scholarly journals Iron and Neurodegeneration in Multiple Sclerosis

2011 ◽  
Vol 2011 ◽  
pp. 1-6 ◽  
Author(s):  
Michael Khalil ◽  
Charlotte Teunissen ◽  
Christian Langkammer

Increased iron deposition might be implicated in multiple sclerosis (MS). Recent development of MRI enabled to determine brain iron levels in a quantitative manner, which has put more interest on studying the role of iron in MS. Evidence for abnormal iron homeostasis in MS comes also from analyses of iron and iron-related proteins in CSF and blood and postmortem MS brain sections. However, it is not yet clear if iron accumulation is implicated in MS pathology or merely reflects an epiphenomenon. Further interest has been generated by the idea of chronic cerebrospinal venous insufficiency that might be associated with brain iron accumulation due to a reduction in venous outflow, but its existence and etiologic role in MS are currently controversially debated. In future studies, combined approaches applying quantitative MRI together with CSF and serum analyses of iron and iron-related proteins in a clinical followup setting might help to elucidate the implication of iron accumulation in MS.

Neurology ◽  
2011 ◽  
Vol 76 (24) ◽  
pp. 2130-2132
Author(s):  
S. R. Brenner ◽  
A. Sena ◽  
R. Pedrosa ◽  
V. Ferret-Sena ◽  
A. Petzold ◽  
...  

2017 ◽  
Vol 01 (04) ◽  
pp. E294-E306 ◽  
Author(s):  
Mike Wattjes ◽  
Peter Raab

AbstractMagnetic resonance imaging (MRI) plays an important role in the diagnosis of multiple sclerosis and has been incorporated into the McDonald diagnostic criteria for MS. In particular, for the exclusion of important differential diagnosis and comorbidities, new MRI markers have been established such as the “central vein sign”. In addition to diagnostic purposes, the role of MRI in MS monitoring is becoming increasingly important, particularly for pharmacovigilance. This includes treatment efficacy monitoring, prediction of treatment response and safety monitoring. Quantitative MRI methods and ultra-high-field MRI offer the opportunity for the quantitative assessment of damage in normal-appearing brain tissue. However, the standardization of these techniques with the goal of implementation in clinical routine will be one of the major challenges in the near future.


Molecules ◽  
2020 ◽  
Vol 25 (8) ◽  
pp. 1997 ◽  
Author(s):  
Romina Mancinelli ◽  
Luigi Rosa ◽  
Antimo Cutone ◽  
Maria Stefania Lepanto ◽  
Antonio Franchitto ◽  
...  

The liver is a frontline immune site specifically designed to check and detect potential pathogens from the bloodstream to maintain a general state of immune hyporesponsiveness. One of the main functions of the liver is the regulation of iron homeostasis. The liver detects changes in systemic iron requirements and can regulate its concentration. Pathological states lead to the dysregulation of iron homeostasis which, in turn, can promote infectious and inflammatory processes. In this context, hepatic viruses deviate hepatocytes’ iron metabolism in order to better replicate. Indeed, some viruses are able to alter the expression of iron-related proteins or exploit host receptors to enter inside host cells. Lactoferrin (Lf), a multifunctional iron-binding glycoprotein belonging to the innate immunity, is endowed with potent antiviral activity, mainly related to its ability to block viral entry into host cells by interacting with viral and/or cell surface receptors. Moreover, Lf can act as an iron scavenger by both direct iron-chelation or the modulation of the main iron-related proteins. In this review, the complex interplay between viral hepatitis, iron homeostasis, and inflammation as well as the role of Lf are outlined.


2012 ◽  
Vol 189 (6) ◽  
pp. 2897-2908 ◽  
Author(s):  
Jacqueline A. Quandt ◽  
Jaebong Huh ◽  
Mirza Baig ◽  
Karen Yao ◽  
Naoko Ito ◽  
...  

2009 ◽  
Vol 15 (9) ◽  
pp. 1048-1054 ◽  
Author(s):  
M Khalil ◽  
C Enzinger ◽  
C Langkammer ◽  
M Tscherner ◽  
M Wallner-Blazek ◽  
...  

Background Increased iron deposition has been implicated in the pathophysiology of multiple sclerosis (MS), based on visual analysis of signal reduction on T2-weighted images. R2* relaxometry allows to assess brain iron accumulation quantitatively. Objective To investigate regional brain iron deposition in patients with a clinically isolated syndrome (CIS) or relapsing–remitting MS (RRMS) and its associations with demographical, clinical, and conventional magnetic resonance imaging (MRI) parameters. Methods We studied 69 patients (CIS, n = 32; RRMS, n = 37) with 3T MRI and analyzed regional R2* relaxation rates and their correlations with age, disease duration, disability, T2 lesion load, and normalized brain volumes. Results Basal ganglia R2* relaxation rates increased in parallel with age ( r = 0.3–0.6; P < 0.01) and were significantly higher in RRMS than in CIS ( P < 0.05). Using multivariate linear regression analysis, the rate of putaminal iron deposition was independently predicted by the patients’ age, disease duration, and gray matter atrophy. Conclusions Quantitative assessment by R2* relaxometry suggests increased iron deposition in the basal ganglia of MS patients, which is associated with disease duration and brain atrophy. This technique together with long-term follow-up thus appears suited to clarify whether regional iron accumulation contributes to MS morbidity or merely reflects an epiphenomenon.


2012 ◽  
Vol 18 (12) ◽  
pp. 1791-1796 ◽  
Author(s):  
MP Amato ◽  
V Saia ◽  
B Hakiki ◽  
M Giannini ◽  
L Pastò ◽  
...  

Objective: Chronic cerebrospinal venous insufficiency (CCSVI) was hypothesized to play a causative role in multiple sclerosis (MS). The assessment of pediatric-onset MS (POMS) may provide a unique window of opportunity to study hypothesized risk factors in close temporal association with the onset of the disease. Methods: Internal jugular veins, vertebral veins and intracranial veins were evaluated with extracranial and intracranial ultrasound in 15 POMS and 16 healthy controls. Assessor’s blinding was maintained during the study. We considered subjects positive to CCSVI when at least two criteria were fulfilled. Results: CCSVI frequency was comparable between POMS and controls ( p > 0.05). Clinical features were not significantly different between CCSVI-positive and CCSVI-negative patients. Conclusions: Our findings add to previous data pointing against a causative role of CCSVI in MS.


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