dyshomeostasis can cause neuronal damage to iron-sensitive brain regions. Neurodegeneration with brain iron accumulation reflects a group of disorders caused by iron overload in the basal ganglia. High iron levels and iron related pathogenic triggers have also been implicated in sporadic neurodegenerative diseases including Alzheimer's disease (AD), Parkinson's disease (PD), and multiple system atrophy (MSA). Iron-induced dyshomeostasis within vulnerable brain regions is still insufficiently understood. Here, we summarize the modes of action by which iron might act as primary or secondary disease trigger in neurodegenerative disorders. In addition, available treatment options targeting brain iron dysregulation and the use of iron as biomarker in prodromal stages are critically discussed to address the question of cause or consequence.
引用
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页数:15
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