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Saturday, October 29, 2011

How cannabis causes ‘cognitive chaos’ in the brain

Cannabis use is associated with disturbances in concentration and memory. New research by neuroscientists at the University of Bristol, published in the Journal of Neuroscience [25 October], has found that brain activity becomes uncoordinated and inaccurate during these altered states of mind, leading to neurophysiological and behavioural impairments reminiscent of those seen in schizophrenia.The collaborative study, led by Dr Matt Jones from the University’s School of Physiology and Pharmacology, tested whether the detrimental effects of cannabis on memory and cognition could be the result of ‘disorchestrated’ brain networks.

Brain activity can be compared to performance of a philharmonic orchestra in which string, brass, woodwind and percussion sections are coupled together in rhythms dictated by the conductor. Similarly, specific structures in the brain tune in to one another at defined frequencies: their rhythmic activity gives rise to brain waves, and the tuning of these brain waves normally allows processing of information used to guide our behaviour.

Using state-of-the-art technology, the researchers measured electrical activity from hundreds of neurons in rats that were given a drug that mimics the psychoactive ingredient of marijuana. While the effects of the drug on individual brain regions were subtle, the drug completely disrupted co-ordinated brain waves across the hippocampus and prefrontal cortex, as though two sections of the orchestra were playing out of synch.  Both these brain structures are essential for memory and decision-making and heavily implicated in the pathology of schizophrenia.

The results from the study show that as a consequence of this decoupling of hippocampus and pre-frontal cortex, the rats became unable to make accurate decisions when navigating around a maze.


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"Friendly" Gut Bacteria, May NOT BE friendly for those with MS

In an astonishing new study published in Naturetoday, researchers at the Max Planck Institute of Neurobiology in Martinsried in Munich, Germany say they have found evidence that suggests multiple sclerosis (MS) is triggered by natural intestinal flora, the so-called friendly bacteria that reside in the gut. They found genetically engineered mice with normal gut bacteria developed brain inflammation similar to MS in humans. They say the bacteria first activated the immune T-cells, then the B-cells, which resulted in an attack on the myelin layer in the brain. The same could happen in humans with a corresponding genetic predisposition, they say.

The human gut is home to some 100 billion bacteria from 2,000 different species, comprising 10 to 100 times more genes than in our entire genome. Some scientists refer to this world within a world as an "extended self".

These microorganisms not only help us digest food, they are also essential for gut development. And they also play a role in promoting autoimmune disease, say the Max Planck researchers.

MS is an autoimmune disorder where the body's own immune system attacks and damages the myelin sheath that insulates the axons which are like the "cabling" that connects nerve cells or neurons to one another. The term multiple sclerosis refers to the numerous scars that result from loss of myelin: particularly in the white matter of the brain and spinal cord, most of which is made of myelin.

Although we know quite a lot about the mechanisms of myelin loss, we know very little about the causes of MS. Some have said it is genetic, others that it is triggered by environmental factors like infections, and many say it's probably a bit of both.

In their background information, the Max Planck researchers refer to previous research that shows active MS lesions have "inflammatory changes suggestive of a combined attack by autoreactive T and B lymphocytes against brain white matter." (Lymphocytes are the white blood cells of the immune system).

They explain that T and B cells are normally innocuous members of a healthy immune system, but it appears something triggers them to become "autoaggressive", and the cause is commonly assumed to be environmental, with infection (ie an external pathogen) being the most common reason given.

So, they decided to investigate further using a new type of laboratory mice that have been genetically engineered to spontaneously develop relapsing-remitting autoimmune brain inflammation that is similar to MS in humans.

They found that the gut microorganisms that are necessary to keep the gut and the body healthy (the so-called "commensal gut flora") were essential to triggering the immune processes that led to "a relapsing-remitting autoimmune disease driven by myelin-specific CD4+ T cells".

They discovered this by allowing some of the genetically modifed mice to continue with their normal gut bacteria intact, while removing the intestinal flora in the others and keeping them under sterile conditions.

In time, the mice that kept their gut bacteria developed MS-like symptoms.

But the mice that had their gut bacteria removed remained healthy, despite their genetic predisposition to MS. They also had fewer T-cells in their gut, their spleens produced fewer inflammatory substances like cytokines, and their B-cells produced few if any antibodies against myelin.

However, when they then inoculated these mice with normal gut flora, their T-cells and B-cells increased, as did their cytokine and antibody production, and they eventually developed symptoms and fell ill.

In a final experiment the researchers also found that a protein called MOG has to be present for the immune cells to be able to trigger the autoimmune process:

"We show further that recruitment and activation of autoantibody-producing B cells from the endogenous immune repertoire depends on availability of the target autoantigen, myelin oligodendrocyte glycoprotein (MOG), and commensal microbiota."

"Our observations identify a sequence of events triggering organ-specific autoimmune disease and these processes may offer novel therapeutic targets," concluded the researchers.

Senior author Gurumoorthy Krishnamoorthy told the press:

"It appears that the immune system is activated in two stages: to begin, the T cells in the lymph vessels of the intestinal tract become active and proliferate. Together with the surface proteins of the myelin layer, these then stimulate the B cells to form pathogenic antibodies."

"Both processes trigger inflammatory reactions in the brain which progressively destroy the myelin layer - a process that is very similar to the way multiple sclerosis develops in humans."

