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News Archive

2008

November

Genetic study provides new insights into molecular basis of language development

Scientists have identified the first gene that is associated with a common childhood language disorder, known as specific language impairment (SLI). The gene – CNTNAP2 – has also been recently implicated in autism, and could represent a crucial genetic link between the two disorders.

Although most children acquire proficient spoken language almost automatically and with little conscious effort, a significant number develop unexplained difficulties in producing and understanding language. SLI is the most common such disorder, affecting up to 7% of pre-school children.

In a study published today in the New England Journal of Medicine, researchers at the Wellcome Trust Centre for Human Genetics, University of Oxford, discovered that particular variants of the CNTNAP2 gene were significantly associated with language deficits in a large sample of families with SLI.

"It has long been suspected that inherited factors play an important role in childhood language disorders," says Dr Simon Fisher, a Royal Society Research Fellow at the Wellcome Trust Centre, who led the research. "But this is the first time that we have been able to implicate variants of a specific gene in common forms of language impairment."

The trail to this new finding began with studies of another language-related gene, called FOXP2, previously found to be mutated in rare cases of a severe speech and language disorder. Versions of FOXP2 are found in many animals, including primates, birds, bats and mice. In birds, for example, it has been linked to song, in mice to learning of sequences of movement, and in bats it may relate to echo-location.

FOXP2 acts to regulate other genes in the brain, switching them on and off. Dr Fisher and colleagues began analysing human neurons grown in the laboratory in order to search for these target genes. They identified CNTNAP2 as a key part of the network.

When the scientists went on to investigate CNTNAP2 in 184 families with common language impairments, they found that children who carried certain variants of the gene displayed reduced language abilities, most strikingly for a measure of nonsense-word repetition that is known to be a strong indicator of SLI.

Recent studies have also implicated CNTNAP2 in autism, a syndrome characterised by communication deficits, impaired social interaction, and repetitive behaviours. In particular, one investigation uncovered an association between variants of CNTNAP2 and delayed language development in children with autism.

"Our findings suggest that similar changes in the regulation or function of this gene could be involved in language deficits in both SLI and autism," says Dr Fisher. "This supports the emerging view that autism involves the convergence of a number of distinct problems underpinned by different genetic effects."

Professor Dorothy Bishop, a Wellcome Trust Principal Research Fellow at the University of Oxford, who specialises in the study of children's communication impairments, comments:

"All too often parents of language-impaired children are blamed for their children's difficulties, even though the evidence has been around for a while that genes are implicated.  These are important yet neglected disorders that can have long term effects on educational and social outcomes. This landmark study provides an important first step in unravelling the complex biological factors that determine susceptibility to language difficulties."

It is not yet known exactly how changes to CNTNAP2 interfere with language development, but there are some tantalising clues. The gene makes a type of protein called a neurexin, which sits in the membranes of neurons, controlling interactions between different cells during the development and wiring up of the nervous system. In early development, the protein appears to be strongly expressed in parts of the human brain which go on to become important for language processing, such as the frontal lobes.

The researchers are now investigating whether variations in CNTNAP2 contribute to natural variation in linguistic abilities in the general population.

"Genes like CNTNAP2 and FOXP2 are giving us an exciting new molecular perspective on speech and language development, one of the most fascinating but mysterious aspects of being human," says Dr. Fisher "There are likely to be more answers buried in our genome. This work promises to shed light on how networks of genes help to build a language-ready brain."

Overview of FOXP2:  http://www.newscientist.com/channel/being-human/mg19926691.800-the-evolutionary-story-of-the-language-gene.html

Eurekalert:  http://www.eurekalert.org/pub_releases/2008-11/wt-gsp110308.php

Reuters 5 November:  http://www.reuters.com/article/healthNews/idUSTRE4A4B5N20081105

Science Online 5 November:  http://sciencenow.sciencemag.org/cgi/content/full/2008/1105/4

Science News 5 November:  http://www.sciencenews.org/view/generic/id/38326/title/A_genetic_pathway_to_language_disorders

