Professor Tony Holland, of the Cambridge Intellectual and Developmental Disabilities Research Group, who is leading the research, said: ”Almost 100% of people with DS develop pathological signs of Alzheimer’s, and clinical symptoms are seen in DS around 40 years earlier than in the general population.”

The research team is looking for individuals with DS to volunteer to take part in the study. The team has produced a short film – www.youtube.com/user/downsproject – to explain the testing process.

“People with DS are living longer lives, and better lives, but this can be a poisoned chalice, as with this comes a real risk of Alzheimer’s,” said Professor Holland. “Now we need volunteers to come forward to help us explore what is happening to the brain.”

This four-year study aims to determine the role of beta amyloid, a key factor in causing Alzheimer’s. People with DS may be more vulnerable to this type of dementia as they have more amyloid in their brains (a key amyloid gene is located on chromosome 21, which is triplicated in people with DS). Investigating amyloid in this way will also help understand Alzheimer’s development in the general population.

The term ‘dementia’ describes a set of symptoms which can include loss of memory, mood changes, and problems with communication and reasoning. As the disease progresses, people with Alzheimer’s need more support from those who care for them. Eventually, they need help with all their daily activities.

The project is funded by a grant from the Medical Research Council, and is being run in partnership with the Down’s Syndrome Association (DSA).

If you have Down’s syndrome or know someone with Down’s syndrome over the age of 30, who might be interested to hear more about this study, please contact either Tiina or Liam by email on the details below.

Tiina: ta337@medschl.cam.ac.uk

Liam: lrw34@medschl.cam.ac.uk

Telephone: 01223 746127 (voice mail after office hours)

Modern radiotherapy machines can now deliver highly targeted radiotherapy treatment. However, the use of high precision radiotherapy techniques is extremely demanding in terms of hours spent, from the physician who defines the tumour target and healthy tissues, to the physicist who has to calculate a plan of optimum beam angles and trajectories for the treatment, and the radiographer, who must ensure that the treatment is delivered accurately to the target every day during a six or seven week course of radiotherapy.

Accel-RT is an innovative partnership between oncologists, physicists and computer scientists at the Universities of Cambridge and Oxford. Over the next three years the collaborators will develop software tools and processes that will speed up the process of planning of radiotherapy. Once completed, free software tools will be available to radiotherapy treatment centres. These tools will increase patient access to high precision radiotherapy by reducing the bottle-necks in the clinical workflow. The system will operate as a ‘virtual oncologist’, observing what the oncologist is treating and using novel search algorithms to recall similar cases from a clinical archive. Models of tissue structures will be used to help outline normal tissue automatically, as well as to track the movement of these structures during the course of radiotherapy treatment.

Accel-RT is being funded by the Science and Technologies Facilities Council (STFC), through its Innovations Partnership Scheme, and will benefit from the support of Siemens Healthcare, a leading supplier of imaging technology and radiotherapy treatment devices throughout the world.

The key players in the project are established leaders in their fields. At the University of Cambridge, Dr Neil Burnet has been an ‘early adopter’ of novel radiotherapy technologies at Addenbrooke’s, from the commissioning of the first in-house 3D computerised treatment planning system, through to the evaluation of the TomoTherapy image guided intensity modulated radiotherapy system conducted for the Department of Health. At Oxford University, Professor Jim Davies and his team from the Department of Computer Science have experience in the handling of ‘smart’ data systems – using metadata elements to allow data to be searched and processed in more intuitive ways.

Professor Andy Parker and his team at the High Energy Physics group in Cambridge have extensive experience in the storage and handling of large quantities of image data, and the use of grid computing techniques to accelerate this process. “In essence, Accel-RT is helping to identify tumours and surrounding organs during the planning and delivery of radiotherapy treatment. Tracking the change in position and volume of these structures is a complex problem. To perform these calculations in real time for a single patient would require up to 16 Teraflops of processing power – approximately 100 times the power of a standard PC workstation,” said Professor Parker, who is Professor of High Energy Physics at the Cavendish Laboratory and Principal Investigator for Accel-RT.

For more details about the project, and to register for project news emails, go to www.accelrt.org.

In the UK, one in three of all deaths is due to cardiovascular disease. The vast majority of these are caused by atherosclerosis, a ‘furring up’ and blockage of blood vessels. For patients who are unsuitable for conventional stenting or bypass treatment, one option in the future may be to grow new blood vessels to bypass their own blocked vessels.

