Iron quantification in basal ganglia: quantitative susceptibility mapping as a potential biomarker for Alzheimer’s disease – a systematic review and meta-analysis
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SUBMITTER: Ghaderi S
PROVIDER: S-EPMC10925682 | biostudies-literature | 2024 Jan
REPOSITORIES: biostudies-literature
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Project description:Background and purposeT2 hypointensity in the basal ganglia of patients with MS has been associated with clinical progression and cognitive decline. Our objectives were the following: 1) to compare signal in T2WI, R2 (ie, 1/T2), and R2* (ie, 1/T2*) relaxation rates and quantitative susceptibility mapping; and 2) to investigate the associations among MR imaging, clinical scores, and cognitive measures of inhibitory control linked to basal ganglia functioning.Materials and methodsTwenty-nine patients with MS underwent a battery of neuropsychological tests including the Flanker and Stroop tasks. 7T MR imaging included 3D gradient-echo and single-echo multishot spin-echo EPI. Quantitative susceptibility mapping images were calculated by using a Wiener filter deconvolution algorithm. T2WI signal was normalized to CSF. R2 and R2* were calculated by log-linear regression. Average MR imaging metrics for the globus pallidus, putamen, and caudate were computed from manually traced ROIs including the largest central part of each structure.ResultsMarked spatial variation was consistently visualized on quantitative susceptibility mapping and T2/T2*WI within each basal ganglia structure. MR imaging metrics correlated with each other for each basal ganglia structure individually. Notably, caudate and putamen quantitative susceptibility mapping metrics were similar, but the putamen R2 was larger than the caudate R2. This finding suggests that tissue features contribute differently to R2 and quantitative susceptibility mapping. Caudate and anterior putamen quantitative susceptibility mapping correlated with the Flanker but not Stroop measures; R2 did not correlate with inhibitory control measures. Putamen quantitative susceptibility mapping and caudate and putamen R2 correlated with the Expanded Disability Status Scale.ConclusionsOur study showed that quantitative susceptibility mapping and R2 may be complementary indicators for basal ganglia tissue changes in MS. Our findings are consistent with the hypothesis that decreased performance of basal ganglia-reliant tasks involving inhibitory control is associated with increased quantitative susceptibility mapping.
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Project description:BackgroundIn spinocerebellar ataxia type 3 (SCA3), volume loss has been reported in the basal ganglia, an iron-rich brain region, but iron content has not been examined. Recent studies have reported that patients with SCA6 have markedly decreased iron content in the cerebellar dentate, coupled with severe volume loss. Changing brain iron levels can disrupt cognitive and motor functions, yet this has not been examined in the SCAs, a disease in which iron-rich regions are affected.MethodsIn the present study, we used quantitative susceptibility mapping (QSM) to measure tissue magnetic susceptibility (indicating iron concentration), structural volume, and normalized susceptibility mass (indicating iron content) in the cerebellar dentate and basal ganglia in people with SCA3 (n = 10) and SCA6 (n = 6) and healthy controls (n = 9). Data were acquired using a 7T Philips MRI scanner. Supplemental measures assessed motor, cognitive, and mood domains.ResultsPutamen volume was lower in both SCA groups relative to controls, replicating prior findings. Dentate susceptibility mass and volume in SCA6 was lower than in SCA3 or controls, also replicating prior findings. The novel finding was that higher basal ganglia susceptibility mass in SCA6 correlated with lower cognitive performance and greater motor impairment, an association that was not observed in SCA3. Cerebellar dentate susceptibility mass, however, had the opposite relationship with cognition and motor function in SCA6, suggesting that, as dentate iron is depleted, it relocated to the basal ganglia, which contributed to cognitive and motor decline. By contrast, basal ganglia volume loss, rather than iron content, appeared to drive changes in motor function in SCA3.ConclusionThe associations of higher basal ganglia iron with lower motor and cognitive function in SCA6 but not in SCA3 suggest the potential for using brain iron deposition profiles beyond the cerebellar dentate to assess disease states within the cerebellar ataxias. Moreover, the role of the basal ganglia deserves greater attention as a contributor to pathologic and phenotypic changes associated with SCA.