Times Online 6 November:  http://www.timesonline.co.uk/tol/life_and_style/health/article5092857.ece

Times Online 6 November:  http://www.timesonline.co.uk/tol/life_and_style/health/article5092839.ece

Times Online 6 November:  http://www.timesonline.co.uk/tol/life_and_style/health/article5092883.ece

Voice of America 6 November:  http://www.voanews.com/english/2008-11-06-voa47.cfm

Times of India 6 November:  http://timesofindia.indiatimes.com/HealthSci/Gene_behind_language_disorder/articleshow/3680935.cms

Financial Times 7 November:  http://www.ft.com/cms/s/0/102d7a98-ac6f-11dd-bf71-000077b07658.html?nclick_check=1

October

Researchers announce major new study on depression

Researchers from the Wellcome Trust Centre for Human Genetics (WTCHG) at the University of Oxford today announce a major new study into the genetics of major depression in a population of women in China.  The five-year project is funded by a £1.4 million grant from the Wellcome Trust.  One of the largest studies into depression ever carried out in China, the project is collaboration between the University of Oxford, Hua Shan Hospital at Fudan University, China, and the Virginia Commonwealth University (VCU).

In the first stage of the project, interviewers in China will talk to over 6,000 women who have suffered from recurrent lifetime major depression.  They will also interview 6,000 matched controls - women who have never suffered from depression.  In each of 15 hospitals across China, interviewers (psychiatrists trained by the VCU) will complete a detailed questionnaire on each woman who has volunteered to participate.  In the second stage, DNA will be extracted from saliva samples collected from all interviewed women.  The DNA will then be analysed to establish differences between the genetic profiles of the women affected by depression (cases) and those who have never suffered from depression (controls).

Professor Jonathan Flint (WTCHG), a Wellcome Trust Principal Research Fellow and one of the project co-directors, says: “"We know that major depression has a genetic component.  This project aims to identify the specific genes that make some people more susceptible than others to recurrent bouts of major depression.  Knowing more about the biological basis of depression will help researchers develop better therapies ".

This Wellcome Trust funded project follows on from a successful pilot project of 1,000 women funded by the mental health research charity, NARSAD.

Project Homepage: http://www.well.ox.ac.uk/flint/china

Dyslexia gene associated with reading difficulties in general population

A gene thought to be associated with dyslexia is also connected with reading ability in the general population, according to research funded by the Wellcome Trust. A study to be published online today in the journal American Journal of Psychiatry suggests that a common variant of this gene, carried by more than one in seven people, is associated with poor reading ability.

Dyslexia is a learning difficulty which affects the development of literacy and language related skills, such as reading and spelling, but does not affect overall IQ. It is believed that as many as one in ten people are affected by dyslexia to some degree.

Previous research has identified at least six candidate genes that appear to affect susceptibility to developing dyslexia. However, scientists have often failed to replicate these findings, suggesting that their role in causing dyslexia is debatable.

The most promising of the candidates is the gene KIAA0319, which lies on chromosome 6. This gene has been reported in at least three independent studies. Researchers at the Wellcome Trust Centre of Human Genetics, University of Oxford, have previously identified a haplotype – a particular DNA sequence, which spans part of this gene – associated with dyslexia in both a large samples of UK families and a samples of twins in the US. This association was also identified independently by researchers at Cardiff University.

Now, working with a cohort of over 6,000 seven to nine-year old children from Children of the 90s, also know as the Avon Longitudinal Study of Parents and Children (ALSPAC), researchers have looked at the association between this particular haplotype, which is carried by 15% of the population, and general reading ability.

"On average, people carrying this common genetic variant tended to perform poorly on tests of reading ability," says Dr Silvia Paracchini from the Wellcome Trust Centre for Human Genetics, lead author of the study. "However, it's important to note that this is only true for reading ability and not for IQ, so it doesn't appear to be connected to cognitive impairment."

