If you have not completed the ‘stay in touch’ form, please do so ASAP otherwise we will not be able to keep in contact with you via telephone, email or post. If you cannot complete the form, please email Sue with your preferences asap. Many thanks,
If you have not completed the ‘stay in touch’ form, please do so ASAP otherwise we will not be able to keep in contact with you via telephone, email or post. If you cannot complete the form, please email Sue with your preferences asap. Many thanks,
Source Multiple Sclerosis News Today: I’m agonizing over an important decision and it’s driving me crazy. I’m usually a quick decision-maker, but this one is tough.
I’m agonizing over an important decision and it’s driving me crazy. I’m usually a quick decision-maker, but this one is tough. I have my analytical hat on, trying to look at my choices from a scientific standpoint. Unfortunately, my anxiety kicks in, and my hat is blown away. Let me explain.
My MS diagnosis was in 1986, a time before any FDA medication was available. When the first MS medication, Betaseron (interferon beta-1b), was approved, I was at the head of the line to sign up. It was exciting to finally have a treatment for my disease, especially one that promised to decrease the severity of an exacerbation while also delaying progression. Unfortunately, I experienced severe side effects, so I jumped ship after a few months. Read on.
Source Multiple News Today: A molecule responsible for preventing the repair of white matter in the brain, a process critical to treating multiple sclerosis (MS) and cerebral palsy, has been identified.
The research, “A TLR/AKT/FoxO3 immune-tolerance like pathway disrupts the repair capacity of oligodendrocyte progenitors,” was published in The Journal of Clinical Investigation.
White matter in the brain’s white matter is composed of nerve fibres. Its colour comes from myelin, the protective layer wrapping nerve fibres that work to ensure proper cell communication. Damaged myelin is a hallmark of MS and other disorders.
Myelin is produced by cells called oligodendrocytes. Research shows that, in cases of chronic white matter injury, oligodendrocyte progenitor cells (OPCs) — the precursor cells of oligodendrocytes — accumulate in lesion areas but are unable to produce myelin. Scientists believe this is due to the presence of fragments from a very large molecule called hyaluronic acid (HA); these small fragments also accumulate at lesion sites. Read on.
Cakes needed for next Friday 11th please for the MEPC cake sale, you can bring in Wed/Thur/Fri a.m, and I will look after here.
Many thanks.
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Source Royal Holloway University: We are looking for volunteers with Relapsing Remitting MS to take part in a new study investigating the relationship between specific mental skills and employment in Multiple Sclerosis. We will be using a new, computer-based test which we hope will be able to produce information more closely related to real life experiences.
You will complete a series of neuropsychological tests and questionnaires which should take no more than 2 hours. We will be arranging a suitable location for testing.
If you are interested and would like more information, please take a stub below and contact the researcher, Laura Clemens, Trainee Clinical Psychologist, who will give you an information leaflet and discuss the study in detail. For more information email Laura.
Source Neurology Advisor: In patients with relapsing-remitting multiple sclerosis (RRMS), fingolimod may protect against deep gray matter (dGM) and thalamus volume loss and may also lead to slower disability progression compared with placebo, according to an analysis published in Neurology.
The investigators analyzed pooled data from the FTY720 Research Evaluating Effects of Daily Oral Therapy in Multiple Sclerosis FREEDOMS and FREEDOMS II phase 3 trials, using data from the fingolimod program. In the pooled analysis, a total of 2064 participants with RRMS received 0.5 mg fingolimod (n=783), 1.25 mg fingolimod, or placebo (n=773). At 12 and 24 months, the investigators evaluated baseline changes in dGM and thalamic volumes. White matter and ventricular volume changes were also evaluated. Read on.
Source MS Society: Researchers at the MS Society Edinburgh Centre for MS Research have found that extra myelin can be sent to the wrong part of the nerve – an important insight for MS treatments.
Professor David Lyons and his team looked at what happens in zebrafish and mice when myelin making cells (known as oligodendrocytes) make more myelin than the nerve fibres need.
Too much of a good thing?
Professor Lyons, MS researcher at the University of Edinburgh and lead author, said: “We were surprised to find that when more oligodendrocytes and myelin were present than the nerve fibre needed, the excess myelin was sent to the wrong part of the nerve.”
It’s important to consider where extra myelin ends up because treatments for MS often involve increasing myelin production to repair damage done to nerve fibres. Read on.