Study: Oxidative Stress and Neurodegenerative Diseases

A forum to discuss Chronic Cerebrospinal Venous Insufficiency and its relationship to Multiple Sclerosis.

Study: Oxidative Stress and Neurodegenerative Diseases

Postby sou » Mon Jan 11, 2010 7:32 am

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:


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

Bayani Uttara Ajay V. Singh, Paolo Zamboni and R.T. Mahajan

Abstract: Free radicals are common outcome of normal aerobic cellular metabolism. In-built antioxidant system of body
plays its decisive role in prevention of any loss due to free radicals. However, imbalanced defense mechanism of antioxidants,
overproduction or incorporation of free radicals from environment to living system leads to serious penalty leading
to neuro-degeneration. Neural cells suffer functional or sensory loss in neurodegenerative diseases. Apart from several
other environmental or genetic factors, oxidative stress (OS) leading to free radical attack on neural cells contributes calamitous
role to neuro-degeneration. Though, oxygen is imperative for life, imbalanced metabolism and excess reactive
oxygen species (ROS) generation end into a range of disorders such as Alzheimer’s disease, Parkinson’s disease, aging
and many other neural disorders. Toxicity of free radicals contributes to proteins and DNA injury, inflammation, tissue
damage and subsequent cellular apoptosis. Antioxidants are now being looked upon as persuasive therapeutic against solemn
neuronal loss, as they have capability to combat by neutralizing free radicals. Diet is major source of antioxidants, as
well as medicinal herbs are catching attention to be commercial source of antioxidants at present. Recognition of upstream
and downstream antioxidant therapy to oxidative stress has been proved an effective tool in alteration of any neuronal
damage as well as free radical scavenging. Antioxidants have a wide scope to sequester metal ions involved in neuronal
plaque formation to prevent oxidative stress. In addition, antioxidant therapy is vital in scavenging free radicals and ROS
preventing neuronal degeneration in post-oxidative stress scenario.

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Postby frodo » Mon Jan 11, 2010 7:47 am

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.
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Postby Algis » Mon Jan 11, 2010 7:51 am

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 :oops:
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iron removbal crosses bbb for ms pd and ataxia deferiprone

Postby jak7ham9 » Mon Jan 11, 2010 7:55 am

University Hospital, Lille Identifier: NCT00943748

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.
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