Astrocytes and cerebral blood flow

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

Re: Astrocytes and cerebral blood flow

Postby 1eye » Sun Jun 24, 2012 3:09 pm

Cell culture work showed that lack of iron reduces the ability of microglia to express cytokines (TNF-α and IL-1β) involved in remyelination
I suspect tumour necrosis and tumour growth are connected to "MS", because of the seeming inability of "MS" and cancer to coexist. This may in turn relate to the necessity of angiogenesis (although perhaps flawed) for carcinogenesis. Perhaps the low level of oxygen in CCSVI blood is somehow connected to the inability of astrocytes to provide iron?
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Re: Astrocytes and cerebral blood flow

Postby Bethr » Mon Jun 25, 2012 5:27 am

I think there is a correlation with cancer too. The connection is iron metabolism and the immune system being one in the same system. Ferroportin is the iron exporter. It gets iron out of storage. Iron is hidden from invaders (cancer, virus etc) in an immune response as these invaders need iron to thrive. A fault in ferroportin makes that stored iron unavailable again, maybe permanently, iron remains in storage where it can do damage, oxidation, stopping remyelisation?

It seems the majority of PWMS have low iron. Or is it just unavailable, ie: a fault in ferroportin?
Genmati from memory found a high number of FPN genes in more advanced MS.
I really need to go back and read his papers from IVSND again I think.
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Cece's post on cerebral blood flow model

Postby MarkW » Mon Jun 25, 2012 7:48 am

Cece wrote:http://www.springerlink.com/content/phpvyh4yfhv1q4f5/
DIAGNOSTIC NEURORADIOLOGY
The anatomy of collateral venous flow from the brain and its value in aetiological interpretation of intracranial pathology
J. Andeweg
Abstract
For more than a century, available data concerning collateral venous outflow from the brain have received insufficient attention, as existing theories did not assign practical importance to them. Ideas concerning arterial blood supply and circulation of cerebrospinal fluid were considered more relevant. But available data afford a schematic model of cerebral venous outflow that does have important pathophysiological consequences. Principal outflow through the internal jugular veins can be substituted completely by the large vertebral plexuses, through communications at the cranial base. Emissary veins of the skull vault are small and few in number. Outflow from the deep venous system through the great vein of Galen can be substituted by choroidal, thalamic and striate anastomoses toward the basal vein. So-called intracerebral venous anastomoses through the centrum semiovale towards the convexity are nonexistent or negligible. Instead, a venous watershed exists separating paraventricular white matter from a layer of subcortical white matter. In most infants, the cavernous sinus is not yet connected to the cerebral veins. Once such communications have been formed, important collateral pathways exist through basal and Sylvian veins via the cavernous sinus to the pterygoid plexuses. Simultaneous hindrance of principal and collateral venous outflow will lead to elevated venous pressure and eventual insufficiency of cerebral blood flow (CBF). This will cause increased intracranial pressure, and ventricular enlargement due to periventricular atrophy. The slow phase of the two-compartment model of CBF coincides with the paraventricular white matter area of the deep venous system. In the neonate CBF was found to be still very low, and in the two compartments CBF increases at a different rate to a maximum in childhood. In hydrocephalus, measurement of CBF in the slow deep compartment, rather than the fast cortical one, will be most informative.

The slow phase of the two-compartment model of cerebral blood flow coincides with the paraventricular white matter area of the deep venous system.
Periventricular white matter lesions are especially common in MS.
If even in a healthy person, flow is slow through this section of the brain, then damage due to unnaturally slowed flow due to outflow obstructions could be expected to accumulate here.
Mark Walker - Oxfordshire, England. Registered Pharmacist (UK). 11 years of study around MS.
Mark's CCSVI Report 7-Mar-11:
http://www.telegraph.co.uk/health/8359854/MS-experts-in-Britain-have-to-open-their-minds.html
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Re: Astrocytes and cerebral blood flow

Postby MarkW » Mon Jun 25, 2012 7:51 am

Bethr wrote:...........It seems the majority of PWMS have low iron. Or is it just unavailable, ie: a fault in ferroportin?
Genmati from memory found a high number of FPN genes in more advanced MS.
I really need to go back and read his papers from IVSND again I think.

Looking forward to your comments...................MarkW
Mark Walker - Oxfordshire, England. Registered Pharmacist (UK). 11 years of study around MS.
Mark's CCSVI Report 7-Mar-11:
http://www.telegraph.co.uk/health/8359854/MS-experts-in-Britain-have-to-open-their-minds.html
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Re: Astrocytes and cerebral blood flow

Postby 1eye » Mon Jun 25, 2012 9:58 am

What evidence is there for saying the majority of "MS" patients have low iron? I have heard of a few people on this forum having regular phlebotomy because it make their "MS" feel better. If anything, that would come from the initial condition being an overload of iron.