Lead author of the research, Dr Sanjay Sinha, Wellcome Trust Intermediate Clinical Fellow at the University of Cambridge said: “This research represents an important step in being able to generate the right kind of smooth muscle cells to help construct these new blood vessels. Other patients who may benefit from new blood vessels include those with renal failure, who need vascular grafts for dialysis.”

For the research, the scientists used embryonic stem cells (or similar cells derived from a patient’s skin sample), which have the potential to form any cell type in the body, known as human pluripotent stem cells (hPSCs).  Using hPSCs, they discovered a method for creating high purity vascular smooth muscle.  Although blood and cardiac cells from hPSCs have been created before, this is the first time that all the major types of vascular smooth muscle cells have been developed and done so in a system which would be easy to scale up for clinical-grade production.

Vascular smooth muscle cells originate from different tissues in the early embryo, and the scientists were able to reproduce three distinct types of embryonic tissue in the culture dish.  Interestingly, these SMCs responded differently to vascular disease causing substances, such as growth factors, depending on which embryonic pathway they had come from.  They conclude that differences in embryonic origin may play a part in determining where and when common vascular diseases such as aortic aneurysms or atherosclerosis develop.

Dr Sinha added:  “Using this system, we can begin to understand how SMC origin affects development of vascular disease and why some parts of the vasculature are protected from disease.

“Additionally, there are many patients who have a genetic disorder, such as Marfans Syndrome, that affects their vascular smooth muscle cells and leads to premature death and disability. With this research, and using hPSCs generated from patient skin samples, we will be able to generate smooth muscle cells with the genetic abnormality in a culture dish. This type of ‘disease in a dish’ modelling will allow us to understand the disease better and will allow us to screen for new treatments.”

Crucially, they also found that within these more aggressive breast cancers, the oestrogen receptor (ER) was being ‘redirected’ to a different part of the genome by a protein called FOXA1. So drugs that specifically block FOXA1 could help treat patients who do not respond to conventional hormone treatments, such as tamoxifen.

The researchers used state of the art technology, called ChIP sequencing, to analyse ER-genome interactions in frozen breast tumour samples and create a map of all of the sites in the human genome where ER attaches itself to the DNA and switches on particular genes.

This map was used to compare where in the genome ER attached in tumours from people that responded well to treatment, versus those that went on to relapse or were resistant to treatment from the start.

This revealed almost 500 contact points that were common across all the samples analysed, but also a distinct set of contact points specific to patients with different clinical outcomes – of which 599 were associated with good response to treatment and 1,192 with poor response.

Studying patterns of gene activity in these two areas of the genome allowed the researchers to identify a subset of genes that are more active in tumours that return and spread.

Carlos Caldas, Professor of Cancer Medicine at the Department of Oncology at the University of Cambridge and the Cancer Research UK Cambridge Research Institute said: “Some breast cancers are treated with hormone treatments, such as tamoxifen, which work by blocking oestrogen receptors. But we know that about a third of patients either fail to respond to this type of treatment, or go on to relapse at a later date.

“Understanding the genetic differences that determine who will or won’t respond to a given treatment is a vital step in being able to choose the right drugs for individual patients. The next step will be to see if these findings can be repeated in larger groups of patients.”

Cancer Research UK’s Dr Jason Carroll, who jointly led the study with Professor Caldas, said: “These findings suggest that ER binds to different regions of the genome DNA in breast cancer patients that respond to treatment, compared to those that relapse and whose cancer spreads.

“We know from previous studies involving breast cancer cells growing in the lab that a protein called FOXA1 is needed for oestrogen receptors to interact with the DNA and switch on genes that fuel cancer growth. But this is the first time we’ve examined frozen tumour samples and shown that FOXA1 redirects ER to different locations within the DNA in patients with different outcomes. This switches on different sets of genes, which in turn affect the outcome of the patient. We now hope to develop ways of blocking FOXA1 to help treat patients who no longer respond to standard treatments.”

Tumour samples were obtained with support from the NIHR Cambridge Biomedical Research Centre and Cancer Research UK’s Cambridge Experimental Cancer Medicine Centre.