Dr Paracchini and colleagues have previously shown that the same haplotype is associated with reduced expression of the KIAA0319 gene during development of the foetus – in other words, it acts like a dimmer switch, reducing the power of the gene to do its normal job as the foetus grows. This affects development of the cerebral cortex, the area of the brain responsible for thought processes. In animal studies, switching off KIAA0319 affects neuronal migration, the process that enables nerve cells created in the inner layer of the cerebral cortex area to migrate outwards to their destination.

"This is clearly only part of the jigsaw puzzle that explains why some people have poorer reading ability than others or develop dyslexia," says Dr Paracchini. "There are likely to be many other contributing factors, but our research provides some valuable clues. We need to carry out studies into the exact role that this gene plays in brain development and how this affects people's reading ability."

Full text article: http://ajp.psychiatryonline.org/cgi/reprint/appi.ajp.2008.07121872v1

BBC News Online 1 October: http://news.bbc.co.uk/1/hi/health/7643760.stm

BBC Radio 5 live 1 October

Reuters 1 October: http://uk.reuters.com/article/domesticNews/idUKTRE49012H20081001

Daily Mail 1 October: http://www.dailymail.co.uk/health/article-1065696/Dyslexia-gene-discovery-improve-treatment-millions.html

Daily Mirror 1 October: P27 and http://www.mirror.co.uk/news/top-stories/2008/10/01/dyslexia-gene-hits-reading-115875-20763608/

Evening Standard 1 October: http://www.thisislondon.co.uk/standard/article-23562445-details/Dyslexia+gene+discovery+brings+hope+to+sufferers/article.do

Oxford Mail 1 October: http://www.oxfordmail.co.uk/news/3717902.Genes_link_to_reading_skills/

PhysOrg.com 1 October: http://www.physorg.com/news142091390.html

TheMedGuru 1 October: http://www.themedguru.com/articles/gene_variation_blamed_for_reading_difficulty-86112737.html

Science News 3 October: http://www.sciencenews.org/view/generic/id/37222/title/Genetic_link_to_dyslexia

Times Online 25 October: http://www.timesonline.co.uk/tol/life_and_style/education/article5006527.ece

September

Evolution marches on

Professor Gil McVean of the Wellcome Trust Centre for Human Genetics, who studies genetic variation in the human population, believes that the basic elements that drive human evolution are alive and well and man is continuing to evolve even in a modern environment.

The Independent 9 September: http://www.independent.co.uk/life-style/health-and-wellbeing/health-news/surgery-is-only-means-to-healthy-weight-loss-923481.html

University of Oxford Science blog 15 September: http://www.ox.ac.uk/media/science_blog/080915.html

Human trials of new 'flu vaccine begin

Clinical trials of a new vaccine that could protect against multiple types of flu are beginning at Oxford University. If successful, the ‘universal’ ‘flu injection would transform the way we vaccinate against influenza and could offer immunity to a bird flu pandemic.

Current vaccines are only effective against certain strains of ‘flu. New formulations have to be developed every year according to which types of ‘flu are thought likely to be circulating that winter.

“This approach to influenza vaccination is unsatisfactory for use against seasonal influenza, and of little use when new types of ‘flu begin to infect humans from birds,” says Dr Sarah Gilbert of the Jenner Institute, University of Oxford. “It leaves manufacturers with a few months to produce the necessary stocks, the vaccine has to be administered to at-risk populations within a short time window, and those receiving the injection will all have to be vaccinated again the following year."

Existing ‘flu vaccines work by inducing protective antibodies to proteins on the outer surface of the influenza virus. These proteins differ between strains and change over time, so each vaccine only works against a specific strain.

The Oxford scientists led by Dr Gilbert are taking a new approach. They have developed a novel vaccine that targets internal proteins essential to the ‘flu virus that change very little over time or between strains.

“By targeting the internal proteins of the virus, we can come up with a universal ‘flu jab,” explains Dr Gilbert. “The same vaccine would work against all seasonal flu and protect against bird ‘flu.”

Such a universal vaccine would not change from year to year, removing the need for annual immunisations. All ages could receive the injection at any time of year, and manufacturers would be able to produce supplies continuously at a sufficient level.

