Ten organisations account for half of all animal research in Great Britain in 2018

Posted: by Hannah Hobson on 18/07/19

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Ten organisations account for half of all animal research in Great Britain in 2018
  • Ten organisations account for nearly half of all animal research in Great Britain

  • Top universities are among the largest users of animals in research in Great Britain

  • All ten organisations have signed up to Concordat on Openness on Animal Research in the UK

Understanding Animal Research, an organisation promoting greater openness about animal research, has today released a list of the ten organisations in Great Britain that carry out the highest number of animal procedures – those used in medical, veterinary and scientific research. These statistics are freely available on the organisations’ websites as part of their ongoing commitment to transparency and openness around the use of animals in research.

The figures show that these ten organisations collectively carried out nearly half of all animal research in Great Britain in 2018*.

These ten organisations carried out 1.69 million procedures, 48% of the 3.52 million procedures carried out in Great Britain in 2018. More than 99% of these 1.69 million procedures were carried out on rodents or fish.

The ten organisations are listed below alongside the total number of procedures that they carried out in 2018. Each organisation’s name links to its animal research webpage which includes more detailed statistics. This is the fourth year in a row that organisations have come together to publicise their collective numbers and examples of their research.


Number of Procedures

Medical Research Council


The Francis Crick Institute


University of Oxford


University of Edinburgh




University of Cambridge


University of Glasgow


King's College London


University of Manchester


Imperial College London




All organisations are committed to the ‘3Rs’ of replacement, reduction and refinement. This means avoiding or replacing the use of animals where possible; minimising the number of animals used per experiment and optimising the experience of the animals to improve animal welfare. However, as institutions expand and conduct more research, the total number of animals used can rise even if fewer animals are used per study.

All ten organisations are signatories to the Concordat on Openness on Animal Research in the UK, a commitment to be more open about the use of animals in scientific, medical and veterinary research in the UK. More than 120 organisations have signed the concordat including UK universities, medical research charities, research funders, learned societies and commercial research organisations.

Wendy Jarrett, Chief Executive of Understanding Animal Research, which developed the Concordat on Openness, said:

“Since the publication of the Concordat on Openness on Animal Research in the UK in 2014, organisations that carry out research using animals have been increasingly transparent. These organisations are providing an unprecedented level of information about how and why they conduct medical, veterinary and scientific research using animals. Facts, figures, case studies, and photos about the use of animals in research are now provided directly by the organisations that carry out the research, so that it has never been easier for members of the public to find out why those animals were used in research.“

Frances Rawle, Director of Policy, Ethics and Governance at the Medical Research Council, said:

“The use of animals in medical research remains essential for us to develop new and better treatments and to understand the biology of disease. If researchers are applying for funding for studies involving animals, they must give clear scientific reasons for using them and explain why there are no realistic alternatives. The MRC is committed to ensuring that these programmes are carried out to the highest possible levels of animal welfare and to replacing, refining and reducing the use of animals in research.”

Professor Julian Downward, Associate Research Director at The Francis Crick Institute, said:

“As the country’s largest biomedical research institute, we have a particular responsibility to be open about our use of animals in research. The Crick is home to around 100 labs, and half of us use animals in our research. While we use alternatives wherever possible, living animals are incredibly complex and there are many processes we simply can’t simulate. For example, my colleagues recently discovered that when antibiotics kill gut bacteria in mice, their lungs become more vulnerable to flu. We still don’t understand how organs communicate with each other, so this discovery would never have been possible without the study of real living animals. In my lab, we are trying to understand how different genes lead to cancers and how best to treat them. We hope to target the way that tumour cells hide from the immune system, to help the body’s own defences kill off the cancer. This requires understanding of how dozens of different cell types interact with the tumour and simply cannot be addressed solely by studying cultured cells or computational simulations.”

inforgraphics university 2019.png



Total Procedures (2018)






Non-Human Primates


Medical Research Council









The Francis Crick Institute









University of Oxford









University of Edinburgh


















University of Cambridge









University of Glasgow









King's College London









University of Manchester









Imperial College London



















Medical Research Council
Mouse study of human neural activity offers neurological condition insight

The inability to study human neurons in humans has been an important problem that Dr Vincenzo De Paola and his team at the MRC London Institute of Medical Sciences, as well as other researchers around the world, have been thinking about for a long time.