I’m abruptly woken by the buzzing of my mobile phone. It’s 2 am. It’s the intensive care unit, seeking my input on a patient who has meningitis (bacteria infecting the lining of the brain). The patient has deteriorated because of a complication that we sometimes see in this condition. About a minute into the conversation with the doctor on the other end, I realise that I need to go into the hospital to take a look at what’s happening. I get there and organise an emergency brain scan. An hour later, we have the results of the scan; as I suspected, we need to organise a brain shunt to release the pressure that is compressing the patient’s brain. It’s now 4 am. Rather than driving home, I decide it would be better to try to sleep somewhere in the hospital. I end up in the Doctor’s Mess, on the last remaining bean bag, in between an array of fatigued on-call medics. As it turns out, I’m glad I stay – within an hour, I need to assess a stroke patient for clot-busting treatment. It’s a typical night on-call.

As I drive home, I recall the lectures I heard a few weeks before at a scientific conference. One set of authors had found that shift-work and jet-lag can cause serious problems with a person’s metabolism and can sometimes predispose to cancer. I’d also heard about an interesting study on junior doctors and their lack of responsiveness while driving home after a sleep-deprived shift on-call. How apt. Not only was I actually experiencing this for myself, but my research also focuses on these types of problems.

My laboratory works on the molecular mechanisms of the biological clock (also known as the circadian clock), which are the cycles of physiology and behaviour that govern the daily life of organisms, from bacteria to humans. These incredible in-built mechanisms allow us to anticipate and adapt to the solar cycle of night and day. We now know that disruption of our circadian programming through neurological disease, old age, and even shift-work, is a growing cause of significant morbidity.

As any clock biologist will tell you, researching the biological clock requires a commitment to working at odd times of the day. Surely enough, after recovering from my weekend on-call, I am thrown straight into another disrupted night. When we do clock experiments, we have to take samples ‘around the clock’, often for 3–4 days on the trot. This time, although lucky to be taking mostly daytime samples, I have to do one of the night shifts, taking skin cells (called fibroblasts) from a petri dish and freezing them down. Laboratories aren’t the best place to catch 40 winks. However, I manage to fall asleep in my office chair at about 3 am. Another buzzing awakens me. It’s my mobile phone alarm this time: the 4 am time-point needs taking. A night in the life of a clock biologist…

Dr Akhilesh B. Reddy

Ak Reddy is from the University of Cambridge’s Department of Clinical Neurosciences and the Institute of Metabolic Science, and a fellow at St John’s College. He splits his time between the research laboratory and clinical medicine as a Consultant Neurologist at Addenbrooke’s Hospital, Cambridge. His laboratory studies the biological circadian clock and sleep, and their relationships to metabolism at the molecular level, and receives funding from the Wellcome Trust, the European Research Council and the European Molecular Biology Organisation.

The research, published this week in the Journal of Experimental Medicine, involved molecular virologists working in collaboration with neuroscientists to share their expertise across disciplines. Building on an earlier study published in 2007, the researchers have now shown proof of principle for their methodology which offers a potential novel disease -modifying approach to treating PD. The researchers’ work in harnessing the behaviour of viruses may have wider applications for the treatment of other neurodegenerative diseases – including Alzheimer’s and Huntington’s disease.

Although the age of onset varies considerably, PD is strongly associated with the elderly, with an average age of onset of around 70 years. Around 120,000 people in the UK are directly affected by the disorder with the numbers diagnosed likely to rise as the average age of the population increases. The disease results from a loss of many different types of nerve cells in the brain but especially a population that produces dopamine, a chemical that relays signals from one neuron to another. It is not known why these cells die, but when they do the people affected experience problems with walking and moving quickly.
Current treatments for PD centre on symptomatic drugs which, though they help treat some of the motor features of PD, are not able to stop the disease from progressing. Indeed, over time these drugs can produce their own side-effects.

The novel methodology developed by the Cambridge researchers stemmed from the work of Professor John Sinclair and colleagues at the Department of Medicine in studying the ways in which common viruses – such as herpes – seek to survive and replicate in cells in the body. When these viruses invade a cell, a tiny component of the virus called the Beta2.7 gene guards the mitochondria from damage for an interval of time – typically five days – so that the virus can replicate and spread from cell to cell.

In looking at how the virus gene functions, Professor Sinclair spotted the potential for harnessing this protective function to help cells survive attack by neurological disorders such as PD. The component of the virus that protects the cells’ mitochondria is a section of RNA (ribonucleic acid) which, like DNA, is essential for life. The molecular virologists led by Professor Sinclair used a method of complexing (mixing) the RNA derived from a human cytomegalovirus to a protein of a rabies virus. This protein was selected as it enables the beta2.7 to cross into the brain when the whole complex is given into the circulation, and, as only of a portion of the rabies and herpes viruses are used, there is no danger of contracting any disease from either virus.

