̽��ֱ�� of Cambridge - Angela Roberts

Marmoset study identifies brain region linking actions to their outcomes

Anonymous — Thu, 24 Jun 2021 15:00:00 +0000

̽��ֱ��study, published today in the journal Neuron, found that marmoset monkeys could no longer make an association between their behaviour and a particular outcome when a region of their brain called the anterior cingulate cortex was temporarily switched off.

This finding is important because the compulsive behaviours in OCD and addiction are thought to result from impairments in the 'goal-directed system' in the brain. In these conditions worrying, obsessions or compulsive behaviour such as drug seeking may reflect an alternative, habit-based system at work in the brain in which behaviours are not correctly linked with their outcomes.

It also sheds more light on how healthy people behave in a goal-directed way, which is needed to respond to changing environments and goals.

“We have identified the very specific region of the brain involved in goal-directed behaviour. When we temporarily turned this off, behaviour became more habitual - like when we go onto autopilot,” said Lisa Duan in the ̽��ֱ�� of Cambridge’s Department of Psychology, first author of the report.

Marmosets were used because their brains share important similarities with human brains, and it is possible to manipulate specific regions of their brains to understand causal effects.

In the experiment, marmosets were first taught a goal-directed behaviour: by tapping a coloured cross when it appeared on a touchscreen, they were rewarded with their favourite juice to drink. But this connection between action and reward was randomly uncoupled so that they sometimes received the juice without having to respond to the image. They quickly detected this change and stopped responding to the image, because they saw they could get juice without doing anything.

Using drugs, the researchers temporarily switched off the anterior cingulate cortex including its connections with another brain region called the caudate nucleus. Repeating the experiment, they found when the connection between tapping the cross and receiving juice was randomly uncoupled, the marmosets did not change their behaviour but kept tapping the cross when it appeared.

Such habitual responding to the coloured cross was not observed when several other neighbouring regions of the brain’s prefrontal cortex - known to be important for other aspects of decision-making - were switched off. This shows the specificity of the anterior cingulate region for goal-directed behaviour.

A similar effect has been observed in computer-based tests on patients with Obsessive Compulsive Disorder (OCD) or addiction - when the relationship between an action and an outcome is uncoupled the patients continue to respond as though the connection is still there.

Previous evidence from patients suffering brain damage, and from brain imaging in healthy volunteers, shows that part of the brain called the prefrontal cortex is involved in goal-directed behaviour. However, the prefrontal cortex is a complex structure with many regions, and it has not previously been possible to identify the specific part responsible for goal-directed behaviour from human studies alone.

“We think this is the first study to have established the specific brain circuitry that controls goal-directed behaviour in primates, whose brains are very similar to human brains,” said Professor Angela Roberts in the ̽��ֱ�� of Cambridge’s Department of Physiology, Development and Neuroscience, joint senior author of the report.

“This is a first step towards identifying suitable molecular targets for future drug treatments, or other forms of therapy, for devastating mental health disorders such as OCD and addiction,” added Professor Trevor Robbins in the ̽��ֱ�� of Cambridge’s Department of Psychology, joint senior author of the report.

This research was conducted in the ̽��ֱ�� of Cambridge’s Behavioural and Clinical Neuroscience Institute, and was funded by Wellcome.

Reference

Duan, L.Y. et al. ‘Controlling one’s world: identification of sub-regions of primate PFC underlying goal-directed behaviour.’ Neuron, June 2021. DOI: 10.1016/j.neuron.2021.06.003

Researchers have discovered a specific brain region underlying ‘goal-directed behaviour’ – that is, when we consciously do something with a particular goal in mind, for example going to the shops to buy food.

This is a first step towards identifying suitable molecular targets for future drug treatments, or other forms of therapy, for devastating mental health disorders such as OCD and addiction.

Trevor Robbins

Marmoset

̽��ֱ��text in this work is licensed under a Creative Commons Attribution 4.0 International License. Images, including our videos, are Copyright © ̽��ֱ�� of Cambridge and licensors/contributors as identified. All rights reserved. We make our image and video content available in a number of ways – as here, on our main website under its Terms and conditions, and on a range of channels including social media that permit your use and sharing of our content under their respective Terms.

Yes

Marmoset study finds single brain region linking depression and anxiety, heart disease, and people’s sensitivity to treatment

Anonymous — Mon, 26 Oct 2020 10:00:00 +0000

A new study, published today in the journal Nature Communications, suggests that sgACC is a crucial region in depression and anxiety, and targeted treatment based on a patient’s symptoms could lead to better outcomes.