Synapses are so small they cannot be studied within the human brain with current imaging methods, but with the breakthrough of induced pluripotent stem cells (iPSCs) a few years ago, the study of human neurons was able to advance. Traditionally, researchers would use model organisms such as mice, flies, fish and worms, to investigate neuron and synapse development. This, however, raises the question of how well this relates to understanding neurons in humans – observations and predictions made within these traditional types of study may lose some of their impact.

In this pioneering study, published in Science, human neurons were created by reverse-engineering skin cells from two individuals with Down syndrome. The cells were implanted in the brains of mice, creating a model where the development of the neurons and synapses can be observed in real time.

There were three key findings of the study: the first was that when the human neurons were transplanted connections developed with similar timing and extent to the human foetal cortex. The second, that transplanted human neurons function as expected, with spontaneously synchronised activity similar to the human foetal cortex. The third, that spontaneous neural activity is markedly reduced in individuals with Down syndrome.

The third finding, which shows clear differences in the activity of the neurons and synapses in healthy individuals and those with Down syndrome, is a very important one. The different synchronised activity may have to do with cognitive function. The team will be exploring this next, as they believe there are candidate molecules involved in the markedly reduced activity and are eager to investigate them.


The Francis Crick Institute
Antibiotics weaken flu defences in the lung

Antibiotics can leave the lung vulnerable to flu viruses, leading to significantly worse infections and symptoms, finds a new study in mice led by the Francis Crick Institute.

The research, published in Cell Reports, discovered that signals from gut bacteria help to maintain a first line of defence in the lining of the lung. When mice with healthy gut bacteria were infected with the flu, around 80% of them survived. However, only a third survived if they were given antibiotics before being infected.

The study found that type I interferon signalling, which is known to regulate immune responses, was key to early defence. Among the genes switched on by interferon is a mouse gene, Mx1, which is the equivalent of the human MxA gene. This antiviral gene produces proteins that can interfere with influenza virus replication. Although often studied in immune cells, the researchers found that microbiota-driven interferon signals also keep antiviralgenes in the lung lining active, preventing the virus from gaining a foothold.

To test whether the protective effect was related to gut bacteria rather than local processes in the lung, the researchers treated mice with antibiotics and then repopulated their gut bacteria through faecal transplant. This restored interferon signalling and associated flu resistance, suggesting that gut bacteria play a crucial role in maintaining defences.


University of Oxford
Fish genes hold key to repairing damaged hearts

The Mexican tetra fish (Astyanax Mexicanus) can repair its heart after damage — something researchers have been striving to achieve in humans for years. Research led by Oxford University suggests that a gene called lrrc10 may hold the key to this fish’s remarkable ability.

Tetra fish in one particular cave, called Pachón, have lost this ability, leading the researchers to compare the genetic code of the river fish to that of the cave fish to discover what mechanisms are required for heart repair. They found three areas of the fish genome were implicated in the fish’s ability to repair their hearts.

The researchers also compared the activity of genes in the river versus the cave fish in the period after heart injury. Two genes, lrrc10 and caveolin, were much more active in the river fish and could be key in allowing the river fish to repair their hearts.

Lrrc10 is already linked to a heart condition called dilated cardiomyopathy (DCM) in people. Studies in mice have previously shown that this gene is involved in the way that heart cells contract with every heartbeat.

The researchers went on to study the effect of this gene in the zebrafish, another fish which has the remarkable ability to heal its own heart. When the team inactivated the lrrc10 gene in zebrafish they saw that the fish could no-longer fully repair their hearts.

