scholarly journals Assessment of brain iron accumulation in Alzheimer's disease with quantitative susceptibility mapping

2020 ◽  
Vol 16 (S4) ◽  
Author(s):  
Xiang Fan ◽  
Xueru Liu ◽  
Lirong Yan ◽  
Vincent C. T. Mok ◽  
Kuncheng Li
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Susceptibility Mapping ◽  
Iron Accumulation ◽  
Brain Iron ◽  
Quantitative Susceptibility Mapping

scholarly journals Cellular Senescence and Iron Dyshomeostasis in Alzheimer’s Disease

2019 ◽  
Vol 12 (2) ◽  
pp. 93 ◽  
Author(s):  
Shashank Masaldan ◽  
Abdel Ali Belaidi ◽  
Scott Ayton ◽  
Ashley I. Bush
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Hydroxyl Radicals ◽  
Iron Accumulation ◽  
Brain Iron ◽  
Dependent Cell ◽  
Cellular Dysfunction ◽  
The Impact ◽  
The Brain

Iron dyshomeostasis is a feature of Alzheimer’s disease (AD). The impact of iron on AD is attributed to its interactions with the central proteins of AD pathology (amyloid precursor protein and tau) and/or through the iron-mediated generation of prooxidant molecules (e.g., hydroxyl radicals). However, the source of iron accumulation in pathologically relevant regions of the brain and its contribution to AD remains unclear. One likely contributor to iron accumulation is the age-associated increase in tissue-resident senescent cells that drive inflammation and contribute to various pathologies associated with advanced age. Iron accumulation predisposes ageing tissue to oxidative stress that can lead to cellular dysfunction and to iron-dependent cell death modalities (e.g., ferroptosis). Further, elevated brain iron is associated with the progression of AD and cognitive decline. Elevated brain iron presents a feature of AD that may be modified pharmacologically to mitigate the effects of age/senescence-associated iron dyshomeostasis and improve disease outcome.

Quantitative Susceptibility Mapping of Amyloid-β Aggregates in Alzheimer’s Disease with 7T MR

2018 ◽  
Vol 64 (2) ◽  
pp. 393-404 ◽  
Author(s):  
Solveig Tiepolt ◽  
Andreas Schäfer ◽  
Michael Rullmann ◽  
Elisabeth Roggenhofer ◽  
Hermann-Josef Gertz ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Amyloid Β ◽  
Susceptibility Mapping ◽  
Quantitative Susceptibility Mapping

P1-477: A QUANTITATIVE SUSCEPTIBILITY MAPPING STUDY IN ALZHEIMER'S DISEASE

2006 ◽  
Vol 14 (7S_Part_9) ◽  
pp. P507-P508
Author(s):  
Xiang Fan ◽  
Zhigang Qi ◽  
Yanhui Yang ◽  
Hui Li ◽  
Kuncheng Li
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Susceptibility Mapping ◽  
Mapping Study ◽  
Quantitative Susceptibility Mapping

scholarly journals Dysregulation of Iron Metabolism in Alzheimer's Disease, Parkinson's Disease, and Amyotrophic Lateral Sclerosis

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Satoru Oshiro ◽  
Masaki S. Morioka ◽  
Masataka Kikuchi
Keyword(s):  
Oxidative Stress ◽  
Alzheimer’S Disease ◽  
Parkinson’S Disease ◽  
Alzheimer's Disease ◽  
Amyotrophic Lateral Sclerosis ◽  
Iron Metabolism ◽  
Iron Homeostasis ◽  
Iron Accumulation ◽  
Brain Iron ◽  
Lateral Sclerosis

Dysregulation of iron metabolism has been observed in patients with neurodegenerative diseases (NDs). Utilization of several importers and exporters for iron transport in brain cells helps maintain iron homeostasis. Dysregulation of iron homeostasis leads to the production of neurotoxic substances and reactive oxygen species, resulting in iron-induced oxidative stress. In Alzheimer's disease (AD) and Parkinson's disease (PD), circumstantial evidence has shown that dysregulation of brain iron homeostasis leads to abnormal iron accumulation. Several genetic studies have revealed mutations in genes associated with increased iron uptake, increased oxidative stress, and an altered inflammatory response in amyotrophic lateral sclerosis (ALS). Here, we review the recent findings on brain iron metabolism in common NDs, such as AD, PD, and ALS. We also summarize the conventional and novel types of iron chelators, which can successfully decrease excess iron accumulation in brain lesions. For example, iron-chelating drugs have neuroprotective effects, preventing neural apoptosis, and activate cellular protective pathways against oxidative stress. Glial cells also protect neurons by secreting antioxidants and antiapoptotic substances. These new findings of experimental and clinical studies may provide a scientific foundation for advances in drug development for NDs.

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