Depression is a debilitating disorder affecting hundreds of millions of people worldwide, but people experience it differently. Some mainly have symptoms of elevated negative emotion like guilt and anxiety; some have a loss of ability to experience pleasure (called anhedonia); and others a mix of the two.

Research at the ̽��ֱ�� of Cambridge has found that increased activity in sgACC – a key part of the emotional brain– could underlie increased negative emotion, reduced pleasure and a higher risk of heart disease in depressed and anxious people. More revealing still is the discovery that these symptoms differ in their sensitivity to treatment with an antidepressant, despite being caused by the same change in brain activity.

Using marmosets, a type of non-human primate, the team of researchers infused tiny concentrations of an excitatory drug into sgACC to over-activate it. Marmosets are used because their brains share important similarities with those of humans and it is possible to manipulate brain regions to understand causal effects.

̽��ֱ��researchers found that sgACC over-activity increases heart rate, elevates cortisol levels and exaggerates animals’ responsiveness to threat, mirroring the stress-related symptoms of depression and anxiety.

“We found that over-activity in sgACC promotes the body’s ‘fight-or-flight’ rather than ‘rest-and-digest’ response, by activating the cardiovascular system and elevating threat responses,” said Dr Laith Alexander, one of the study’s first authors from the ̽��ֱ�� of Cambridge’s Department of Physiology, Development and Neuroscience.

“This builds on our earlier work showing that over-activity also reduces anticipation and motivation for rewards, mirroring the loss of ability to experience pleasure seen in depression.”

To explore threat and anxiety processing, the researchers trained marmosets to associate a tone with the presence of a rubber snake, an imminent threat which marmosets find innately stressful. Once marmosets learnt this, the researchers ‘extinguished’ the association by presenting the tone without the snake. They wanted to measure how quickly the marmosets could dampen down and ‘regulate’ their fear response.

“By over-activating sgACC, marmosets stayed fearful for longer as measured by both their behaviour and blood pressure, showing that in stressful situations their emotion regulation was disrupted,” said Alexander.

Similarly, when the marmosets were confronted with a more uncertain threat in the form of an unfamiliar human, they appeared more anxious following over-activation of sgACC.

“ ̽��ֱ��marmosets were much more wary of an unfamiliar person following over-activation of this key brain region - keeping their distance and displaying vigilance behaviours,” said Dr Christian Wood, one of the lead authors of the study and senior postdoctoral scientist in Cambridge’s Department of Physiology, Development and Neuroscience.

̽��ֱ��researchers used brain imaging to explore other brain regions affected by sgACC over-activity during threat. Over-activation of sgACC increased activity within the amygdala and hypothalamus, two key parts of the brain’s stress network. By contrast, it reduced activity in parts of the lateral prefrontal cortex – a region important in regulating emotional responses and shown to be underactive in depression.

“ ̽��ֱ��brain regions we identified as being affected during threat processing differed from those we’ve previously shown are affected during reward processing,” said Professor Angela Roberts in the ̽��ֱ�� of Cambridge’s Department of Physiology, Development and Neuroscience, who led the study.

“This is key, because the distinct brain networks might explain the differential sensitivity of threat-related and reward-related symptoms to treatment.”

̽��ֱ��researchers have previously shown that ketamine – which has rapidly acting antidepressant properties – can ameliorate anhedonia-like symptoms. But they found that it could not improve the elevated anxiety-like responses the marmosets displayed towards the human intruder following sgACC over-activation.

“We have definitive evidence for the differential sensitivity of different symptom clusters to treatment – on the one hand, anhedonia-like behaviour was reversed by ketamine; on the other, anxiety-like behaviours were not,” Professor Roberts explained.

“Our research shows that the sgACC may sit at the head and the heart of the matter when it comes to symptoms and treatment of depression and anxiety.”

This research was funded by Wellcome.

Reference
Alexander, L. et al; ‘Over-activation of primate subgenual cingulate cortex enhances the cardiovascular, behavioural and neural responses to threat.’ Nature Communications, October 2020. DOI: 10.1038/s41467-020-19167-0

Over-activity in a single brain region called the subgenual anterior cingulate cortex (sgACC) underlies several key symptoms of mood and anxiety disorders, but an antidepressant only successfully treats some of the symptoms.

We found that over-activity in sgACC promotes the body’s ‘fight-or-flight’ rather than ‘rest-and-digest’ response, by activating the cardiovascular system and elevating threat responses.