Hundreds of thousands of people in the UK are living with debilitating heart failure, often as a result of a heart attack. During a heart attack, the heart is deprived of oxygen leading to the death of heart muscle cells and their replacement by scar tissue. This stops the heart muscle from contracting properly and reduces the heart’s ability to pump blood around the body. People suffering from heart failure can’t regenerate their damaged hearts, and often the only cure is a heart transplant.


University of Edinburgh
Early statin treatment may help children with Fragile X Syndrome

Research with rats suggests children with an inherited form of intellectual disability and autism could be helped by a medicine commonly used to lower cholesterol, if used early in life. The drug – a type of statin called lovastatin – corrected learning and memory problems in rats with a form of Fragile X Syndrome.

Fragile X Syndrome is one of the most common genetic causes of intellectual disability. It is often associated with autism and attention deficit and hyperactivity disorder, or ADHD. Many affected individuals also have seizures.

Researchers at the University of Edinburgh studied rats with a genetic alteration similar to that found in people with Fragile X Syndrome. These rats have problems completing certain memory tasks when compared with typical rats.

Treatment with lovastatin between five and nine weeks of age – the precise window when they are developing these memory abilities – restored normal development in the rats. The animals were able to complete the memory tasks more than three months after treatment ended, indicating the effects of the drug were long-lasting.

The researchers say they will next focus on whether there is a critical time-window during development when treatment is more effective.


UCL (University College London)
Fetal gene therapy prevents fatal disease in mouse studies

A fatal neurodegenerative condition known as Gaucher disease can be prevented in mice following fetal gene therapy, finds a research team led by Professor Simon Waddington of the UCL Institute for Women’s Health.

Scientists used a viral vector to deliver genetic material into the brains of fetal mice carrying neuropathic Gaucher disease, caused by mutations in the GBA gene. Mice who received the gene therapy exhibited less brain degeneration and survived considerably longer than untreated mice – they were healthy for up to 18 weeks compared to 15 days for the untreated mice.

The researchers are now working with an international team of scientists to develop a gene therapy that could work in people.

Professor Waddington’s lab also develops ways to reduce the number of animals needed for medical research. One method involves injecting newborn mice with firefly genes that glow in the presence of certain molecules, so that researchers can get molecular-level data of disease progression by taking a photo with specialist equipment, without needing to cull and perform an autopsy. An experiment that previously needed 60 mice can be done with 15 mice thanks to the new technique, with more reliable results.



University of Cambridge
Blood pressure drug shows promise for treating Parkinson’s and dementia in animal studies

A prescription drug to treat high blood pressure has shown promise against conditions such as Parkinson’s, Huntington’s and forms of dementia in studies carried out in mice and zebrafish at the University of Cambridge.

A common feature of neurodegenerative diseases is the build-up of misfolded proteins. In healthy individuals, the body uses a mechanism known as autophagy, or ‘self-eating’, to prevent the build-up of such toxic materials. There are currently no drugs that can induce autophagy effectively in patients.

In addition to searching for new drugs, scientists often look to re-purpose existing drugs. These have the advantage that they have already been shown to be safe for use in humans. If they can be shown to be effective against the target diseases, then the journey to clinical use is much faster.

Scientists at Cambridge have shown in mice that felodipine, a hypertension drug, may be a candidate for re-purposing. The team used mice that had been genetically modified to express mutations that cause Huntington’s disease or a form of Parkinson’s disease, and zebrafish that model a form of dementia.

Felodipine was effective at reducing the build-up of aggregates in the mice with the Huntington’s and Parkinson’s disease mutations and in the zebrafish dementia model. The treated animals also showed fewer signs of the diseases.

Studies in mice often use doses that are much higher than those known to be safe to use in humans. Professor Rubinsztein and colleagues showed in the Parkinson’s mice that it is possible to show beneficial effects even at concentrations similar to those tolerated by humans. They did so by controlling the concentrations using a small pump under the mouse’s skin.