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Project description:Systemic lupus erythematosus (SLE) is an auto-immune disease characterized by multi-organ involvement. Although uncommon, central nervous system involvement in SLE, termed neuropsychiatric SLE (NPSLE), is not an exception. Current knowledge on underlying pathogenic mechanisms is incomplete, however, neuroinflammation is thought to play a critical role. Evidence from neurodegenerative diseases and multiple sclerosis suggests that neuroinflammation is correlated with brain iron accumulation, making quantitative susceptibility mapping (QSM) a potential hallmark for neuroinflammation in vivo. This study assessed susceptibility values of the thalamus and basal ganglia in (NP)SLE patients and further investigated the in vivo findings with histological analyses of postmortem brain tissue derived from SLE patients. We used a 3T MRI scanner to acquire single-echo T2*-weighted images of 44 SLE patients and 20 age-matched healthy controls. Of the 44 patients with SLE, all had neuropsychiatric complaints, of which 29 were classified as non-NPSLE and 15 as NPSLE (seven as inflammatory NPSLE and eight as ischemic NPSLE). Mean susceptibility values of the thalamus, caudate nucleus, putamen, and globus pallidus were calculated. Formalin-fixed paraffin-embedded post-mortem brain tissue including the putamen and globus pallidus of three additional SLE patients was obtained and stained for iron, microglia and astrocytes. Susceptibility values of SLE patients and age-matched controls showed that iron levels in the thalamus and basal ganglia were not changed due to the disease. No subgroup of SLE showed higher susceptibility values. No correlation was found with disease activity or damage due to SLE. Histological examination of the post-mortem brain showed no increased iron accumulation. Our results suggest that neuroinflammation in NPSLE does not necessarily go hand in hand with iron accumulation, and that the inflammatory pathomechanism in SLE may differ from the one observed in neurodegenerative diseases and in multiple sclerosis.
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Project description:PurposesTo evaluate the feasibility of simultaneous quantification of liver iron concentration (LIC) and fat fraction (FF) using water-fat separation and quantitative susceptibility mapping (QSM).MethodsForty-five patients suspected of liver iron overload (LIO) were included. A volumetric interpolated breath-hold examination sequence for QSM and FF, a fat-saturated gradient echo sequence for R2*, a spin echo sequence for LIC measurements and MRS analyses for FF (FF-MRS) were performed. Magnetic susceptibility and FF were calculated using a water-fat separation method (FF-MRI). Correlation and receiver operating characteristic analyses were performed.ResultsMagnetic susceptibility showed strong correlation with LIC (rs=0.918). The optimal susceptibility cut-off values were 0.34, 0.63, 1.29 and 2.23 ppm corresponding to LIC thresholds of 1.8, 3.2, 7.0 and 15.0 mg/g dry weight. The area under the curve (AUC) were 0.948, 0.970, 1 and 1, respectively. No difference in AUC was found between susceptibility and R2* at all LIC thresholds. Correlation was found between FF-MRI and FF-MRS (R2=0.910).ConclusionsQSM has a high diagnostic performance for LIC quantification, similar to that of R2*. FF-MRI provides simultaneous fat quantification. Findings suggest QSM in combination with water-fat separation has potential value for evaluating LIO, especially in cases with coexisting steatosis.Key points• Magnetic susceptibility showed strong correlation with LIC (r s =0.918). • QSM showed high diagnostic performance for LIC, similar to that of R 2* . • Simultaneously estimated FF-MRI showed strong correlation with MR-Spectroscopy-based FF (R 2 =0.910). • QSM combining water-fat separation has quantitative value for LIO with coexisted steatosis.
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Project description:BackgroundThis study explores the magnetostatic properties of the Alzheimer's disease brain using a recently proposed, magnetic resonance imaging, postprocessed contrast mechanism. Quantitative susceptibility mapping (QSM) has the potential to monitor in vivo iron levels by reconstructing magnetic susceptibility sources from field perturbations. However, with phase data acquired at a single head orientation, the technique relies on several theoretical approximations and requires fast-evolving regularisation strategies.MethodsIn this context, the present study describes a complete methodological framework for magnetic susceptibility measurements with a review of its theoretical foundations.Findings and significanceThe regional and whole-brain cross-sectional comparisons between Alzheimer's disease subjects and matched controls indicate that there may be significant magnetic susceptibility differences for deep brain nuclei--particularly the putamen--as well as for posterior grey and white matter regions. The methodology and findings described suggest that the QSM method is ready for larger-scale clinical studies.
