Increased brain iron deposition in patients with sickle cell disease: an MRI quantitative susceptibility mapping study.
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ABSTRACT:
SUBMITTER: Miao X
PROVIDER: S-EPMC6182265 | biostudies-literature | 2018 Oct
REPOSITORIES: biostudies-literature
Publications
Increased brain iron deposition in patients with sickle cell disease: an MRI quantitative susceptibility mapping study.
Miao Xin X Choi Soyoung S Tamrazi Benita B Chai Yaqiong Y Vu Chau C Coates Thomas D TD Wood John C JC
Blood 20180725 15
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Project description:Background The underlying brain structural changes in type 2 diabetes mellitus (T2DM) patients have attracted increasing attention. The insulin-resistant state causes iron overload in neurons and leads to lesions in the central nervous system. Quantitative susceptibility mapping (QSM) can provide a noninvasive quantitative analysis of brain iron deposition. We aimed to compare the difference of brain iron deposition in the gray matter nucleus between T2DM patients and healthy elderly individuals using QSM. Methods Thirty-two T2DM patients and thirty-two age- and gender-matched healthy controls (HCs) were enrolled in this research. Twenty-three patients and twenty-six HCs underwent cognitive assessments. Brain QSM maps were computed from multiecho GRE data using morphology-enabled dipole inversion with automatic uniform cerebrospinal fluid zero reference algorithm (MEDI+0). ITK-SNAP was used to measure the susceptibility values reflecting the content of iron in the regions of interest (ROIs). Results The study included thirty-two T2DM patients (20 males and 12 females; mean age of 61.09 ± 9.99 years) and 32 HCs (14 males and 18 females; mean age of 59.09 ± 9.77 years). These participants had no significant difference in age or gender (P > 0.05). Twenty-three patients with T2DM (11 males and 12 females; mean age, 64.65 ± 8.44 years) and twenty-six HCs (14 males and 12 females; mean age, 62.30 ± 6.13 years) received an assessment of cognitive function. T2DM patients exhibited an obviously (t = 3.237, P = 0.003) lower Montreal Cognitive Assessment (MoCA) score (26.78 ± 2.35; HCs, 28.42 ± 0.64; normal standard ?26) and a higher Stroop color-word test (SCWT)-C score [87(65,110); HC, 63(60,76.75), Z = ?2.232, P = 0.003] than HCs. The mean susceptibility values in the putamen appeared obviously higher in T2DM patients than in HCs (t = ?3.994, P < 0.001). The susceptibility values and cognitive assessment scores showed no obvious association (P > 0.05). However, an obvious correlation was observed between the changes in the susceptibility values in the putamen and the thalamus/dentate nucleus (r = 0.404, P < 0.001; r = 0.423, P < 0.001). Conclusion T2DM patients showed increased susceptibility values in the putamen and had declines in executive functions, but the linear association between them was not statistically significant. Changes in susceptibility values in the putamen indicated increased iron deposition and might be used as a quantitative imaging marker of central nervous system injury in T2DM patients. QSM might be able to help probe micro neuronal damage in gray matter and provide information on diabetic encephalopathy.
| S-EPMC7533753 | biostudies-literature
Project description:BACKGROUND AND PURPOSE:In patients with premanifest (nonsymptomatic) and advanced Huntington disease, changes in brain iron levels in the basal ganglia have been previously reported, especially in the striatum. Quantitative susceptibility mapping by using MR phase imaging allows in vivo measurements of tissue magnetic susceptibility, which has been shown to correlate well with iron levels in brain gray matter and is believed to be more specific than other imaging-based iron measures. The purpose of this study was to investigate the use of magnetic susceptibility as a biomarker of disease progression. MATERIALS AND METHODS:Fifteen subjects with premanifest Huntington disease and 16 age-matched healthy controls were scanned at 7T. Magnetic susceptibility, effective relaxation, and tissue volume in deep gray matter structures were quantified and compared with genetic and clinical measures. RESULTS:Subjects with premanifest Huntington disease showed significantly higher susceptibility values in the caudate nucleus, putamen, and globus pallidus, indicating increased iron levels in these structures. Significant decreases in magnetic susceptibility were found in the substantia nigra and hippocampus. In addition, significant volume loss (atrophy) and an increase effective relaxation were observed in the caudate nucleus and putamen. Susceptibility values in the caudate nucleus and putamen were found to be inversely correlated with structure volumes and directly correlated with the genetic burdens, represented by cytosine-adenine-guanine repeat age-product-scaled scores. CONCLUSIONS:The significant magnetic susceptibility differences between subjects with premanifest Huntington disease and controls and their correlation with genetic burden scores indicate the potential use of magnetic susceptibility as a biomarker of disease progression in premanifest Huntington disease.