“Children would be protected, we’d see economic benefits through reduced sickness in people of working age, and the elderly, who respond less well to vaccination, would be better off through lack of exposure to ‘flu,” explains Dr Gilbert.

In the Phase I clinical trial, 12 healthy volunteers are receiving the single injection of the new vaccine. Their immune response will then be monitored over time. Should this trial be successful, further clinical trials will be necessary before the vaccine can be approved. The research is funded by the Wellcome Trust.

The vaccine developed by Dr Gilbert and colleagues induces T cells, part of the body’s immune system, to kill any cells infected by the flu virus, so controlling the infection. The body maintains a low-level T cell response to flu from previous flu infections which the vaccine should boost to levels high enough to protect against subsequent infection.

July

Royal Society honours Oxford researchers

Four researchers from the University of Oxford have been honoured by the Royal Society in this year’s Royal Society Awards, Medals, and Prize lectures announced today.

Dr Simon Fisher, a Royal Society University Research Fellow at Oxford’s Wellcome Trust Centre for Human Genetics, has been awarded the Francis Crick Prize Lecture for his ground breaking research in human language.

Dr Fisher’s work combines a number of disciplines such as genetics, neuroscience and psychology to investigate what makes us human. He was co-discoverer of the FOXP2 gene and the revolutionary finding that people with faulty versions of this gene have difficulty developing normal speech and language.

Dr Fisher said: 'I feel deeply honoured to have been chosen to deliver the Crick Prize Lecture at the Royal Society. Francis Crick was a truly inspirational scientist; not only was he a pioneer of molecular biology, laying the foundations for modern genetics, but he went on tackle some of the most challenging questions facing the field of neuroscience.'

Sir Roger Penrose, Emeritus Rouse Ball Professor of Mathematics at Oxford, has been awarded the Royal Society’s Copley medal – the world’s oldest prize for scientific achievement – for his exceptional contributions to geometry and mathematical physics.

Sir Roger said: 'The award of the Royal Society's Copley Medal came as a complete surprise to me. It is an extraordinary honour, this being the Royal Society's oldest and most distinguished award, first given just 200 years before I was born. I feel most humbled for my name to be added to that enormously distinguished list of previous recipients.'

The Copley medal was first awarded in 1731. It is awarded for outstanding achievements in scientific research and has been awarded to such eminent scientists as Charles Darwin, Michael Faraday, Albert Einstein and Stephen Hawking.

Professor Robert Hedges, Deputy Director of the Laboratory of Archaeology and the History of Art at Oxford has been awarded a Royal Medal for his contribution to the rapid development of accelerator mass spectrometry and radiocarbon dating techniques.

His research focuses on the recovery of information about human and animal diets, and ancient environments, from archaeological sites. This work includes identifying surviving biological molecules and understanding how such molecules degrade over time.

Professor James Murray, Emeritus Professor of Mathematical Biology at Oxford, has been awarded the Bakerian Prize Lecture, the Royal Society's premier lecture in the physical sciences. The award has been made for his groundbreaking work in mathematical biology.

Professor Murray was formerly Director of the Centre for Mathematical Biology at Oxford. He also recently received the Gold Medal of the Institute of Mathematics and its Applications (IMA).

More information from the Royal Society: http://royalsociety.org/news.asp?id=7877

June

Genetic complexity of Crohn's disease revealed

New research has trebled the number of genetic regions known to be implicated in Crohn's disease, a form of inflammatory bowel disease, to over thirty. The research, published today in the journal Nature Genetics, has identified a number of potential new targets for drug development as well as providing surprising new links between the condition and other common diseases including asthma.

Crohn's disease affects between 1 in 500 and 1 in 1000 people within the UK, causing inflammation of gastrointestinal tract and leading to pain, ulcers and diarrhoea. The disease can strike at any age, but onset is typically between 15 and 40 years old. As many as 80% of people suffering from the disease will require surgery at some point.