University of Glasgow
Sugar supplement slows tumour growth and can improve cancer treatment

The University of Glasgow, along with our close collaborators at the Beatson Institute for Cancer Research, have a world-leading reputation for translational cancer research. Recent studies on the importance of metabolism in cancer – and how modulating metabolic pathways can directly impinge on cancer development – have been proven using in vitro and in vivo models.

For example, a recent Nature-published study showed that supplementation of the sugar mannose slowed tumour growth in different mouse models of cancer, as well as enhancing the effects of chemotherapy. The results make an important step towards understanding how mannose could, in future, be used to help treat cancer in patients, and human clinical trials with mannose are now being pursued.


King's College London
Genetic therapy heals damage caused by heart attack

Myocardial infarction, more commonly known as a heart attack, caused by the sudden blocking of one of the cardiac coronary arteries, is the main cause of heart failure, a condition that now affects over 23 million population in the world, according to the World Health Organisation.

At present, when a patient survives a heart attack, they are left with permanent structural damage to their heart through the formation of a scar, which can lead to heart failure in the future. In contrast to fish and salamander, which can regenerate the heart throughout life. 

In this study the team of investigators delivered a small piece of genetic material, called microRNA-199, to the heart of pigs, after a myocardial infarction which resulted in the almost complete recovery of cardiac function at one month later.

This is the first demonstration that cardiac regeneration can be achieved by administering an effective genetic drug that stimulates cardiac regeneration in a large animal, with heart anatomy and physiology like that of humans.


University of Manchester
Sex drug effective as heart failure treatment

A drug used to treat erectile dysfunction has been found by University of Manchester scientists to slow or even reverse the progression of heart failure in sheep.

The British Heart Foundation funded study is a breakthrough in the treatment for the disease in which five year survival rates are lower than most common cancers.

The study of Tadalafil – which is in the same class as Viagra – proves that the drug is biologically effective as a treatment for heart failure in sheep.

However, lead author Professor Andrew Trafford argues the effect is likely to also be shown in humans. The study is published in the journal Scientific Reports.

Heart failure is a devastating condition, occurring when the heart is too weak to pump enough blood to meet the body's needs.

It also causes a build-up of fluid that backs up into the lungs, resulting in breathlessness as well as fluid retention, resulting in swelling of different parts of the body.

Most current treatments are ineffective.

Sheep were used by the team as the physiology of their hearts is similar to human hearts.

When the animals had heart failure – induced by pace makers – which was sufficiently advanced to need treatment, the team administered the drug. Within a short period the progressive worsening of the heart failure was stopped and, importantly, the drug reversed the effects of heart failure.

The biological cause of breathlessness in heart failure – the inability of the heart to respond to adrenaline – was almost completely reversed.

The dose the sheep received was similar to the dose humans are given when being treated for erectile dysfunction.

Tadalafil blocks an enzyme called Phosphodiesterase 5 or PDE5S for short, which regulates how our tissue responds to hormones like adrenaline.

The research team found that in heart failure, the drug altered the signalling cascade – a series of chemical reactions in the body – to restore the heart’s ability to respond to adrenaline.

And that increases the ability of the heart to force blood around the body when working harder.


Imperial College London
Head injury effects halted in mice

Traumatic brain injury (TBI) is the leading cause of death and disability in people under 45 in developed countries. TBI patients who survive the injury have a reduced life expectancy and an increased risk of developing Alzheimer’s disease or other dementias later in life. 

Using a mouse model of TBI, researchers have found that the anaesthetic drug xenon, given shortly after a TBI, prevents early death and long-term cognitive impairment and protects brain tissue itself. The xenon-treated mice had a similar life expectancy, cognitive function, and brain tissue integrity, to mice that had never sustained a TBI.

This new study looked at the effects of xenon over the whole lifespan of mice for the first time.


Last edited: 13 May 2024 09:51

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