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Project description:This study adopted diffusion tensor imaging to detect alterations in the diffusion parameters of the white matter fiber in Alzheimer's disease (AD) and used quantitative susceptibility mapping to detect changes in magnetic susceptibility. However, whether the changes of susceptibility values due to excessive iron in the basal ganglia have correlations with the alterations of the diffusion properties of the white matter in patients with AD are still unknown. We aim to investigate the correlations among magnetic susceptibility values of the basal ganglia, diffusion indexes of the white matter, and cognitive function in patients with AD. Thirty patients with AD and nineteen healthy controls (HCs) were recruited. Diffusion indexes of the whole brain were detected using tract-based spatial statistics. The caudate nucleus, putamen, and globus pallidus were selected as regions of interest, and their magnetic susceptibility values were measured. Compared with HCs, patients with AD showed that there were significantly increased axial diffusivity (AxD) in the internal capsule, superior corona radiata (SCR), and right anterior corona radiata (ACR); increased radial diffusivity (RD) in the right anterior limb of the internal capsule, ACR, and genu of the corpus callosum (GCC); and decreased fractional anisotropy (FA) in the right ACR and GCC. The alterations of RD values, FA values, and susceptibility values of the right caudate nucleus in patients with AD were correlated with cognitive scores. Besides, AxD values in the right internal capsule, ACR, and SCR were positively correlated with the magnetic susceptibility values of the right caudate nucleus in patients with AD. Our findings revealed that the magnetic susceptibility of the caudate nucleus may be an MRI-based biomarker of the cognitive dysfunction of AD and abnormal excessive iron distribution in the basal ganglia had adverse effects on the diffusion properties of the white matter.
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Project description:Background and purposeIn 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 methodsFifteen 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.ResultsSubjects 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.ConclusionsThe 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.
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Project description:ObjectivesQuantitative mapping of T1 relaxation in the rotating frame (T1ρ) is a magnetic resonance imaging technique sensitive to pH and other cellular and microstructural factors, and is a potentially valuable tool for identifying brain alterations in bipolar disorder. Recently, this technique identified differences in the cerebellum and cerebral white matter of euthymic patients vs healthy controls that were consistent with reduced pH in these regions, suggesting an underlying metabolic abnormality. The current study built upon this prior work to investigate brain T1ρ differences across euthymic, depressed, and manic mood states of bipolar disorder.MethodsForty participants with bipolar I disorder and 29 healthy control participants matched for age and gender were enrolled. Participants with bipolar disorder were imaged in one or more mood states, yielding 27, 12, and 13 imaging sessions in euthymic, depressed, and manic mood states, respectively. Three-dimensional, whole-brain anatomical images and T1ρ maps were acquired for all participants, enabling voxel-wise evaluation of T1ρ differences between bipolar mood state and healthy control groups.ResultsAll three mood state groups had increased T1ρ relaxation times in the cerebellum compared to the healthy control group. Additionally, the depressed and manic groups had reduced T1ρ relaxation times in and around the basal ganglia compared to the control and euthymic groups.ConclusionsThe study implicated the cerebellum and basal ganglia in the pathophysiology of bipolar disorder and its mood states, the roles of which are relatively unexplored. These findings motivate further investigation of the underlying cause of the abnormalities, and the potential role of altered metabolic activity in these regions.
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Project description:ObjectiveRecurrence is the most significant feature of depression and the relationship between iron and recurrent depression is still lack of direct evidence in vivo.MethodsTwenty-one patients with depression and twenty control subjects were included. Gradient-recalled echo, T1 and T2 images were acquired using a 3.0T MRI system. After quantitative susceptibility mapping were reconstructed and standardized, a whole-brain and the regions of interest were respectively analyzed.ResultsSignificant increases in susceptibility were found in multiple recurrent depression patients, which involved several brain regions (frontal lobes, temporal lobe structures, occipital lobes hippocampal regions, putamen, thalamus, cingulum, and cerebellum). Interestingly, no susceptibility changes after treatment compared to pre-treatment (all p>0.05) and no significant correlation between susceptibility and Hamilton Depression Rating Scale were found. Besides, it was close to significance that those with a higher relapse frequency or a longer mean duration of single episode had a higher susceptibility in the putamen, thalamus, and hippocampus. Further studies showed susceptibility across the putamen (ρ2=0.27, p<0.001), thalamus (ρ2=0.21, p<0.001), and hippocampus (ρ2=0.19, p<0.001) were strongly correlated with total course of disease onset.ConclusionBrain iron deposition is related to the total course of disease onset, but not the severity of depression, which suggest that brain iron deposition may be a sign of brain damage in multiple recurrent depression.
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