Clinical features and dysfunctions of iron metabolism in Parkinson disease patients with hyper echogenicity in substantia nigra: a cross-sectional study

Yu, Shuyang; Cao, Chen-Jie; Zuo, Lijun; Chen, Ze-Jie; Lian, Ting; Wang, Fang; Hu, Yang; Piao, Ying-shan; Li, Lixia; Guo, Ping; Liu, Li; Yu, Qing; Wang, Ruidan; Chan, Piu; Chen, Shengdi; Wang, Xiaomin; Zhang, Wei

doi:10.1186/s12883-018-1016-5

Cited by 31 publications

(25 citation statements)

References 21 publications

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“…A large prospective study showed that elevated systemic Fe can impair dexterity in healthy elderly men [11]. In PD patients, systemic Fe correlated with brain Fe [12], but less is known about the effects of brain Fe on fine motor functions.…”

Section: Introductionmentioning

confidence: 99%

Impairment of Motor Function Correlates with Neurometabolite and Brain Iron Alterations in Parkinson’s Disease

Pesch

Casjens

Woitalla

et al. 2019

Cells

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We took advantage of magnetic resonance imaging (MRI) and spectroscopy (MRS) as non-invasive methods to quantify brain iron and neurometabolites, which were analyzed along with other predictors of motor dysfunction in Parkinson’s disease (PD). Tapping hits, tremor amplitude, and the scores derived from part III of the Movement Disorder Society-Sponsored Revision of the Unified Parkinson Disease Rating Scale (MDS-UPDRS3 scores) were determined in 35 male PD patients and 35 controls. The iron-sensitive MRI relaxation rate R2* was measured in the globus pallidus and substantia nigra. γ-aminobutyric acid (GABA)-edited and short echo-time MRS was used for the quantification of neurometabolites in the striatum and thalamus. Associations of R2*, neurometabolites, and other factors with motor function were estimated with Spearman correlations and mixed regression models to account for repeated measurements (hands, hemispheres). In PD patients, R2* and striatal GABA correlated with MDS-UPDRS3 scores if not adjusted for age. Patients with akinetic-rigid PD subtype (N = 19) presented with lower creatine and striatal glutamate and glutamine (Glx) but elevated thalamic GABA compared to controls or mixed PD subtype. In PD patients, Glx correlated with an impaired dexterity when adjusted for covariates. Elevated myo-inositol was associated with more tapping hits and lower MDS-UPDRS3 scores. Our neuroimaging study provides evidence that motor dysfunction in PD correlates with alterations in brain iron and neurometabolites.

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Section: Introductionmentioning

confidence: 99%

Impairment of Motor Function Correlates with Neurometabolite and Brain Iron Alterations in Parkinson’s Disease

Pesch

Casjens

Woitalla

et al. 2019

Cells

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“…* Jinzhou Tian jztian@hotmail.com severer motor and non-motor symptoms [6][7][8]; however, visual hallucinations (VH), one of the most common psychotic symptoms, which was reported to affect 9.8 to 82.7% of PD population in different stages [9][10][11], in relation to SN, have not been reported before. Our objective is to evaluate the validity of TCS for the diagnosis of PD in Chinese population, and to investigate the correlation of sonographic manifestations with clinical features, especially in VH.…”

Section: Introductionmentioning

confidence: 99%

Increased substantia nigra echogenicity correlated with visual hallucinations in Parkinson’s disease: a Chinese population-based study

Shi

Qin

et al. 2019

Neurol Sci

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As a noninvasive technique, transcranial sonography (TCS) of substantia nigra (SN) has gradually showed its effectiveness not only in diagnosis but also in understanding clinical features of Parkinson's Disease (PD). This study aimed to further evaluate TCS for clinical diagnosis of PD, and to explore the association between sonographic manifestations and visual hallucinations (VH). A total of 226 subjects including 141 PD patients and 85 controls were recruited. All participants received TCS. A series of rating scales to evaluate motor and non-motor symptoms were performed in PD patients. Results showed that 172 subjects were successfully assessed by TCS. The area of SN was greater in PD patients than that in controls (P < 0.001). As receiver-operating characteristic (ROC) curve analysis showed, the best cutoff value for the larger SN echogenicity size was 23.5 mm 2 (sensitivity 70.3%, specificity 77.0%). Patients with VH had larger SN area (P = 0.019), as well as higher Non-Motor Symptoms Scale (NMSS) scores (P = 0.018). Moreover, binary logistic regression analysis indicated that SN hyperechogenicity (odds ratio = 4.227, P = 0.012) and NMSS scores (odds ratio = 0.027, P = 0.042) could be the independent predictors for VH. In conclusion, TCS can be used as an auxiliary diagnostic tool for Parkinson's disease. Increased SN echogenicity is correlated with VH in Parkinson's disease, possibly because the brain stem is involved in the mechanism in the onset of VH. Further studies are needed to confirm these findings.

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“…However, excess iron is involved in the formation of free radicals and has been associated with oxidative damage to neuronal or other brain cells . Abnormally increased brain iron has been observed in various neurodegenerative disorders including neurodegeneration with brain iron accumulation (NBIA), Alzheimer's disease (AD), Parkinson's disease (PD), Huntington's disease (HD), multiple sclerosis, Wilson's disease, and amyotrophic lateral sclerosis . During past decades, a great number of studies have focused on addressing whether the abnormally increased brain iron is an initial cause for the development of neurodegeneration and neuronal death.…”

Section: Brain Iron Misregulation Is a Common Pathway In Neurodegenermentioning

confidence: 99%

Hepcidin and its therapeutic potential in neurodegenerative disorders

Qian

2019

Medicinal Research Reviews

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Abnormally high brain iron, resulting from the disrupted expression or function of proteins involved in iron metabolism in the brain, is an initial cause of neuronal death in neuroferritinopathy and aceruloplasminemia, and also plays a causative role in at least some of the other neurodegenerative diseases including Alzheimer's disease, Parkinson's disease, Huntington's disease, and Friedreich's ataxia. As such, iron is believed to be a novel target for pharmacological intervention in these disorders. Reducing iron toward normal levels or hampering the increases in iron associated with age in the brain is a promising therapeutic strategy for all iron‐related neurodegenerative disorders. Hepcidin is a crucial regulator of iron homeostasis in the brain. Recent studies have suggested that upregulating brain hepcidin levels can significantly reduce brain iron content through the regulation of iron transport protein expression in the blood‐brain barrier and in neurons and astrocytes. In this review, we focus on the discussion of the therapeutic potential of hepcidin in iron‐associated neurodegenerative diseases and also provide a systematic overview of recent research progress on how misregulated brain iron metabolism is involved in the development of multiple neurodegenerative disorders.

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Clinical features and dysfunctions of iron metabolism in Parkinson disease patients with hyper echogenicity in substantia nigra: a cross-sectional study

Cited by 31 publications

References 21 publications

Impairment of Motor Function Correlates with Neurometabolite and Brain Iron Alterations in Parkinson’s Disease

Impairment of Motor Function Correlates with Neurometabolite and Brain Iron Alterations in Parkinson’s Disease

Increased substantia nigra echogenicity correlated with visual hallucinations in Parkinson’s disease: a Chinese population-based study

Hepcidin and its therapeutic potential in neurodegenerative disorders

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