Having identified the potential offered by the virus as an agent for ‘search and rescue’, Professor Sinclair collaborated with Professor Roger Barker and colleagues at the Cambridge Centre for Brain Repair to see whether this novel protein/RNA complex could protect neurons from cell death associated with PD. Using rat models, the results have been promising and resulted in a further tranche of research funding from the Michael J Fox Foundation to take work in the laboratory forward to help develop the novel therapeutic for eventual clinical use.

The researchers emphasise that much work remains to be done in taking the therapy to the point at which clinical trials can be undertaken. “Our results with rat models are tremendously encouraging, but we need to do a lot more in terms of refining and optimising the therapy before it could be used in patients. For example, we don’t know what the dosages or frequency of treatment might need to be in treating humans,” said Professor Sinclair.

“What we have established is proof of principle – essentially showing that this is a truly novel and highly promising pathway for treating not just the dopamine cell loss in Parkinson’s but also all cell losses in this condition, as well as other chronic neurodegenerative disorders.”

The novel therapy offers a number of significant advantages over all currently used surgical and drug therapies. Professor Barker explained: “In many ways the therapy we’ve developed is a beautiful treatment. It can be delivered through an injection direct into the bloodstream, for example into the arm of the patient. This makes it much easier to use than many other putative disease-modifying therapies such as growth factors which have to be injected directly into the brain. This new agent also appears to be non-immunogenic – in other words it does not trigger an immune response so it can be used repeatedly and should still maintain its potency. Finally, it appears to go only into the brain and nowhere else in the body and then to target only cells that are unwell.”
The next stage of the research will be to test the novel therapy in other models of PD to help define the dosage and time course of delivery.

Around 12 million people in the UK are diagnosed with hypertension, a condition which greatly increases the risk of having a heart attack or stroke. For most people with hypertension there is no single underlying cause, but in a small minority there is a specific condition that causes blood pressure to rise. One of these conditions is called Conn’s syndrome – the most common curable cause of high blood pressure.

Conn’s syndrome is difficult to diagnose but an accurate diagnosis often leads to successful treatment. It’s caused by a benign tumour called an adenoma – about the size of a 5-pence coin – in one of the adrenal glands, which lie close to the kidneys. The tumour causes the over-production of a key blood pressure-regulating hormone called aldosterone. It can be treated either by surgically removing an affected gland, or by using a drug to block the effects of aldosterone.

The new test, studied in 44 patients at Addenbrooke’s Hospital in Cambridge, scans the abdomen using ‘positron emission tomography with x-ray computer tomography’ technology, better known as a PET-CT and more commonly used in cancer diagnosis. The researchers developed a special radioactive tracer called 11C-metomidate, which lights up culprit adenomas in the scan. The test takes around 45 minutes.

The current standard test for Conn’s syndrome relies on taking blood samples from a vein supplying the adrenal gland to measure the aldosterone level, a complex and difficult procedure which often fails to confirm the diagnosis. However, the researchers showed that their scan picked up adenomas causing hypertension in the majority of study patients, making it a potentially useful alternative to the standard test.

Morris Brown, Professor of Clinical Pharmacology at the University of Cambridge, who led the study, said:  “We were excited to see our technique work so well, and shortcut the delays and discomforts associated with the alternative test. We’re using PET-CT on our patients already, but we also plan a larger study to work out who will benefit the most. The test could be especially important for older patients – we often see growths in the adrenal glands during a routine CT scan. Often these growths are not Conn’s adenomas, but it’s difficult to be sure and they create a lot of anxiety in patients and doctors. In the future PET-CT could be a quick way to reassure a lot of patients without the need for detailed investigations.”

Dr Shannon Amoils, Research Advisor at the BHF, said: “Conn’s syndrome is the most common curable cause of high blood pressure. And although it affects only a small fraction of people with hypertension, it’s almost certainly more widespread than we previously thought.  There are drugs that can control the high blood pressure caused by Conn’s syndrome, but the only cure is surgery, so making the diagnosis is very important. This new approach, using a PET-CT scan, offers real hope that more people with Conn’s syndrome will be accurately diagnosed in the future.”

