New drug may possibly treat Multiple Sclerosis

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New drug may possibly treat Multiple Sclerosis

Postby MSUK » Tue Jul 24, 2012 11:47 pm

New drug may possibly treat Multiple Sclerosis, Alzheimer's and brain injury

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A new class of drug developed at Northwestern University Feinberg School of Medicine shows early promise of being a one-size-fits-all therapy for Alzheimer's disease, Parkinson's disease, multiple sclerosis and traumatic brain injury by reducing inflammation in the brain.

Northwestern has recently been issued patents to cover this new drug class and has licensed the commercial development to a biotech company that has recently completed the first human Phase 1 clinical trial for the drug.

The drugs in this class target a particular type of brain inflammation, which is a common denominator in these neurological diseases and in traumatic brain injury and stroke. This brain inflammation, also called neuroinflammation, is increasingly believed to play a major role in the progressive damage characteristic of these chronic diseases and brain injuries.... Read More - http://www.msrc.co.uk/index.cfm/fuseact ... ageid/1397
MS-UK - http://www.ms-uk.org/
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Re: New drug may possibly treat Multiple Sclerosis

Postby cheerleader » Wed Jul 25, 2012 7:50 am

Proinflammatory cytokines will become a new target for pharma. All neurodegenerative conditions that exhibit hypoperfusion (slowed cerebral bloodflow) and ischemic injury have proinflammatory cytokines. This includes stroke, TBI, Alzheimer's, Parkinsons, and MS. It was only a matter of time for pharma to look at this. Of course, the next question should be why is there hypoperfusion? And is there anything else to be done?

Mounting clinical and experimental evidence indicates that Alzheimer Disease can be caused by vascular-related factors that directly reduce cerebral perfusion to a critical level of dysfunction. This evidence can be summarized as follows: (1) epidemiological studies show that risk factors thus far described for AD have a vascular basis; (2) most of the risk factors for AD are also associated with VaD; (3) practically all drugs reported to slow the development of AD improve or increase cerebral perfusion; (4) development of AD can be predicted preclinically by measuring regional cerebral perfusion deficits; (5) clinical evidence exists that AD symptoms are related to brain microvascular hemodynamic pathology; (6) clinical symptomatology is similar in AD and VaD; (7) cerebrovascular pathological lesions often overlap in AD and VaD; and (8) evidence that cerebral hypoperfusion appears to precede the hypometabolic, cognitive, and degenerative pathology that is present in AD.

http://stroke.ahajournals.org/content/33/4/1152.long

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.

http://iiumedic.com/eimj/v1/wp-content/ ... p05-08.pdf

BTW--there's already a wonderful, non-toxic substance on the market that deals with proinflammatory cytokines in the human brain. EGCG.


EGCG significantly suppressed the LPS-induced expression of IL-1beta and TNF-alpha in hCMECs. EGCG also inhibited the expression of MCP-1/CCL2, VCAM-1 and ICAM-1. Functional analysis showed that EGCG induced the expression of tight junction proteins (Occludin and Claudin-5) in hCMECs. Investigation of the mechanism showed that EGCG had the ability to inhibit LPS-mediated NF-kappaB activation. In addition, 67-kD laminin receptor was involved in the anti-inflammatory effect of EGCG.

Conclusions
Our results demonstrated that LPS induced inflammatory cytokine production in hCMECs, which could be attenuated by EGCG. These data indicate that EGCG has a therapeutic potential for endotoxin-mediated endothelial inflammation.

http://www.jneuroinflammation.com/conte ... 1/abstract

interesting,
cheer
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