Previous studies have already identified 11 genes and loci (regions of the genome typically including one or more genes) that increase susceptibility to the disease. Now an international collaboration of researchers has identified a further 21 new genes and loci. The team of scientists and clinicians involved used DNA samples from almost 12,000 people. Many were from UK patient collections and analysed originally in the Wellcome Trust Case Control Consortium – the largest study ever undertaken into the genetics underlying common diseases – with others coming from European and North American collections.

"We now know of more than thirty genetic regions that affect susceptibility to Crohn's disease," says Dr Jeffrey Barrett from the Wellcome Trust Centre for Human Genetics at the University of Oxford, lead author of the study. "These explain only about a fifth of the genetic risk, which implies that there may be hundreds of genes implicated in the disease, each increasing susceptibility by a small amount.

"Whilst this study shows the power of genome wide association studies to reveal the genetics behind common diseases, it also highlights the complexity of diseases such as Crohn's."

Genome wide association studies have led to an explosion in the number of genes known to be implicated in complex diseases such as diabetes, heart disease and Crohn's disease. The first two Crohn's disease susceptibility genes were discovered in 2001, followed by a third in 2006. The Wellcome Trust Case Control Consortium and parallel studies took that number above ten the following year using genome wide association studies. This number has now almost trebled to thirty-two.

Amongst the findings are loci containing genes known to be implicated in a number of other common diseases including diabetes, rheumatoid arthritis and psoriasis.  However, the genetic relationship between Crohn's and these other diseases is not always straightforward.  For example, the genetic variant PTPN2 appears to increase susceptibility to both Crohn's disease and type 1 diabetes.  But the similarly named PTPN22 increases the risk of developing type 1 diabetes, yet appears to offer protection from Crohn's.

Although some of the disease connections were unsurprising – there is already a known epidemiological correlation between Crohn's disease and psoriasis, for example – the ORMDL3 gene on chromosome 17 provided the most unexpected link. ORMDL3 was already known to be a genetic risk factor for childhood asthma, but until now, no epidemiological link had ever been seen between asthma and Crohn's disease. 

"It's too early for us to say how Crohn's disease and many of these other diseases, including asthma, are linked at a biological level," says Dr Miles Parkes, Consultant Gastroenterologist at Addenbrooke's Hospital and the University of Cambridge, who also worked on the study. "However, we are building up a picture of the biology underlying Crohn's disease, and the more we understand about the underlying biology of these diseases, the better equipped we will be to treat them.

"Studies such as this are not about developing diagnostic tests, but about identifying targets for new drugs therapies. Crohn's disease can be a very serious condition, often requiring surgery, and the sooner we can understand the underlying causes, the sooner we will be able to devise new treatments to help our patients."

Some of the most likely candidates for so-called "druggable" targets include the CCR6 gene, which is thought to be part of the signalling machinery that causes white blood cells in the gut to become over-active, leading to inflammation. These particular white blood cells, known as Th17 cells, are also present in inflamed joints, implying that CCR6 may also be relevant to rheumatoid arthritis, and therefore of added interest to the pharmaceutical industry.

"Genetics, and particularly the large scale approach of genome wide association studies, offers much hope for understanding the biological causes of complex diseases," says Dr Mark Walport, Director of the Wellcome Trust. "Studies such as this also highlight the important relationships between different diseases and, as such, may offer valuable insights into the pathways that lead to common symptoms such as inflammation."

The collection of samples was supported by the National Association for Colitis and Crohn's Disease.

Science Codex 29 June: http://www.sciencecodex.com/complexity_of_crohns_disease_revealed_as_gene_count_tops_30

Reuters 29 June: http://www.reuters.com/article/scienceNews/idUSL276667620080629

Washington Post 30 June: http://www.washingtonpost.com/wp-dyn/content/article/2008/06/30/AR2008063000615.html

Science Daily 30 June: http://www.sciencedaily.com/releases/2008/06/080629130751.htm

New York Sun 30 June: http://www.nysun.com/health-fitness/the-brains-sense-of-adventure-is-identified/80903/

NHS News 1 July: http://www.nhs.uk/news/2008/06June/Pages/GenesforCrohnsidentified.aspx