| S-EPMC4867278 | biostudies-literature
Project description:BackgroundDysfunction of iron metabolism, especially in substantia nigra (SN), is widely acknowledged in Parkinson's disease (PD), but the genetic influence on iron deposition remains largely unknown. Thus, in this study, we aimed to investigate potential genetic impacts on iron deposition in PD.MethodsSeventy-four subjects, including 38 patients with PD and 36 age-matched normal controls, participated in this study. Imaging genetic association analysis was used to identify the specific influence of single nucleotide polymorphism (SNP) on iron-related quantitative traits (QT). Genetic effects on iron deposition at the disease level, SNP level, and their interactive effect were highlighted.ResultsFour strong SNP-QT associations were detected: rs602201-susceptibility of bilateral SN, rs198440-susceptibility of left SN, and rs7895403-susceptibility of left caudate head. Detailed analyses showed that: (1) significant iron deposition was exclusively found in bilateral SN in PD; (2) altered polymorphisms of the A allele/A- genotype of rs602201 and G allele/G- genotype of rs198440 and rs7895403 were more frequently observed in PD; (3) for rs602201, among all subjects, A- genotype carriers showed significantly increased iron content than TT genotype in bilateral SN; for rs198440 and rs7895403, G- carriers showed increased iron content than AA genotype in left SN and left caudate head, respectively; and (4) rs602201 exhibited significant SNP-by-disease interaction in bilateral SN.ConclusionsThis study shows that rs602201 and rs198440 have a stimulative impact on nigral iron deposition in PD, which provides improved understanding of iron-related pathogenesis in PD, and specifically, that vulnerability to iron deposition in SN is genetic-based.
| S-EPMC10324346 | biostudies-literature
Project description:BackgroundRegional excessive iron overload is pernicious to motor functions and cognitive functioning of the brain. The aim of this research was to utilize quantitative susceptibility mapping (QSM) to inspect brain iron accumulation in patients with hypertension (HP), and to evaluate whether it is correlated with physiological parameters.MethodsThirty-one HP and 31 age- and sex-matched healthy controls (HC) were included. All participants underwent brain magnetic resonance imaging (MRI), and QSM data were obtained. Differences in brain iron deposition in deep gray matter nuclei of participants were compared between HP and HC. The correlations between iron deposition, body mass index (BMI), maximum systolic blood pressure (SBP), and diastolic blood pressure (DBP) were analyzed.ResultsThe HP group showed increased susceptibility values in the caudate nucleus (CA), putamen (PU), globus pallidus (GP), and dorsal thalamus (TH), compared with the HC group. There was a significant positive correlation between BMI and the susceptibility values in the dentate nucleus (DN); the maximum SBP and DBP were positively correlated with magnetic susceptibility of the CA, PU, GP, and TH, respectively.ConclusionsThese results are indicative of the role of overload brain iron in deep brain gray matter nuclei in HP and suggest that HP is associated with excess brain iron in certain deep gray matter regions.
| S-EPMC8576670 | biostudies-literature
Project description: Not available
| S-EPMC11250300 | biostudies-literature
Project description:The proper microstructural arrangement of complex neural structures is essential for establishing the functional circuitry of the brain. We present an MRI method to resolve tissue microstructure and infer brain cytoarchitecture by mapping the magnetic susceptibility in the brain at high resolution. This is possible because of the heterogeneous magnetic susceptibility created by varying concentrations of lipids, proteins and irons from the cell membrane to cytoplasm. We demonstrate magnetic susceptibility maps at a nominal resolution of 10-?m isotropic, approaching the average cell size of a mouse brain. The maps reveal many detailed structures including the retina cell layers, olfactory sensory neurons, barrel cortex, cortical layers, axonal fibers in white and gray matter. Olfactory glomerulus density is calculated and structural connectivity is traced in the optic nerve, striatal neurons, and brainstem nerves. The method is robust and can be readily applied on MRI scanners at or above 7T.
| S-EPMC5201162 | biostudies-literature
Project description:BackgroundPsychosis is related to neurochemical changes in deep-brain nuclei, particularly suggesting dopamine dysfunctions. We used an magnetic resonance imaging-based technique called quantitative susceptibility mapping (QSM) to study these regions in psychosis. QSM quantifies magnetic susceptibility in the brain, which is associated with iron concentrations. Since iron is a cofactor in dopamine pathways and co-localizes with inhibitory neurons, differences in QSM could reflect changes in these processes.MethodsWe scanned 83 patients with first-episode psychosis and 64 healthy subjects. We reassessed 22 patients and 21 control subjects after 3 months. Mean susceptibility was measured in 6 deep-brain nuclei. Using linear mixed models, we analyzed the effect of case-control differences, region, age, gender, volume, framewise displacement (FD), treatment duration, dose, laterality, session, and psychotic symptoms on QSM.ResultsPatients showed a significant susceptibility reduction in the putamen and globus pallidus externa (GPe). Patients also showed a significant R2* reduction in GPe. Age, gender, FD, session, group, and region are significant predictor variables for QSM. Dose, treatment duration, and volume were not predictor variables of QSM.ConclusionsReduction in QSM and R2* suggests a decreased iron concentration in the GPe of patients. Susceptibility reduction in putamen cannot be associated with iron changes. Since changes observed in putamen and GPe were not associated with symptoms, dose, and treatment duration, we hypothesize that susceptibility may be a trait marker rather than a state marker, but this must be verified with long-term studies.
