This Is MS Multiple Sclerosis Community: Knowledge & Support

Hi all.

I have found this very interesting study and I would like to share it with you. Not very related to CCSVI itself, but it discusses some ways the neural cells die, including Fe poisoning and Fe induced inflammation.

Here is the full text:

link

If somebody could upload it somewhere, because I don't know how long I could keep it here for.



sou(r)

_________________
Shortest joke: "We may not be able to cure MS but we can manage its symptoms."

Some years ago there was some clinical trials with inosine, with good results, but like all non-pharma treatments it was simply forgotten.

No more trials have been published. The relationship with this is that it was supposed to work as an antioxidant.

I - For sure - do not know exactly how does oxidative stress - works or if it directly relates to stress - But I can guarantee that any stress situation would make me worse than usual.

Not sure if my remark is relevant tho

University Hospital, Lille
ClinicalTrials.gov Identifier: NCT00943748

Purpose
In general, there are few available drugs for slowing the progression of neurodegenerative pathologies such as Parkinson's disease (PD). One of the recent hypotheses concerning the reduction of oxidative stress and neuron death features a harmful effect of iron, which may reach abnormally high levels in the substantia nigra pars compacta. In fact, iron overload has been seen in the substantia nigra in parkinsonian patients and in the 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) mouse model of PD. Iron overload is harmful because it reacts with hydrogen peroxide (H2O2) produced during the oxidative deamination of dopamine, generating hydroxyl radicals which then damage proteins, DNA and phospholipid membranes and may be responsible for neuron death. The use of an iron chelator (clioquinol) produces a reduction in neuron death in the MPTP mouse model. In humans, a special, partially refocused interleaved multiple echo (PRIME) MR sequence has been used to study the relaxation time (T2*) and quantify iron overload in the substantia nigra of PD patients and the nucleus dentatus of patients with Friedreich's ataxia. T2* sequences have revealed a decrease in iron overload following treatment with the chelator deferiprone (Ferriprox®), in parallel with a clinical improvement in these patients. Furthermore, the very recent open label use of deferiprone in rare serious, systemic, neurological iron overload diseases (Neurodegeneration with Brain Iron Accumulation , NBIA) has revealed a clinical improvement after 6 months, with 2 case reports from our group and another from an Italian group (Forni et al., 2008). The safety of the low dosages of deferiprone (20 to 30 mg/kg/day) used in neurology appears to be much greater than for the high dosages (75 to 100 mg/kg/day in 3 doses) used in hematology to decrease post-transfusion iron overloads in thalassemia major.

Hence, the investigators wish to evaluate the effect of treatment with an oral iron chelator which is capable of crossing the blood-brain barrier (deferiprone, Ferriprox®) on iron overload in the substantia nigra (as assessed by the T2* sequence) with respect to the progression of clinical sign in PD. The investigators expect a 6-month course of deferiprone to produce a moderate reduction in iron overload of the substantia nigra, associated with a drop in the motor handicap score (relative to the placebo group). Depending on the risk/benefit balance determined in this initial pilot study, a larger, multicenter neuroprotection study could be envisaged.