In vivo assessment of iron content of the cerebral cortex in healthy aging using 7-Tesla T2*-weighted phase imaging

Buijs, Mathijs; Doan, Nhat Trung; Rooden, Sanneke van; Versluis, Mieke; Lew, Baldur van; Milles, Julien; Buchem, Mark A. van

doi:10.1016/j.neurobiolaging.2016.09.005

Cited by 36 publications

(30 citation statements)

References 46 publications

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“…Brain iron levels inevitably rise during aging and in degenerative diseases, which can be detected both in post-mortem analysis as well as in living individuals; such increases could contribute to an age-dependent risk of ferroptosis (Belaidi and Bush, 2016; Buijs et al, 2017). Genetic evidence also links brain degeneration to ferroptosis: inducible deletion of gpx4 in adult mice causes hippocampal neuronal loss with astrogliosis, as seen in AD (Yoo et al, 2012).…”

Section: Links Between Ferroptosis and Pathologymentioning

confidence: 99%

Ferroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease

Stockwell

Angeli

Bayır

et al. 2017

Cell

4,465

4,352

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Summary Ferroptosis is a form of regulated cell death characterized by the iron-dependent accumulation of lipid hydroperoxides to lethal levels. Emerging evidence suggests that ferroptosis represents an ancient vulnerability caused by the incorporation of polyunsaturated fatty acids into cellular membranes, and that cells have developed complex systems that exploit and defend against this vulnerability in different contexts. The sensitivity to ferroptosis is tightly linked to numerous biological processes, including amino acid, iron and polyunsaturated fatty acid metabolism, and the biosynthesis of glutathione, phospholipids, NADPH and coenzyme Q10. Ferroptosis has been implicated in the pathological cell death associated with degenerative diseases (i.e., Alzheimer's, Huntington's, and Parkinson's diseases), carcinogenesis, stroke, intracerebral hemorrhage, traumatic brain injury, ischemia-reperfusion injury, and kidney degeneration in mammals and is also implicated in heat stress in plants. Ferroptosis may also have a tumor suppressor function that could be harnessed for cancer therapy. This Primer reviews the mechanisms underlying ferroptosis, highlights connections to other areas of biology and medicine, and recommends tools and guidelines for studying this emerging form of regulated cell death.

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Section: Links Between Ferroptosis and Pathologymentioning

confidence: 99%

Ferroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease

Stockwell

Angeli

Bayır

et al. 2017

Cell

4,465

4,352

View full text Add to dashboard Cite

show abstract

“…After the formal concept of ferroptosis publishing, the researchers began to believe that ferroptosis is the main driver of neuronal death in diseases such as PD, AD, and HD (Guiney et al, 2017;Morris et al, 2018;Mi et al, 2019). In animal models of aging and neurodegenerative diseases and human anatomy studies, iron levels in the brain were found to rise to varying degrees, and it was concluded that this increase may lead to age-dependent ferroptosis (Belaidi and Bush, 2016;Buijs et al, 2017). And studies also found that chronic exposure to iron for mice caused a disorder of membrane-transport protein function and intracellular iron homeostasis and resulted in a significant increase in ROS and free radical MDA, ultimately leading to neuron and glial cell dysfunction and even neuron loss .…”

Section: Research Progress On Ferroptosis and Neurodegenerative Diseasesmentioning

confidence: 99%

Nrf2 and Ferroptosis: A New Research Direction for Neurodegenerative Diseases

2020

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“…Mutation in WDR45 , leading to decreased autophagy, has been identified in a number of patients with Neurodegeneration with Brain Iron Accumulation (NBIA) [75]. In general, as autophagy levels decrease with age [76], iron levels increase [77]. As defective autophagy is associated with ND, this suggests a more complex relationship of ferritinophagy activity to ND.…”

Section: Ferritinophagy and Ferroptosis In Diseasementioning

confidence: 99%

The Role of NCOA4-Mediated Ferritinophagy in Health and Disease

2018

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Nuclear receptor coactivator 4 (NCOA4) is a selective cargo receptor that mediates the autophagic degradation of ferritin (“ferritinophagy”), the cytosolic iron storage complex. NCOA4-mediated ferritinophagy maintains intracellular iron homeostasis by facilitating ferritin iron storage or release according to demand. Ferritinophagy is involved in iron-dependent physiological processes such as erythropoiesis, where NCOA4 mediates ferritin iron release for mitochondrial heme synthesis. Recently, ferritinophagy has been shown to regulate ferroptosis, a newly described form of iron-dependent cell death mediated by excess lipid peroxidation. Dysregulation of iron metabolism and ferroptosis have been described in neurodegeneration, cancer, and infection, but little is known about the role of ferritinophagy in the pathogenesis of these diseases. Here, we will review the biochemical regulation of NCOA4, its contribution to physiological processes and its role in disease. Finally, we will discuss the potential of activating or inhibiting ferritinophagy and ferroptosis for therapeutic purposes.

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In vivo assessment of iron content of the cerebral cortex in healthy aging using 7-Tesla T2*-weighted phase imaging

Cited by 36 publications

References 46 publications

Ferroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease

Ferroptosis: A Regulated Cell Death Nexus Linking Metabolism, Redox Biology, and Disease

Nrf2 and Ferroptosis: A New Research Direction for Neurodegenerative Diseases

The Role of NCOA4-Mediated Ferritinophagy in Health and Disease

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