Contribution of metals to brain MR signal intensity: review articles

Kanda, Tomonori; Nakai, Yudai; Aoki, S; Oba, Hiroshi; Toyoda, Keiko; Kitajima, Kazuhiro; Furui, Shigeru

doi:10.1007/s11604-016-0532-8

Cited by 33 publications

(30 citation statements)

References 112 publications

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“…For example, iron, in addition to myelin, has been found to contribute to cortical MR image contrast (Shafee et al, 2015). Indeed, most metal deposition, including iron, causes high signal intensity on T1w images and/or low signal intensity on T2w images (Kanda et al, 2016). In the present study, we found that T2w images in the high PiB-BP ND group had a significantly lower intensity compared to the low PiB-BP ND group, and the increased T1w/T2w ratio is primarily due to differences in the T2w image.…”

Section: Discussionmentioning

confidence: 99%

Use of T1-weighted/T2-weighted magnetic resonance ratio to elucidate changes due to amyloid β accumulation in cognitively normal subjects

Yasuno

Kazui

Morita

et al. 2017

NeuroImage: Clinical

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The ratio of signal intensity in T1-weighted (T1w) and T2-weighted (T2w) magnetic resonance imaging (MRI) was recently proposed to enhance the sensitivity of detecting changes in disease-related signal intensity. The objective of this study was to test the effectiveness of T1w/T2w image ratios as an easily accessible biomarker for amyloid beta (Aβ) accumulation. We performed the T1w/T2w analysis in cognitively normal elderly individuals. We applied [11C] Pittsburgh Compound B (PiB)-PET to the same individuals, and Aβ deposition was quantified by its binding potential (PiB-BPND). The subjects were divided into low and high PiB-BPND groups, and group differences in regional T1w/T2w values were evaluated. In the regions where we found a significant group difference, we conducted a correlation analysis between regional T1w/T2w values and PiB-BPND. Subjects with high global cortical PiB-BPND showed a significantly higher regional T1w/T2w ratio in the frontal cortex and anterior cingulate cortex. We found a significant positive relationship between the regional T1w/T2w ratio and Aβ accumulation. Moreover, with a T1w/T2w ratio of 0.55 in the medial frontal regions, we correctly discriminated subjects with high PiB-BPND from the entire subject population with a sensitivity of 84.6% and specificity of 80.0%. Our results indicate that early Aβ-induced pathological changes can be detected using the T1w/T2w ratio on MRI. We believe that the T1w/T2w ratio is a prospective stable biological marker of early Aβ accumulation in cognitively normal individuals. The availability of such an accessible marker would improve the efficiency of clinical trials focusing on the initial disease stages by reducing the number of subjects who require screening by Aβ-PET scan or lumbar puncture.

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Section: Discussionmentioning

confidence: 99%

Use of T1-weighted/T2-weighted magnetic resonance ratio to elucidate changes due to amyloid β accumulation in cognitively normal subjects

Yasuno

Kazui

Morita

et al. 2017

NeuroImage: Clinical

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“…This observation could be interpreted as evidence that these neuroanatomic regions have less robust capillary basement membranes or that this deposition is a consequence of localization to areas of the brain that are susceptible to cellular stress. Reports of similar MR signal intensity changes in the dentate and/or deep gray nuclei in patients with multiple sclerosis, neurofibromatosis, hypoparathyroidism, inherited metabolic disorders, and Fahr disease corroborate this theory and may suggest that these areas are uniquely susceptible to mineral or metal deposition or injury (12,13). Furthermore, it remains possible that inflammatory and malignant intracranial processes, even when distant from some of the more gadolinium-avid neuroanatomic locations, may increase the permeability of the blood-brain barrier in these locations.…”

Section: Neuroradiology: Gadolinium Deposition In Human Brain At Contmentioning

confidence: 94%

Gadolinium Deposition in Human Brain Tissues after Contrast-enhanced MR Imaging in Adult Patients without Intracranial Abnormalities