Chris Wood, 56, who was diagnosed as having Conn’s syndrome by the new test, said: “When I had blood tests before, the results were never clear. I enrolled in Professor Brown’s study I had the scan, which took less than an hour, and immediately after the scan they showed me the pictures of the lump in my adrenal gland that was causing the problem. Getting the definitive diagnosis is fantastic because it removes all the worry, and because I’m on much much less medication than I had been for 15 years. I feel absolutely great.”

The study was published online in the Journal of Clinical Endocrinology and Metabolism. The work was funded mainly by the BHF and the National Institute for Health Research (NIHR), the research funding arm of the NHS.

Researcher Roger Foo explains: “By going wider and scanning the genome in greater detail this time – we now have a clear picture of the ‘fingerprint’ of the missing link, where and how epigenetics in heart failure may be changed and the parts of the genome where diet or environment or other external factors may affect outcomes.”

The study originally began investigating the differences in DNA methylation found in the human heart. Researchers compared data from a small number of people with end-stage cardiomyopathy who were undergoing heart transplantation, and the healthy hearts of age-matched victims of road traffic accidents.

DNA methylation leaves indicators, or “marks”, on the genome and there is evidence that these “marks” are strongly influenced by external factors such as the environment and diet. The researchers have found that this process is different in diseased and normal hearts. Linking all these things together suggest this may be the “missing link” between environmental factors and heart failure.

The findings deepen our understanding of the genetic changes that can lead to heart disease and how these can be influenced by our diet and our environment. The findings can potentially open new ways of identifying, managing and treating heart disease.

The DNA that makes up our genes is made up of four “bases” or nucleotides – cytosine, guanine, adenine and thymie, often abbreviated to C, G, A and T. DNA methylation is the addition of a methyl group (CH3) to cytosine.

When added to cytosine, the methyl group looks different and is recognised differently by proteins, altering how the gene is expressed i.e. turned on or off.

DNA methylation is a crucial part of normal development, allowing different cells to become different tissues despite having the same genes. As well as happening during development, DNA methylation continues throughout our lives in a response to environmental and dietary changes which can lead to disease.

As a result of the study, Foo likens DNA methylation to a fifth nucleotide: “We often think of DNA as being composed of four nucleotides. Now, we are beginning to think there is a fifth – the methylated C.”

Foo also alludes to what the future holds for the study: “…and more recent basic studies now show us that our genome has even got 6th, 7th and 8th nucleotides… in the form of further modifications of cytosines. These are hydroxy-methyl-Cytosine, formylCytosine and carboxylCytosine = hmC, fC and caC! These make up an amazing shift in the paradigm…”

As in most studies, as one question is resolved, another series of mysteries form in its place. The study shows that we are still on the frontier of Epigenetics and only just beginning to understand the link between the life we lead and the body we have.

Wakefulness and energy expenditure rely on “orexin cells”, which secrete a stimulant called orexin/hypocretin in the brain. Reduced activity in these unique cells results in narcolepsy and has been linked to weight gain.

Scientists at the University of Cambridge compared actions of different nutrients on orexin cells. They found that amino acids – nutrients found in proteins such as egg whites – stimulate orexin neurons much more than other nutrients.

“Sleep patterns, health, and body weight are intertwined. Shift work, as well as poor diet, can lead to obesity,” said lead researcher Dr Denis Burdakov of the Department of Pharmacology and Institute of Metabolic Science. “Electrical impulses emitted by orexin cells stimulate wakefulness and tell the body to burn calories. We wondered whether dietary nutrients alter those impulses.”

To explore this, the scientists highlighted the orexin cells (which are scarce and difficult to find) with genetically targeted fluorescence in mouse brains. They then introduced different nutrients, such as amino acid mixtures similar to egg whites, while tracking orexin cell impulses.

They discovered that amino acids stimulate orexin cells. Previous work by the group found that glucose blocks orexin cells (which was cited as a reason for after-meal sleepiness), and so the researchers also looked at interactions between sugar and protein. They found that amino acids stop glucose from blocking orexin cells (in other words, protein negated the effects of sugar on the cells).

These findings may shed light on previously unexplained observations showing that protein meals can make people feel less calm and more alert than carbohydrate meals.

“What is exciting is to have a rational way to ‘tune’ select brain cells to be more or less active by deciding what food to eat,” Dr Burdakov said. “Not all brain cells are simply turned on by all nutrients, dietary composition is critical.