Laith Alexander

Daniel Dino-Slofer from Pixabay

Network

Yes

Genetic variation linked to response to anxiety could inform personalised therapies

cjb250 — Mon, 01 Jul 2019 19:16:51 +0000

Some individuals are at greater risk of developing anxiety and depression than others and this depends in part upon the interaction between our genes and our environment, such as stressful or adverse events in our lives. Moreover, some of those who develop anxiety or depression may respond better to treatment while others struggle to benefit.

Although much research has been dedicated to finding effective treatments, we still have a poor understanding of how mental health disorders such as these develop and of the underlying brain mechanisms.

A study published today in PNAS has identified specific brain mechanisms that may underlie how genetic variation in the serotonin transporter gene, a key gene that regulates mood and stress responses, can influence the way we respond to perceived threat.

In a previous study working with marmoset monkeys, Dr Andrea Santangelo in the laboratory of Professor Angela Roberts at the ̽��ֱ�� of Cambridge showed that the particular variant of the gene carried by a monkey will influence whether it perceives an ambiguous stimulus as being high or low threat. This characteristic of an individual’s personality is called ‘trait anxiety’.

High trait anxiety is a risk factor in humans for developing anxiety and mood disorders, and genetic variation in the serotonin transporter gene has been linked with an increased likelihood of developing these disorders.

But in this earlier study, the researchers showed that variants of the gene also affected how a monkey responds to certain medicines. Specifically, individuals carrying the variant of the gene associated with high anxiety actually increased their anxiety towards a threat immediately after treatment with a commonly-used antidepressant known as a ‘selective serotonin re-uptake inhibitor’, or SSRI. This so called ‘anxiogenic’ effect is often seen in patients in the early stages of treatment and is thought to be part of the reason why these patients do not respond favourably to SSRIs.

In this new study, Dr Santangelo and Professor Roberts, along with colleagues including those at the Wolfson Brain Imaging Centre and Translational Neuroimaging Laboratory, have revealed how variation in the serotonin transporter gene has an impact on the number of a specific type of serotonin receptor, known as the type 2A receptor, in a specific brain area. Receptors are proteins in the brain that enable particular molecules – in this case serotonin – to affect the function of nerve cells. Monkeys carrying the variant of the gene associated with high anxiety had lower numbers of this receptor, hence changing the way in which serotonin-based drugs act upon them.

Medicines targeting these receptors have recently been used in the treatment of anxiety and mood disorders, so these findings suggest that it could be important in the future to know what variant of the serotonin transporter gene an individual is carrying when deciding on a treatment strategy.

̽��ֱ��specific brain area where the number of receptors was reduced was the insula cortex, an important site for integrating information about sensations coming from the body with cognitive information processed in other areas to generate feelings and self-awareness, and to help guide decision-making.

This new finding suggests that those cognitive behavioural therapies (CBT) that focus on controlling sensations from the body could help patients in whom SSRI drugs are not effective.

“As many as one in three people affected by anxiety and depression does not respond to anti-depressants, so we need to find better treatments to help improve their quality of life,” says Dr Santangelo from the Department of the Physiology, Development and Neuroscience at the ̽��ֱ�� of Cambridge.

“Our research suggests that differences in our DNA may help predict which of us will respond well to these medicines and which of us require a different approach. This could be assessed using genetic testing.”

̽��ֱ��research was carried out using marmoset monkeys because this type of genetic variation in the serotonin transporter gene is only present in humans, apes and monkeys, and not rodents. Moreover, the marmoset’s brain shares many similarities with the human brain, so using monkeys in research allows us to identify exactly which mechanisms are behind conditions such as anxiety and depression, helping inform the development of much needed new treatments.

̽��ֱ��research was funded by the Medical Research Council.

Reference
Insula serotonin 2A receptor binding and gene expression contribute to serotonin transporter polymorphism anxious phenotype in primates. PNAS; 1 July 2019; DOI: 10.1073/pnas.1902087116

A new study in marmoset monkeys suggests that individual variation in genes alters our ability to regulate emotions, providing new insights that could help in the development of personalised therapies to tackle anxiety and depression.

As many as one in three people affected by anxiety and depression does not respond to anti-depressants, so we need to find better treatments to help improve their quality of life

Andrea Santangelo

Kevin Lee

Date night

Yes

Licence type:

Public Domain

Marmoset study gives insights into loss of pleasure in depression

cjb250 — Tue, 04 Dec 2018 16:00:03 +0000

Now, in a study involving marmosets, scientists at the ̽��ֱ�� of Cambridge have identified the region of the brain that contributes to this phenomenon, and shown that the experimental antidepressant ketamine acts on this region, helping explain why this drug may prove effective at treating anhedonia.