Cordis News 1 July: http://cordis.europa.eu/fetch?CALLER=EN_NEWS&ACTION=D&SESSION=&RCN=29606

News-Medical.net 2 July: http://www.news-medical.net/?id=39712

Tehran Times 3 July: http://www.tehrantimes.com/index_View.asp?code=172220

Health News 13 July: http://www.healthnews.com/medical-updates/complexities-crohns-disease-brought-light-1393.html

May

Second genetic link to obesity identified

A study of almost 90,000 people has identified a second genetic variant that influences body fat, weight and risk of obesity. The first, a variant of a gene called FTO, was uncovered in 2007. The new variant is closely related to a gene called MC4R. Mutations in MC4R are the most common genetic cause of severe obesity within families.

The study also revealed that people who carry variants of both the FTO and MC4R genes have an increased risk of becoming obese and are on average 3.8kg heavier than those who don’t carry these genetic variations. The results are published this week in Nature Genetics. 

Dr Cecilia Lindgren, joint first author (together with Dr. Ruth Loos and Dr. Shengxu Li), of the Wellcome Trust Centre for Human Genetics at the University of Oxford explains: “Several research groups had shown that rare variants in the MC4R gene are responsible for severe, genetic forms of obesity but this collaboration has uncovered variants that affect more people. This discovery was made possible by the pooling of research data from international teams of scientists. It highlights the power of large collections of samples from volunteers in looking for common genetic variants that can influence health.”

The study involved scientists from University of Oxford, Cambridge Genetics of Energy Metabolism Consortium, the Wellcome Trust Sanger Institute, the MRC Epidemiology Unit and 77 other research institutions from the UK, USA, France, Germany, Italy, Finland and Sweden.

The protein that the MC4R gene provides instructions to make plays a pivotal role in many aspects of physiology, including regulation of appetite and energy expenditure to keep body weight in balance.

It is already known that the most severe form of MC4R-related obesity is caused by alterations in the MC4R gene that in turn create an inactive or less active MC4R protein. The variants uncovered in this research collaboration are much more common throughout the population than the mutated genes that cause severe conditions. They have a less dramatic effect on the normal function of the gene than the rare mutations that cause extreme obesity.

Rather than being located within the gene itself, these common variants lie some distance from the MC4R gene and so the team suspects that the variant changes gene activity. It might do this by disrupting the DNA regions required for the MC4R gene’s normal activity thereby preventing a standard version of the MC4R protein from being made.

The next step for the research collaboration is to figure out exactly how variations in DNA near the MC4R gene influence the activity of the MC4R protein and in doing so disrupt its ability to keep body weight in check.

Dr Lindgren concludes: ‘‘Although this research shows that genetic variants can influence a person’s risk of becoming obese, it is important to remember that lifestyle choices like eating healthily and taking regular exercise have an impact too.’’

April

Rat survey may help identify human disease genes

A survey of genetic variation in laboratory rats which may help identify human disease genes is published this week in Nature Genetics.

A consortium of European laboratories, including Professor Dominique Gauguier at the Wellcome Trust Centre for Human Genetics, University of Oxford, has published a survey of genetic variation in the laboratory rat.  This survey is based on 3 million single nucleotide polymorphisms (SNPs) and represents a solid foundation for disease gene discovery in rats and important perspectives in translational medicine.

The laboratory rat is a major experimental system for modelling human disease, and is used in physiology, pharmacology, toxicology, nutrition, immunology, genetics and genomics.  The complete rat genome was sequenced in 2004 and has been shown to have many genetic similarities to the human genome.  The discovery of over 3 million SNPs in the rat genome and the characterization of genetic polymorphism for 20,000 of them provide crucial resources for identifying genes underlying complex traits relevant to human disorders.

This research is published in a special issue of Nature Genetics which celebrates the Chinese Year of the Rat, along with a community view on rat genetics and other papers reporting findings linking rat genomic studies to human genetics.  This demonstrates the importance of rat genetic and genomic research in modern biomedical genetics.

This work was funded by the European Commission and the Wellcome Functional Genomic grant for Cardiovascular Functional Genomics.
 