“To combat obesity and insomnia in today’s society, we need more information on how diet affects sleep and appetite cells. For now, research suggests that if you have a choice between jam on toast, or egg whites on toast, go for the latter! Even though the two may contain the same number of calories, having a bit of protein will tell the body to burn more calories out of those consumed.”

In 1975 Cambridge scientists Cesar Milstein and George Kohler at the Laboratory for Molecular Biology (LMB) invented the technology to make large quantities of a monoclonal antibody of any specificity, for which they would later receive the Nobel Prize for Physiology or Medicine.  Building on this research, Herman Waldmann, Geoff Hale and Mike Clark, University of Cambridge, with Greg Winter and Lutz Riechmann, LMB, produced the first humanised monoclonal antibody for use as a medicine, Campath-1H (now known as alemtuzumab).

Campath-1H was licensed for the treatment of chronic lymphocytic leukaemia, but in the 1980s Cambridge clinical scientists also began to explore its use in diseases where the immune system is overactive.

In 1991, Professor Alastair Compston (current Head of the Department of Clinical Neurosciences) began to explore the use of alemtuzumab as a treatment for the autoimmune disease multiple sclerosis.  He and Dr Alasdair Coles (currently University Lecturer in the same department), led the subsequent phases of development of alemtuzumab in multiple sclerosis, in a fruitful partnership with the company Genzyme, now a Sanofi company. In 2008, they announced the results of a phase 2 trial and, in October 2011, they reported the results of the first of two phase 3 trials (CARE-MS1).

Today, Monday 14 November, the successful top line results from the second of the two Phase III trials (CARE – MS2) were announced.  The trial was overseen by Professor Compston as the Chair of the Steering Committee.

“CARE-MS2 represents the culmination of many years clinical and laboratory research aimed at demonstrating the potential for alemtuzumab as a highly effective treatment for multiple sclerosis and understanding mechanisms involved in the complex natural history of the disease,” said Professor Alastair Compston, Chair of the Steering Committee overseeing the conduct of the study. “Taken together, the phase II and III clinical trial data illustrate the promise that alemtuzumab holds as a transformative treatment for a broad range of people with relapsing multiple sclerosis.”

Dr Alasdair Coles said: “Three important results emerge from these trials. First, they show that just eight days of alemtuzumab significantly reduces the risk of having another relapse of multiple sclerosis or becoming disabled over the next 3 to 5 years, compared to the standard active drug, interferon-beta. Secondly, many patients on alemtuzumab experience an improvement in disability, which is not seen after standard treatment. Finally, although alemtuzumab causes potentially serious side-effects, these can be identified and treated provided a monitoring schedule is carefully followed.”

Multiple sclerosis is an autoimmune disease, in which the body’s immune system mistakes friend as foe. Immune cells mistakenly attack nerve fibres and their protective insulation, the myelin sheath, in the central nervous system. The resulting damage prevents the nerves from ‘firing’ properly and ultimately leads to their destruction, resulting in physical and intellectual disabilities.

“Alemtuzumab works by inflicting a short sharp shock to the immune system, by depleting a key cell type called lymphocytes, which then ‘reboot’, leading to a modified immune repertoire that no longer regards myelin and nerves as an invading bug. In so doing, roughly one third of patients after alemtuzumab develop another autoimmune disease, mainly against the thyroid gland and rarely against platelets in the blood,” explains Dr Coles.

Dr Coles’ research team is investigating how to detect people who are susceptible to this particular side-effect, with generous funding from the Grand Charity of the Freemasons, UK and the Evelyn Trust. Additionally, the Moulton Charitable Trust and the Medical Research Council have agreed to fund a trial of alemtuzumab in combination with a novel drug to reduce the risk of autoimmune disease. (Several years ago, the Moulton Charitable Trust also funded Dr Coles’ group to test a strategy to reduce the chance that the immune system will “reject” alemtuzumab after multiple doses.)

It is hoped the drug will be approved by the UK and US regulatory bodies in the next two years, concluding the 36 year epic journey from fundamental research to a new, effective treatment for MS.

Multiple sclerosis affects almost 100,000 people in the United Kingdom, 400,000 in the United States and several million worldwide. Symptoms of the disease can include loss of physical skills, sensation, vision, bladder control, and intellectual abilities.