Depression is a common and debilitating condition which is recognised as a leading cause of disability worldwide. A survey published in 2016 found that 3.3 out of every 100 UK adults had experienced depression in the week before being interviewed.

A key symptom of depression is anhedonia, typically defined as the loss of ability to experience pleasure. However, anhedonia also involves a lack of motivation and lack of excitement in anticipation of events. All these aspects have proven difficult to treat. One major issue slowing down progress in developing new treatments is that the brain mechanisms that give rise to anhedonia remain largely unknown.

“Imaging studies of depressed patients have given us a clue about some of the brain regions that may be involved in anhedonia, but we still don't know which of these regions is causally responsible,” says Professor Angela Roberts from the Department of Physiology, Development and Neuroscience at the ̽��ֱ�� of Cambridge.

“A second important issue is that anhedonia is multi-faceted – it goes beyond a loss of pleasure and can involve a lack of anticipation and motivation, and it’s possible that these different aspects may have distinct underlying causes.”

In fact, even when existing therapies do work, the reasons why they are effective are not always clear, making it difficult to target these therapies to individuals.

Using marmosets, a type of non-human primate, Professor Roberts and MBPhD student Laith Alexander, along with other colleagues, including those at the Wolfson Brain Imaging Centre and Translational Neuroimaging Laboratory, have shown how over-activity in a specific area of the brain’s frontal lobe blunts the excitement seen when anticipating a reward and the motivation to work for that reward. Their results are published today in the journal Neuron.

In the present study marmosets were trained to respond to two sounds: if they heard sound A, they would receive a treat of marshmallows; if they heard sound B, they would not receive a treat. Once they had learned the association, they would become aroused at sound A, reflected in an increase in blood pressure and excited movements of the head. They would not show the same response to B.

̽��ֱ��researchers then infused either a drug or a saline solution into a region of the brain known as ‘area 25’ through thin cannulae (metal tubes) in the marmosets’ head. Cannulae are inserted during a single surgical procedure, and once the anaesthetic has worn off they do not trouble the animals.

̽��ֱ��effect of the drug was to temporarily make this particular brain region over-active, and this resulted in the marmosets showing less excitement and anticipation at the prospect of a marshmallow treat. They were however as quick to eat the marshmallow treat as before. ̽��ֱ��saline infusion made no difference to the activity in area 25 or to the marmosets’ excitement and anticipation.

In a second task, the marmosets had to make more and more responses to get their reward – while initially they would receive a marshmallow treat after pressing a coloured shape on a touch sensitive computer screen just once, as the task proceeded, they would be required to press the coloured shape an increasing number of times. Eventually, the marmoset would reach a point where it gave up, considering the treat to be no longer worth the effort required.

When the marmosets’ area 25 was over-activated, the researchers observed that the marmosets gave up much faster. This lack of motivation is another key symptom associated with anhedonia.

By using PET scanning techniques to observe activity across the marmoset’s brain the researchers found that over-activity in area 25 had a knock-on effect to other brain regions, which also became more active, indicating that these were all part of brain circuity controlling anticipatory excitement.

Finally, the researchers investigated the effect of the experimental antidepressant, ketamine. Marmosets were given the antidepressant 24 hours ahead of the experiment. This time, even when marmosets were administered the treatment to make area 25 over-active, they still showed excitement and anticipation at the marshmallow reward. PET scanning revealed that the brain circuits were functioning normally. In other words, ketamine had blocked the effects of over-activating area 25, which would otherwise blunt anticipation.

“Understanding the brain circuits that underlie specific aspects of anhedonia is of major importance, not only because anhedonia is a core feature of depression but also because it is one of the most treatment-resistant symptoms,” says Laith Alexander, the study’s first author.

“By revealing the specific symptoms and brain circuits that are sensitive to antidepressants like ketamine, this study moves us one step closer to understanding how and why patients may benefit from different treatments.”

Marmosets are used to study brain disorders such as depression because of the similarity of the frontal lobes to those of humans. Rats, which are often used in psychology studies, have frontal lobes quite different to those of humans, making it less easy to translate studies of frontal lobe circuitry directly into the clinic.