March

Mice reveal clues to the basis of human speech

Human speech requires complex rapid movements of mouth and facial muscles, learned during our early years. Now, research in mice has linked a rare inherited human speech and language disorder to fundamental deficits in learning to make sequences of movements, suggesting that the brain circuits involved in this type of learning are crucial for human speech development.

The human disorder, caused by mutation of the FOXP2 gene, is characterised by disruptions of speech and written language. Difficulties with speaking are thought to be down to problems with learning and/or producing the facial muscle movements needed for speech.

But now Dr Simon E Fisher at the Wellcome Trust Centre for Human Genetics in Oxford and colleagues have found that a mutation in the equivalent gene in mice (Foxp2) causes more general problems with learning of rapid movement sequences when running on wheels or balancing on rotating rods.

Unlike many inherited speech disorders (which involve changes in numerous genes), a mutation at a single DNA base in FOXP2 is enough to cause this condition in humans. This means that scientists can 'knock out' or mutate this gene in animals to produce a model of the human disease, allowing them to investigate what’s happening in the brain.

The researchers produced mice carrying one normal copy of Foxp2 and one mutated version - matching a genetic change observed in affected humans. These mice developed normally in terms of the basics of making and controlling movements, but they had trouble building on these so-called motor skills, for example, taking longer to learn how to run faster and further on a tilted running track.

Further evidence of problems with learning came when the researchers looked at the brain circuits where Foxp2 is known to be active. The way the connections between nerve cells are strengthened or weakened - which is vital for learning - was abnormal in mice carrying the mutated gene.

These findings add weight to the idea that human speech development relies on evolutionarily ancient brain circuits involved in learning of motor skills.

The differences seen between the effects of Foxp2 mutations in mice and FOXP2 mutations in humans raise several interesting questions. Does FOXP2have a different role in humans than it does in mice, or could it be that the gene is involved in learning an animal’s most demanding motor skills, which may for humans - but not mice - be speech?

The team has also generated mice in which Foxp2 can be ‘switched off’ in particular parts of the brain, and is now using these to understand more how different brain regions are involved in the learning problems revealed in this study.

Groszer M et al. Impaired synaptic plasticity and motor learning in mice with a point mutation implicated in human speech deficits.  Curr Biol. 2008 Mar 11;18(5):354-62.

Celebrating Oxfordshire Science

Holograms, prosthetic limbs, honey bees and onion DNA have one thing in common – they’re all part of Oxfordshire Science Week 2008, which runs from 7 – 16 March.  This celebration of local talent brings together scientists and science fans from the University of Oxford, museums and science centres across Oxfordshire for ten days of events at eleven different venues.

This year, for the first time, Oxfordshire Science Week is a real collaboration of county-wide science expertise; notably the University of Oxford (including the Wellcome Trust Centre for Human Genetics and the University Museums), Science Oxford, the Medical Research Council and Rutherford Appleton Laboratory at Harwell, and museums in Wantage, Henley and Banbury.

Oxfordshire Science Week will be launched on Friday 7th March with a debate entitled “How would you spend £2 billion to transform British science?”  Science broadcaster Sue Nelson will join top-level scientists from the UK Atomic Energy Authority, the Rutherford Appleton Laboratory and the University of Oxford, to discuss what they would fund to transform science in Britain and to justify their choices.

Photocall: Media are invited to attend the launch of Science Week.  There will be a photocall at 6:30 pm with speakers and members of the Oxford Science Week team.
To confirm attendance, or for more information, contact: Sarah Richardson at Science Oxford by 12 pm Wednesday 5 March.
P: 01865 728953 E: Sarah.Richardson@oxtrust.org.uk

Saturday 8th March sees one of the week’s largest events, “Wow! How?”  Held at the Oxford University Museum of Natural History and the Pitt Rivers Museum, this family science fair attracts thousands of visitors each year, to stalls run by volunteers showing off their favourite experiments, including how to make slime or what happens to a marshmallow in a vacuum. 