et al. 2017

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Purpose To determine whether gadolinium deposits in neural tissues of patients with intracranial abnormalities following intravenous gadolinium-based contrast agent (GBCA) exposure might be related to blood-brain barrier integrity by studying adult patients with normal brain pathologic characteristics. Materials and Methods After obtaining antemortem consent and institutional review board approval, the authors compared postmortem neuronal tissue samples from five patients who had undergone four to 18 gadolinium-enhanced magnetic resonance (MR) examinations between 2005 and 2014 (contrast group) with samples from 10 gadolinium-naive patients who had undergone at least one MR examination during their lifetime (control group). All patients in the contrast group had received gadodiamide. Neuronal tissues from the dentate nuclei, pons, globus pallidus, and thalamus were harvested and analyzed with inductively coupled plasma mass spectrometry (ICP-MS), transmission electron microscopy with energy-dispersive x-ray spectroscopy, and light microscopy to quantify, localize, and assess the effects of gadolinium deposition. Results Tissues from the four neuroanatomic regions of gadodiamide-exposed patients contained 0.1-19.4 μg of gadolinium per gram of tissue in a statistically significant dose-dependent relationship (globus pallidus: ρ = 0.90, P = .04). In contradistinction, patients in the control group had undetectable levels of gadolinium with ICP-MS. All patients had normal brain pathologic characteristics at autopsy. Three patients in the contrast group had borderline renal function (estimated glomerular filtration rate <45 mL/min/1.73 m) and hepatobiliary dysfunction at MR examination. Gadolinium deposition in the contrast group was localized to the capillary endothelium and neuronal interstitium and, in two cases, within the nucleus of the cell. Conclusion Gadolinium deposition in neural tissues after GBCA administration occurs in the absence of intracranial abnormalities that might affect the permeability of the blood-brain barrier. These findings challenge current understanding of the biodistribution of these contrast agents and their safety. RSNA, 2017.

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“…130 The T 2 * MRI hyperintensity found in the mitochondrial disorder Leigh's disease 131 is caused by spongiform changes and vacuolation of the brain in conjunction with reduced activity of electron transport chain and impaired oxidative phosphorylation. 132 Because brain swMRI intensity can be affected by more than one mineral, 133,134 more research is needed to determine whether the reported links between ZIP12 and brain swMRI are due to altered brain zinc homeostasis or whether other minerals like iron or manganese are affecting the swMRI signal. These future findings may be relevant for determining if ZIP12 affects risks for neurodegenerative diseases, what metals may be responsible for these effects, and whether neuroprotective zinc or iron binding compounds such as DP-b99, 135 PBT2, 136 and PBT434 137 may offset the loss of ZIP12 function.…”

Section: Zip12 Polymorphisms and Relevance To Mitochondria And Neurodmentioning

confidence: 99%

Role of zinc transporter ZIP12 in susceptibility‐weighted brain magnetic resonance imaging (MRI) phenotypes and mitochondrial function

et al. 2020

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Brain zinc dysregulation is linked to many neurological disorders. However, the mechanisms regulating brain zinc homeostasis are poorly understood. We performed secondary analyses of brain MRI GWAS and exome sequencing data from adults in the UK Biobank. Coding ZIP12 polymorphisms in zinc transporter ZIP12 (SLC39A12) were associated with altered brain susceptibility weighted MRI (swMRI). Conditional and joint association analyses revealed independent GWAS signals in linkage disequilibrium with 2 missense ZIP12 polymorphisms, rs10764176 and rs72778328, with reduced zinc transport activity. ZIP12 rare coding variants predicted to be deleterious were associated with similar impacts on brain swMRI. In Neuro‐2a cells, ZIP12 deficiency by short hairpin RNA (shRNA) depletion or CRISPR/Cas9 genome editing resulted in impaired mitochondrial function, increased superoxide presence, and detectable protein carbonylation. Inhibition of Complexes I and IV of the electron transport chain reduced neurite outgrowth in ZIP12 deficient cells. Transcriptional coactivator PGC‐1α, mitochondrial superoxide dismutase (SOD2), and chemical antioxidants α‐tocopherol, MitoTEMPO, and MitoQ restored neurite extension impaired by ZIP12 deficiency. Mutant forms of α‐synuclein and tau linked to familial Parkinson’s disease and frontotemporal dementia, respectively, reduced neurite outgrowth in cells deficient in ZIP12. Zinc and ZIP12 may confer resilience against neurological diseases or premature aging of the brain.

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Contribution of metals to brain MR signal intensity: review articles

Cited by 33 publications

References 112 publications

Use of T1-weighted/T2-weighted magnetic resonance ratio to elucidate changes due to amyloid β accumulation in cognitively normal subjects

Use of T1-weighted/T2-weighted magnetic resonance ratio to elucidate changes due to amyloid β accumulation in cognitively normal subjects

Gadolinium Deposition in Human Brain Tissues after Contrast-enhanced MR Imaging in Adult Patients without Intracranial Abnormalities

Role of zinc transporter ZIP12 in susceptibility‐weighted brain magnetic resonance imaging (MRI) phenotypes and mitochondrial function

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