Krishnamoorthy and colleagues are convinced that the gut flora can also trigger an overreaction of the immune system against the myelin in people who are genetically predisposed to MS.

This study indicates that nutrition may play a key role in the development of MS, since diet largely determines the types of bacteria that colonize the gut.

CONTINUE READING from Medical News Today





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Disclaimer:  'MS Views and News' (MSVN), does not endorse any products or services found on this blog. It is up to you to seek advice from your healthcare provider. The intent of this blog is to provide information on various medical conditions, medications, treatments, and procedures for your personal knowledge and to keep you informed of current health-related issues. It is not intended to be complete or exhaustive, nor is it a substitute for the advice of your physician. Should you or your family members have any specific medical problem, seek medical care promptly.
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Thursday, October 27, 2011

The Potential for another FDA approval for a New Oral MS Medication

AMSTERDAM -- The investigational oral drug teriflunomide (Aubagio) seems to have maintained its effectiveness during up to nine years of follow-up in clinical trial patients with the relapsing form of multiple sclerosis, and no late safety problems have been noticed, researchers said here.

The findings came from open-label extensions of phase II and III studies with teriflunomide, which is now under FDA review as a treatment for relapsing-remitting MS. The results were presented in a series of posters at the joint meeting of the European and American Committees for Treatment and Research in Multiple Sclerosis (ECTRIMS).

Annualized relapse rates during the eight-year extension phase of the phase II study ranged from 0.20 to 0.32, with somewhat lower rates seen with a 14-mg/day dose of teriflunomide relative to 7 mg/day, according to Paul O'Connor, MD, of the University of Toronto, who was a principal investigator for this study and others involving teriflunomide.

The relapse rates were comparable to those seen in the trial's placebo-controlled phase.
Also, EDSS disability scores remained stable in patients taking 14 mg/day during the extension and rose only moderately among those on 7 mg/day.

But with both dosages, other signs of disease activity, such as total MRI lesion burden and brain atrophy, continued to rise during the extension.

Findings were similar in an extension of the phase III TEMSO trial, for which five years of efficacy data are now available, according to O'Connor...


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Breath test to diagnose multiple sclerosis comes closer to reality


Washington, Oct 27 (ANI): Scientists have developed a sensor array that can diagnose multiple sclerosis (MS) from exhaled breath.
Hossam Haick and colleagues report that doctors now diagnose MS based on its characteristic symptoms, which include muscle spasms, numbness, coordination problems and slurred speech. One common tool for confirming the diagnosis and making informed decisions on treatment is magnetic resonance imaging (MRI) of the brain. Another tool is a lumbar puncture or "spinal tap" to analyze the fluid that bathes the brain and spinal cord. But MRI scans are costly, and lumbar punctures are invasive.
To overcome these obstacles, the researchers have identified volatile organic compounds that can be associated with MS from exhaled breath.
Based on these findings, the researchers developed a new sensor array that can diagnose MS by analyzing the determined chemical compounds that appear in the breath of MS patients.
Using the developed sensors, the researchers carried out a proof-of-concept clinical study on 34 MS patients and 17 healthy volunteers and found that the developed sensors are just as accurate as a spinal tap but without the pain or the risk of side effects.
"The results presented here open new frontiers in the development of fast, noninvasive and inexpensive medical diagnosis tools for detection of chronic neurological diseases," the scientists stated.
"The results could serve as a launching pad for the discrimination between different subphases of stages of multiple sclerosis as well as for the identification of multiple sclerosis patients who would respond well to immunotherapy," they added.
The study has been published in the journal ACS Chemical Neuroscience. (ANI)



Source for this article found here


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Researchers at the University of Alberta have discovered a potential new drug target for Multiple Sclerosis that could prevent physical disability


October 27, 2011
Medical researchers at the University of Alberta have discovered a potential new drug target for Multiple Sclerosis that could prevent physical disability associated with the disease, once a new drug is developed.

In the first phase of MS, those with the condition have lots of inflammation of theirbrain cells, resulting in continuous cycles of inflammation attacks followed by recovery periods. In the second phase of the disease, the inflammation isn't as severe, but this is the stage where physical disability sets in due to the effects from substantial numbers of brain cells being killed in the first phase of the disease.

When immune cells become active due to inflammation, they can pass through the blood-brain barrier and enter the central nervous system. Some of these activated immune cells secrete a molecule, known as granzyme B, that can get inside neurons and wreak havoc - ultimately causing brain cell death. Granzyme B is found in MS brain lesions - especially in the early stages of inflammation. This molecule can get into braincells through a "gatekeeper," known as receptor M6PR.

Researchers with the Faculty of Medicine & Dentistry discovered in lab experiments that if they prevent this granzyme B from entering neurons, "we can also prevent the killing of neurons," says principal investigator Fabrizio Giuliani, whose work was recently published in the peer-reviewed publication, The Journal of Immunology.
"It is this loss of brain cells, in the long-term, which induces disability in those with MS," he says. "This is a new drug target for MS that is specific for the neurodegenerative processes following inflammation."

Giuliani, a researcher in the Division of Neurology and a practising neurologist, noted this latest research builds on previous findings by his colleagues within the faculty. Medical researcher and co-author Chris Bleackley made an earlier discovery about how granzyme B enters target cells through the receptor M6PR. Another faculty researcher discovered that the M6PR receptor is found mostly in neurons.



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