Science Week concludes with a two-day event at Science Oxford on Friday 14th and Saturday 15th March.  “Science in the Kitchen” explores scientific phenomenon using household materials and equipment.  Find out how to investigate ink using jelly and batteries, make paint from eggs, or explore the chemistry of polymers using custard powder.  Lending their endorsement to the event on Friday 14th March will be Judith Hann, author of several science books and a presenter of Tomorrow’s World for 20 years, and John Exelby, co-founder of the BBC World Service TV News.  In 2007, Science in the Kitchen attracted several hundred visitors and was listed by The Times as their number one activity for families nationwide that weekend.

Photocall: Media are invited to attend Science in the Kitchen.  There will be a photocall on Friday 14th March at 10:30am, with Judith Hann and John Exelby.

For more information contact: Annabel Cook – see end for details.

This is just a small selection of the events taking place during the week.  A full brochure is available at venues across the County or can be downloaded from http://www.oxtrust.org.uk/festival/

February

Malaria vaccine trials begin using 'chimpanzee virus'

Trials are underway, funded by the Wellcome Trust, for a new vaccine to combat the most deadly form of malaria. For the first time ever, researchers will use a virus found in chimpanzees to boost the efficacy of the vaccine. The trials will take place at the University of Oxford's Jenner Institute, led by its Director, Professor Adrian Hill, following early testing of the vaccine at the Wellcome Trust Centre for Human Genetics.

Malaria, caused by Plasmodium parasites, is one of the world's deadliest killers, killing over a million people each year, mainly women and young children in Africa and SE Asia. The most deadly species , P. falciparum, is responsible for 80% of malaria infections and 90% of deaths. As yet, there is no vaccine against malaria. This is because, for much of their life-cycle, the parasites responsible for infection live inside cells, where they cannot be reached by antibodies.

"We urgently need a vaccine to help in the fight against this deadly killer," says Professor Hill, a Wellcome Trust Principal Research Fellow. "Malaria parasites are able to outwit our immune system by hiding out in the body's cells, however. Finding a way to generate enough immune cells and antibodies to identify and destroy the parasites will be the key to preventing infection."

The vaccine being developed and trialled by Professor Hill's team in collaboration with Okairòs uses the company’s genetically-modified chimpanzee adenovirus to produce the malaria antigen and to stimulate a response to the vaccine in the body. Adenoviruses appear to be particularly potent for increasing the immune response to the malaria vaccine. However, because human adenoviruses, which cause diseases including the common cold and gastroenteritis, are widespread, most people have developed some immunity towards them. Using a chimpanzee adenovirus ensures that a recipient is unlikely to have resistance to this component of the vaccine.

"Chimpanzees have their own set of adenoviruses which rarely infect humans, so we have not built up immunity to them," explains virologist Dr Sarah Gilbert at the Jenner Institute. "This is why we have chosen such a virus to form the backbone of the new vaccine." 

Professor Hill's team is currently recruiting for more volunteers for the first trials, which are to assess the safety of the vaccine. Because the active component of the adenovirus is removed, however, there is no danger of transmission to the human of the original chimpanzee virus.

The trial will also be measuring the response of the immune system. The team hopes to generate a response from CD8+ T-cells (sometimes known as killer cells) that should kill the parasites when they enter the liver, where they multiply undetected. However, if the T-cells do not kill all of the parasites, any that escape from the liver into the bloodstream will still be able to enter red blood cells and cause illness.

The group plans to test a second vaccine which would then target the parasites in the bloodstream and red blood cells.

“Our ultimate goal is a combination product which targets the parasite at both the liver stage and the blood stage,” says Professor Hill.  “Few people still think that you can get really strong protection from malaria based on a single component.”

Over a dozen vaccines have now been made by scientists at the University of Oxford and taken into clinical trials, but this is the first vaccine to have also been manufactured within a UK university, according to Professor Hill.

BBC news online 1 Feb: http://news.bbc.co.uk/1/hi/health/7219371.stm

Daily Mail 1 Feb: http://www.dailymail.co.uk/pages/live/articles/health/healthmain.html?in_article_id=511600&in_page_id=1774