| S-EPMC10483330 | biostudies-literature
Project description:BackgroundAnorexia nervosa (AN) is a potentially fatal psychiatric condition, associated with structural brain changes such as gray matter volume loss. The pathophysiological mechanisms for these changes are not yet fully understood. Iron is a crucial element in the development and function of the brain. Considering the systemic alterations in iron homeostasis in AN, we hypothesized that brain iron would be altered as a possible factor associated with structural brain changes in AN.MethodsIn this study, we used quantitative susceptibility mapping (QSM) magnetic resonance imaging to investigate brain iron in current AN (c-AN) and weight-restored AN compared with healthy individuals. Whole-brain voxel wise comparison was used to probe areas with possible group differences. Further, the thalamus, caudate nucleus, putamen, nucleus accumbens, hippocampus, and amygdala were selected as the regions of interest (ROIs) for ROI-based comparison of mean QSM values.ResultsWhole-brain voxel-wise and ROI-based comparison of QSM did not reveal any differences between groups. Exploratory analyses revealed a correlation between higher regional QSM (higher iron) and lower body mass index, higher illness severity, longer illness duration, and younger age at onset in the c-AN group.ConclusionsThis study did not find evidence of altered brain iron in AN compared to healthy individuals. However, the correlations between clinical variables and QSM suggest a link between brain iron and weight status or biological processes in AN, which warrants further investigation.
| S-EPMC10441741 | biostudies-literature
Project description:Iron has been increasingly implicated in the pathology of neurodegenerative diseases. In the past decade, development of the new magnetic resonance imaging technique, quantitative susceptibility mapping (QSM), has enabled for the more comprehensive investigation of iron distribution in the brain. The aim of this systematic review was to provide a synthesis of the findings from existing QSM studies in neurodegenerative diseases. We identified 80 records by searching MEDLINE, Embase, Scopus, and PsycInfo databases. The disorders investigated in these studies included Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, Wilson's disease, Huntington's disease, Friedreich's ataxia, spinocerebellar ataxia, Fabry disease, myotonic dystrophy, pantothenate-kinase-associated neurodegeneration, and mitochondrial membrane protein-associated neurodegeneration. As a general pattern, QSM revealed increased magnetic susceptibility (suggestive of increased iron content) in the brain regions associated with the pathology of each disorder, such as the amygdala and caudate nucleus in Alzheimer's disease, the substantia nigra in Parkinson's disease, motor cortex in amyotrophic lateral sclerosis, basal ganglia in Huntington's disease, and cerebellar dentate nucleus in Friedreich's ataxia. Furthermore, the increased magnetic susceptibility correlated with disease duration and severity of clinical features in some disorders. Although the number of studies is still limited in most of the neurodegenerative diseases, the existing evidence suggests that QSM can be a promising tool in the investigation of neurodegeneration.
| S-EPMC7930077 | biostudies-literature
Project description:Purpose: This study aimed to use quantitative susceptibility mapping (QSM) to systematically investigate the changes of iron content in gray matter (GM) nuclei in patients with long-term anterior circulation artery stenosis (ACAS) and posterior circulation artery stenosis (PCAS). Methods: Twenty-five ACAS patients, 25 PCAS patients, and 25 age- and sex-matched healthy controls underwent QSM examination. Patients were scored using the National Institutes of Health Stroke Scale (NIHSS) and modified Rankin Scale (mRS) to assess the degree of neural function deficiency. On QSM images, iron related susceptibility of GM nuclei, including bilateral caudate nucleus, putamen (PU), globus pallidus (GP), thalamus (TH), substantia nigra (SN), red nucleus, and dentate nucleus (DN), were assessed. Susceptibility was compared between bilateral GM nuclei in healthy controls, ACAS patients, and PCAS patients. Partial correlation analysis, with age as a covariate, was separately performed to assess the relationships of susceptibility with NIHSS and mRS scores. Results: There were no significant differences between the susceptibilities for left and right hemispheres in all seven GM nucleus subregions for healthy controls, ACAS patients, and PCAS patients. Compared with healthy controls, mean susceptibility of bilateral PU, GP, and SN in ACAS patients and of bilateral PU, GP, SN, and DN in PCAS patients were significantly increased (all P < 0.05). In addition, mean susceptibility of bilateral TH and SN in PCAS patients was significantly higher than in ACAS patients (both P < 0.05). With partial correlation analysis, mean susceptibility at bilateral PU of ACAS patients was significantly correlated with mRS score (r = 0.415, P < 0.05), and at bilateral PU in PCAS patients was correlated with NIHSS score (r = 0.424, P < 0.05). Conclusion: Our findings indicated that abnormal iron metabolism may present in different subregions of GM nuclei after long-term ACAS and PCAS. In addition, iron content of PU in patients with ACAS and PCAS was correlated with neurological deficit scores. Therefore, iron quantification measured by QSM susceptibility may provide a new insight to understand the pathological mechanism of ischemic stroke caused by ACAS and PCAS.
| S-EPMC8766754 | biostudies-literature