“Depression affects many millions of people worldwide, so it’s important we get to the problems within the brain that underlie the various symptoms,” says Professor Roberts. “Studying these symptoms in non-human primates, such as marmosets can help bridge the gap between findings from rodent studies and the clinic.

“Using marmosets, we are able to manipulate the activity in specific brain regions, helping us see which regions are causally involved. These effects are temporary, and wear off after a short time.”

̽��ֱ��research was funded by Wellcome.

Reference
Alexander, L, et al. Fractionating blunted reward processing characteristic of anhedonia by over-activating primate subgenual anterior cingulate cortex. Neuron; 4 Dec 2018; DOI: 10.1016/j.neuron.2018.11.021

‘Anhedonia’ (the loss of pleasure) is one of the key symptoms of depression. An important component of this symptom is an inability to feel excitement in anticipation of events; however the brain mechanisms underlying this phenomenon are poorly understood.

Understanding the brain circuits that underlie specific aspects of anhedonia is of major importance, not only because anhedonia is a core feature of depression but also because it is one of the most treatment-resistant symptoms

Laith Alexander

Free photos

Window view

Yes

Licence type:

Public Domain

Stimulate your brain with the Cambridge BRAINFest 2017

cjb250 — Mon, 05 Jun 2017 09:14:32 +0000

̽��ֱ��three day event, running from 23-25 June, will allow audiences to quiz more than 130 leading Cambridge neuroscientists on everything from dementia and dyslexia through to memory and mental health.

“We’re all fascinated by the brain – its complexity is what makes us so unique as a species,” says Dr Dervila Glynn, coordinator of Cambridge Neuroscience, who is organising the event. “Cambridge is one of the major centres in the UK, if not the world, for studying how the brain works, and why in many cases it goes wrong, leading to disease. Cambridge BRAINFest is our chance to showcase the brilliant work that is taking place across the city.”

Throughout the weekend, the Cambridge Corn Exchange will be transformed into an interactive tour of the brain, with themes including ‘Development’, ‘Brain & Body’, ‘Pain & Pleasure’, Perception & Imagination’ and ‘Learning & Forgetting’ spanning research from molecules to man. Visitors, adults and children alike, will get the opportunity to take part in experiments across 30 different interactive exhibits and even build their own brain. A ‘Secret Cinema’ will show a series of films that illustrate how Cambridge researchers are tackling conditions such as dementia and OCD. Meanwhile, Café Scientifique will explore the breadth of brain science from body clocks and brain networks to the weird and wonderful world of the naked mole-rat.

On 23 June, the opening night, audiences at the Babbage Lecture Theatre will hear from BBC Horizon presenter Dr Giles Yeo about why we are all getting fatter, from Professor Usha Goswami about how dyslexic brains may be in tune but out of time, and from Professor Roger Barker on how we can repair the degenerating brain. Poet Lavinia Greenlaw will perform a moving poem about dementia, while Cambridgeshire-based Dance Ensemblé will explore the story of Parkinson’s disease through the medium of dance.

̽��ֱ��following night, Professor Sir Simon Wessely, President of the Royal College of Psychiatrists, will chair a panel discussion with mental health experts from the ̽��ֱ�� of Cambridge and from Cambridgeshire & Peterborough NHS Foundation Trust, looking at the ongoing research that will help us better understand and treat mental health disorders and how we can bridge the existing gap between neuroscience research and current practice in the health service. ̽��ֱ��panel will look at issues including how the brain and body interact, the stigma surrounding mental health problems and the transition between child and adult psychiatry.

For those wishing to take advantage of the sights around Cambridge, a historical self-guided ‘Neurotrail’ will lead explorers around the places, people, and discoveries that have put our city at the heart of our understanding of the brain. Maps will be available at the Corn Exchange on the weekend.

̽��ֱ��foyer of the Corn Exchange will be transformed by BRAINArt, an exhibition of brain-inspired art by local school children. In the lead up to Cambridge BRAINFest, Dr Glynn visited 1,400 pupils, talked about the brain and enthused her audiences about the body’s most complex organ.

“As a researcher, it can be thrilling to discuss our work with the public,” says Professor Angela Roberts, chair of the organising committee. “It’s an opportunity for us to share some of the excitement that comes from working at the cutting-edge of research. But equally, it’s a chance for us to hear the public’s views about our work. We expect some fascinating – and potentially challenging – discussions will arise.”

Cambridge BRAINFest 2017 builds on the success of major public engagement events organised by the ̽��ֱ�� of Cambridge, including the Cambridge Science Festival in spring and the Festival of Ideas in autumn.