Oxidation and deoxidation are the main function of iron. It is so important because it can so easily combine with oxygen (rust). I think pw"MS" have low oxygen, and that would hinder anything involving iron's role as a carrier of oxygen, whether there is low iron or high iron.

My opinion is the iron problem in pw"MS" is not in the form of a carrier molecule, but in deposits of iron visible on MRI, possibly from blood cells which have decomposed. That blood leaks across the blood-brain-barrier is found using gadolinium dye, which shows active lesions on MRI, because the gadolinium is in the blood.
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Re: Astrocytes and cerebral blood flow

Postby Bethr » Mon Jun 25, 2012 3:22 pm

1eye wrote:What evidence is there for saying the majority of "MS" patients have low iron?

I've gathered that from my readings over the years. I study iron metabolism and MS.
To make things clearer, this would be as shown on an iron test result from blood levels. That does not mean that iron is not in tissues or free iron. See http://www.hindawi.com/journals/msi/2011/606807/ as an example

Iron and Neurodegeneration in Multiple Sclerosis
Michael Khalil,1,2 Charlotte Teunissen,2 and Christian Langkammer1
1Department of Neurology, Medical University of Graz, A-8036 Graz, Austria
2NUBIN, Department of Clinical Chemistry, VU University Medical Center, 1007MB Amsterdam, The Netherlands

Across the general population the majority of women have low iron levels, so to me that state is normal, MS or not. MS predominantly affects women.


I have heard of a few people on this forum having regular phlebotomy because it make their "MS" feel better. If anything, that would come from the initial condition being an overload of iron.


Yeah, I know, I'm still having one pint taken four times a year. Works great for me.
I have high iron levels as does my sister with MS. But from my readings, we are not the average.

Anyway, that's my take on it, and if you think the hemosiderin deposition gets there simply from old blood, that's your take. I think it's more about iron transport and metabolism No doubt they'll get to the bottom of it eventually. I really doubt that one shoe is going to fit all.
\
Cheers..

Mark - Not sure what you want me to comment on.
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Re: Astrocytes and cerebral blood flow

Postby 1eye » Mon Jun 25, 2012 7:38 pm

BethR:

From the reference you gave:
The exact underlying mechanism by which brain iron accumulates in MS is not fully understood. Iron transport across the blood-brain barrier is dependent on iron transport proteins, predominantly by transferring receptors expressed on brain epithelial cells [59]. Other transporters may also facilitate iron transport across the blood-brain barrier, such as the divalent metal transporter (DMT) and the lactoferrin receptor [60]. It is also not yet clear if increased brain iron deposition is implicated in MS pathology or merely reflects an epiphenomenon [3, 61]
I think it may be more fully understood than it used to be. Dr. Zamboni, possibly others, called it extravasation. This sounds to me like actual leakage of venous blood cells (with a very low level of oxygen due to it being around the brain long enough to have gotten all reduced to more elemental iron) across a pathologically permeable blood brain barrier. When these die they leave iron behind. :smile: I don't think it's an epiphenomenon.
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Re: Astrocytes and cerebral blood flow

Postby 1eye » Mon Jun 25, 2012 8:32 pm

BethR wrote:Across the general population the majority of women have low iron levels, so to me that state is normal, MS or not. MS predominantly affects women.
If they have low blood iron levels it could be due to menstrual loss or some BBB leakage added to that. Aren't men with "MS" low in blood iron levels then? Does it mirror the sex of the patient?
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Re: Astrocytes and cerebral blood flow

Postby Bethr » Tue Jun 26, 2012 3:03 pm

Got it now Mark :lol: . Will get back to this as time permits.
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Re: Astrocytes and cerebral blood flow

Postby Cece » Tue Jun 26, 2012 9:17 pm

1eye wrote:BethR:

From the reference you gave:
The exact underlying mechanism by which brain iron accumulates in MS is not fully understood. Iron transport across the blood-brain barrier is dependent on iron transport proteins, predominantly by transferring receptors expressed on brain epithelial cells [59]. Other transporters may also facilitate iron transport across the blood-brain barrier, such as the divalent metal transporter (DMT) and the lactoferrin receptor [60]. It is also not yet clear if increased brain iron deposition is implicated in MS pathology or merely reflects an epiphenomenon [3, 61]
I think it may be more fully understood than it used to be. Dr. Zamboni, possibly others, called it extravasation. This sounds to me like actual leakage of venous blood cells (with a very low level of oxygen due to it being around the brain long enough to have gotten all reduced to more elemental iron) across a pathologically permeable blood brain barrier. When these die they leave iron behind. :smile: I don't think it's an epiphenomenon.

Diapedesis! (Movement of blood cells out of the blood vessel.)
I like 1eye's interpretation.
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