Chronic cerebral hypoperfusion causes delayed white matter l

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Chronic cerebral hypoperfusion causes delayed white matter l

Postby ThisIsMA » Wed Jun 11, 2014 11:29 pm

Interesting research study:

Chronic cerebral hypoperfusion induced by right unilateral common carotid artery occlusion causes delayed white matter lesions and cognitive impairment in adult mice.


http://www.ncbi.nlm.nih.gov/pubmed/18222425

It would seem plausible that chronic outflow obstructions could cause similar white matter lesions as inflow obstructions. We already know that people with MS are prone to hypoperfusion.

I wonder how long the delay was between when they occluded the carotid artery, and when the lesions developed?
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Re: Chronic cerebral hypoperfusion causes delayed white matt

Postby frodo » Sun Jun 22, 2014 1:38 pm

These are great news!! I remember Dr. Fredman requesting mouse models. Now there is one.
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Re: Chronic cerebral hypoperfusion causes delayed white matt

Postby cheerleader » Mon Jun 23, 2014 3:54 pm

That's a terrific paper---I used a reference to it in an article for the CCSVI Alliance site---discussing how hypoperfusion is linked to all diseases of neurodegeneration, and can be related to CCSVI.

3. Hypoperfusion and reduced cerebral blood flow cause neurodegeneration in a mouse model characterizing vascular cognitive impairment and white matter changes.

Introduction: Reduced cerebral blood flow is associated with neurodegenerative disorders and dementia, in particular. Experimental evidence has demonstrated the initiating role of chronic cerebral hypoperfusion in neuronal damage to the hippocampus, the cerebral cortex, the white matter areas and the visual system. Permanent, bilateral occlusion of the common carotid arteries of rats (two vessel occlusion - 2VO) has been introduced for the reproduction of chronic cerebral hypoperfusion as it occurs in Alzheimer’s disease and human aging. Increased generation of free radicals through lipid peroxidation can damage neuronal cell membrane. Markers of lipid peroxidation have been found to be elevated in brain tissues and body fluids in neurodegenerative diseases, including Alzheimer’s disease, Parkinson disease and amyotrophic lateral sclerosis. [8]


Here's more---
http://ccsvi.org/index.php/the-basics/c ... l-diseases
cheer
Husband dx RRMS 3/07
dx dual jugular vein stenosis (CCSVI) 4/09
http://ccsviinms.blogspot.com
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Re: Chronic cerebral hypoperfusion causes delayed white matt

Postby ThisIsMA » Tue Jun 24, 2014 9:42 am

Here's a study that implicates the endothelium in hypoperfusion caused white matter lesions:

J Neurol Sci. 2010 Dec 15;299(1-2):72-80. doi: 10.1016/j.jns.2010.08.035. Epub 2010 Sep 17.
Is endothelial dysfunction of cerebral small vessel responsible for white matter lesions after chronic cerebral hypoperfusion in rats?
Huang Y1, Zhang W, Lin L, Feng J, Chen F, Wei W, Zhao X, Guo W, Li J, Yin W, Li L.
Author information
Department of Neurology, Beijing Military General Hospital, Beijing, China.


http://www.ncbi.nlm.nih.gov/pubmed/20850139

Abstract

Cerebral white matter (WM) lesions contribute to cognitive impairment and motor dysfunction in the elderly. Intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) are two important adhesion molecules that are upregulated during endothelial activation. Data from recent studies have suggested that ICAM-1 levels are related to progression of white matter hyperintensities (WMH) on MRI. In the present study, we hypothesized that ICAM-1 and VCAM-1 are involved in the endothelial dysfunction and the subsequent WM lesions after chronic cerebral hypoperfusion. Rats underwent bilateral common carotid artery ligation. They were divided into the lipoic acid group and the saline (vehicle) group. RT-PCR and double immunofluorescence for ICAM-1, VCAM-1, endothelial cells (staining positive for von Willebrand factor, vWF), reactive astrocytes (GFAP staining) and activated microglia/macrophages/(CD11b/c staining) were analyzed at baseline and at 1, 3, 7, 14 and 28 days after hypoperfusion. The severity of the WM lesions in the corpus callosum, internal capsule, and external capsule of both hemispheres was graded by luxol fast blue staining. RT-PCR and double immunofluorescence analysis of white matter from rats that had received lipoic acid (100mg/kg/day) for 28 days exhibited markedly reduced expression of ICAM-1 and VCAM-1 over endothelial cells compared with that of rats receiving saline. In the rats treated with lipoic acid, the WM lesions after chronic cerebral hypoperfusion were significantly less severe, and the number of reactive astrocytes and activated microglia/macrophages (CD11b/c staining) were also significantly lower as compared with the saline-treated rats. These findings indicate that endothelial dysfunction plays a critical role in overexpression of ICAM-1 and VCAM-1, glial cell activation and WM lesions after chronic cerebral hypoperfusion and suggest the potential value of lipoic acid as a therapeutic tool in cerebrovascular WM lesions. Our results also provide support for endothelial activation being involved in early pathogenesis of WM lesions and suggest that therapies that stabilize the endothelium may have a role in preventing WM lesions progression.

Copyright © 2010 Elsevier B.V. All rights reserved.

PMID: 20850139 [PubMed - indexed for MEDLINE]
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Re: Chronic cerebral hypoperfusion causes delayed white matt

Postby cheerleader » Tue Jun 24, 2014 4:21 pm

Another great paper, ThisIs....
more and more research keeps coming in that shows how endothelial dysfunction initiates hypoperfusion. Just last week Columbia University researchers showed how this happens in humans---by creating oxidative stress and damaging the vascular endothelium, they slowed blood flow to the human brain.

“Our latest finding gives us a new way of thinking about brain disease—that some conditions assumed to be caused by faulty neurons could actually be problems with faulty blood vessels,” Hillman adds. “This gives us a new target to focus on to explore treatments for a wide range of disorders that have, until now, been thought of as impossible to treat. The brain’s vasculature is a critical partner in normal brain function. We hope that we are slowly getting closer to untangling some of the mysteries of the human brain.”

http://ccsviinms.blogspot.com/2014/06/c ... e-new.html

Following the Endothelial Health program can potentially make a difference in healing the vasculature and normalizing cerebral blood flow. http://ccsvi.org/index.php/helping-myse ... ial-health
Seven years since I wrote it up for Jeff. Science keeps confirming the theory...
cheer
(PS...I mentioned on another thread that Dr. Cooke no longer recommends lipoic acid supplementation to his patients, and he suggests raising antioxidant levels and NO thru lifestyle, exercise and nutrition. More ways to heal endothelial dysfunction are listed in the program.)
Husband dx RRMS 3/07
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