Abstract

Whether iron deposition is an epiphenomenon of the multiple sclerosis (MS) disease process or may play a primary role in triggering inflammation and disease development remains unclear at this time, and should be studied at the early stages of disease pathogenesis. However, it is difficult to study the relationship between iron deposition and inflammation in early MS due to the delay between the onset of symptoms and diagnosis, and the poor availability of tissue specimens. In a recent article published in BMC Neuroscience, Williams et al. investigated the relationship between inflammation and iron deposition using an original animal model labeled as "cerebral experimental autoimmune encephalomyelitis", which develops CNS perivascular iron deposits. However, the relative contribution of iron deposition vs. inflammation in the pathogenesis and progression of MS remains unknown. Further studies should establish the association between inflammation, reduced blood flow, iron deposition, microglia activation and neurodegeneration. Creating a representative animal model that can study independently such relationship will be the key factor in this endeavor.

Highlights

  • Whether iron deposition is an epiphenomenon of the multiple sclerosis (MS) disease process or may play a primary role in triggering inflammation and disease development remains unclear at this time, and should be studied at the early stages of disease pathogenesis

  • At this time it is unclear whether iron deposition is an epiphenomenon of the multiple sclerosis (MS) disease process or may play a primary role in triggering inflammation and disease development [1]

  • In a recent article published in BMC Neuroscience, Williams et al [2] investigated the relationship between inflammation and iron deposition using an original animal model labeled as “cerebral experimental autoimmune encephalomyelitis”, which develops CNS perivascular iron deposits

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Summary

Introduction

Whether iron deposition is an epiphenomenon of the multiple sclerosis (MS) disease process or may play a primary role in triggering inflammation and disease development remains unclear at this time, and should be studied at the early stages of disease pathogenesis. In a recent article published in BMC Neuroscience, Williams et al [2] investigated the relationship between inflammation and iron deposition using an original animal model labeled as “cerebral experimental autoimmune encephalomyelitis”, which develops CNS perivascular iron deposits. It was proposed in a pilot study that iron deposits in MS may be related to chronic cerebrospinal venous insufficiency (CCSVI), [6] a vascular condition characterized by anomalies of the main extra-cranial cerebrospinal venous routes that interfere with normal blood outflow of brain parenchyma in patients with MS [12].

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