All events are free, but booking is recommended for the evening events at the Babbage Lecture Theatre. Further details, including how to book, can be found on the Cambridge BRAINFest 2017 website.

Join the #CambridgeBRAINfest conversation on Twitter @CamNeuro and on Facebook.

Why are we getting so fat? Why do teenagers really need to lie-in? And can we fix a broken brain? These are just some of the questions that will be answered at Cambridge BRAINFest 2017, a free public festival celebrating the most complex organ in the body.

Cambridge is one of the major centres in the UK, if not the world, for studying how the brain works, and why in many cases it goes wrong, leading to disease. Cambridge BRAINFest is our chance to showcase the brilliant work that is taking place across the city

Dervila Glynn

affen ajlfe

brain 22

̽��ֱ��text in this work is licensed under a Creative Commons Attribution 4.0 International License. For image use please see separate credits above.

Yes

̽��ֱ��OCD Brain: how animal research helps us understand a devastating condition

cjb250 — Tue, 28 Mar 2017 10:36:15 +0000

When David Adam was just 18, a teasing comment from a university friend triggered a series of thoughts that he had contracted HIV and would die of AIDS. This was around the time of peak hysteria about this new disease, but even so, his thoughts represented more than the worries of a naïve, newly-sexually active young man: the fear was unshakeable and the thoughts consumed him, dominating his life.

For a long time, David remained silent about his obsession, afraid to tell anyone what he was going through. It was only a couple of decades later, when the thoughts began to affect his relationship with his young daughter, to whom he was sure he would transmit his ‘infection’, that he sought help. He was subsequently diagnosed with obsessive compulsive disorder (OCD).

OCD is sometimes viewed as a personality quirk – “I’m a little bit OCD,” people will say as they carefully arrange the books on their shelf. ̽��ֱ��truth is far more devastating. People living with OCD will scrub their hands compulsively, often with bleach, till they are bleeding. Others will check that they have locked the back door thirty, forty times – otherwise, they are sure a family member will come to harm - making going out almost impossible.

David, a journalist and science writer, has written and spoken extensively about his condition. He considers himself fortunate: his condition is under control, thanks to a combination of ‘talking therapies’ and medication. Others are not so fortunate: despite intensive therapy and medication, they are still unable to hold down a job or a relationship, so dominant are their OCD behaviours.

Now, in a series of short films for the ̽��ֱ�� of Cambridge, David has visited leading researchers who study OCD and asks what we know about the underlying biology that leads to the condition: just what is going on in the brain?

In the films, Professor Trevor Robbins, Head of Psychology at Cambridge, introduces David to scientists who use a combination of studies to explore the inner workings of the brain. These include studies involving rats and marmosets (small monkeys), as well as people.

One of the studies is a so-called ‘reversal learning’ test. In this test, the marmoset learns that pressing one button gives it a juice reward, while it gets no reward if it presses a second button. But then, unexpectedly, the buttons swap: how good is the marmoset at changing its thinking to adjust to this new information? A common trait in people with OCD is a tendency to have rigid, obsessive thinking that dominates their behaviour.

By manipulating localised regions of the animals’ brains, either permanently or via temporary drug infusions, scientists are able to understand better the exact pathways within the brain that malfunction in OCD and cause this rigid behaviour. As Professor Robbins explains, this would not be possible in human studies. But this knowledge will help underpin the development of new, more effective treatments – and this is crucial, as around 60% of patients with OCD do not respond to existing treatments.

̽��ֱ��films have been produced as part of the ̽��ֱ�� of Cambridge’s commitment to openness on animal research. In 2014, the ̽��ֱ�� announced that it had signed the Concordat on Openness on Animal Research. ̽��ֱ��following year, it launched its first film on the subject, Fighting Cancer: Animal research at Cambridge.

We welcome comments about this article. However, as with discussions on all of our news and feature pages, comments will be moderated so please do not post contributions that are offensive or contain profanities, and please stay on topic. We do not moderate comments in real-time so there may be a delay before they appear.

OCD can be a devastating condition: therapy and medication often doesn’t work, leaving many people unable to hold down a job or a relationship – or even to leave their house. In our series of films, science writer David Adam looks at how research at Cambridge using animals helps us understand what is happening in the brain – and may lead to better treatments.

Understanding the OCD Brain: OCD and me

̽��ֱ��text in this work is licensed under a Creative Commons Attribution 4.0 International License. For image use please see separate credits above.

Yes