Plasticity in the spinal cord

Siobhan Fitzpatrick’s PhD work aims to give back movement.

Conditions that decrease a person’s ability to control their muscles, such as spinal cord injury and stroke, have devastating and debilitating consequences for individuals and their loved ones.

Siobhan_6030_lrImagine not being able to pick up your mug of coffee, or do up the button on your coat. Small daily tasks, that many take for granted, can prove impossible for those with damage to the neural pathways responsible for muscle control.

My PhD, being conducted within the Taylor Group here at NeuRA, is focused on the use of a variety of brain, spinal cord and nerve stimulation techniques to induce changes (plasticity) at the connections (synapses) between nerve cells in the spinal cord, with the ultimate goal of enhancing the control of muscles.

How to stimulate movement 

Two techniques our group uses are known as transcranial magnetic stimulation (TMS), and electrical peripheral nerve stimulation (PNS); both are non-invasive methods that can be used to stimulate parts of the nervous system.

We can use TMS to stimulate parts of the brain that control specific muscles of the arm, and PNS to excite peripheral nerves that supply the arm. Repetitive pairing of these two stimuli at specific timing intervals can induce synaptic plasticity in the spinal cord in pathways that control voluntary muscle activity.

This technique can enhance muscle activity of the biceps in able-bodied participants  and can improve manual dexterity of the hand in participants with incomplete spinal cord injury.

The technique has the potential for enhancing activity at any remaining synapses in the spinal cord that can transmit commands from the brain to the muscles; therefore this protocol would be more relevant for those with incomplete spinal cord injuries, when some spinal nerve fibers are preserved. However, even with clinically diagnosed complete injuries where there is an absence of all sensory and muscle activity below the site of injury, there could be some nerve cells within the spinal cord that have the potential to respond to the technique.

Although there are a large number of studies that investigate plasticity in the brain, there is limited knowledge of the effects of magnetic and electrical stimulation on plasticity of spinal cord pathways. I am interested in optimising the methods we use. For example, I am asking, is more necessarily better? Indeed, in the most recent study for my PhD, we found that by doubling the number of stimulus pairs we could induce more reliable, longer lasting spinal cord plasticity.

What could this mean in the future? 

What we are aiming for with these methods is small, but functionally relevant improvements in muscle control which, as an example, could be the difference between being able to pick up a cup or not.

Work in this area is still in its early days; however my vision for the future is that an optimised technique could be used clinically in conjunction with other forms of rehabilitation, such as physiotherapy, to improve motor control in those with conditions such as incomplete spinal cord injury and stroke.

A blood test for dementia

Lauren Bartley is part of a team developing a blood test to detect dementia.

A blood test can reveal many things about your physical health, such as your blood glucose levels or an iron deficiency. But what if a simple blood test could reveal what’s happening inside your brain?

Blood 1 As the Biomarker Study Coordinator, I see each participant involved in frontotemporal dementia and Alzheimer’s disease research at NeuRA and take a sample of their blood for analysis.

At the moment, if your doctor suspects you have dementia, you are likely to undergo neuroimaging to look for changes to your brain structure and shape, as well as cognitive and behavioural assessments looking for changes in the way you think, act and process information. When people only have mild changes, it can be difficult to accurately predict the underlying disease process, which can be frustrating for the affected person and their families.

Developing a blood test

At NeuRA, we are currently investigating the concept of a blood test for dementia, with the hope that one day clinicians will be able to easily and quickly discriminate between frontotemporal dementia and Alzheimer’s disease, the two most common forms of younger onset dementia.

Our hope is that this test could further reveal if any medications or therapies might be effective in reducing symptoms and halting the progression of illness. This is important because a medicine that benefits someone with Alzheimer’s disease is unlikely to be effective for someone suffering from frontotemporal dementia.

Our blood test will screen for particular proteins in the blood associated with dementia: Beta Amyloid, Tau, TDP-43 and FUS. We know these proteins are responsible for causing the brain changes in both Alzheimer’s disease and frontotemporal dementia by having performed previous pathological studies on the brain tissue that has been generously donated by former research participants both in Australia and around the world.

These proteins are in everyone’s brains as they age and they carry out important functions in supporting the brain cells. But in some people, these proteins start aggregating in a harmful way that can kill the brain cells and cause the symptoms of dementia.

Our prediction is that a person who has pathological levels of protein massing in their brain will also have increased concentrations in their blood. It’s important for our study to screen the blood of a significant number of older healthy males and females to act as a comparison and help us understand what the respective protein concentrations are in people with no presentation of dementia symptoms.

The people attending the Frontier research clinic at NeuRA to volunteer for frontotemporal dementia research are generally aged between 50 and 75 when their symptoms begin, so we have a wide range of ages to match for. Often the supporting partners of our participants act as controls in the study, and are happy to be offered the opportunity to contribute to our research.

An update on our progress

Our study is a little more than half way through and so far I have collected blood samples from over 500 dementia-affected participants and controls. It’s important to obtain bloods from people with a variety of symptoms so that we can best correlate these symptoms to a protein profile.

I am also collecting further samples from participants at different in their illness to see if there are changes to this profile as the condition progresses.

The only way to quantify our study and determine the accuracy of our results will be to confirm the pathological protein at the end of the participant’s life through our brain donor program (see my previous blog post). In this way, we can ensure our results are meaningful.

The blood samples that I have collected are now in the very early stages of being analysed by the biomarker team, and over the next 18 months we will learn more about the feasibility of the blood test for dementia in everyday community healthcare. We want to be very certain of the accuracy of the test before its release.

Concerned about your memory?

In the meantime, anyone who has concerns about their memory, or who has had changes in their speech or ability to understand language should discuss them with their GP. Sometimes it’s easier for a loved one to recognise these symptoms, along with other clues like changes in personality or behaviour that might be more than just a ‘mid-life crisis’ or the general process of ageing.

How your support has made a difference to NeuRA in 2013

Your donations to NeuRA this year have helped bring certainty to our research initiatives.

Funding for medical research is a roller coaster… sometimes you’re up and sometimes you’re down. Never knowing for certain where funding for the next trial or research initiative will come from is a very real concern for researchers and, frankly, patients and carers.

You often hear people say that ‘the Government should be doing more’, but the reality is the public purse as it stands cannot support every research opportunity. NeuRA applies for research grants predominately from the Australian Research Council (ARC) and the National Health and Medical Research Council (NHMRC); some applications are successful, others are not. Even when successful, the grants typically only cover a proportion of the true costs of running a research project. In addition, funding for the next generation of the brightest scientists working toward their PhD at NeuRA is a stipend of around $25,000, not enough for them to pay the rent, eat and concentrate on work.

Enter our loyal donors.

How your donations make a difference

In my role at the NeuRA Foundation, I am entrusted to share with our donors (via mail and email) the stories of patients and their carers who live with degenerative and chronic diseases. I see firsthand the generosity of people from all stages of life. I am as touched by the donor who gives thousands of dollars as I am by the one who gives five. Every dollar is important. Every donation helps. Every donor contributes to future discoveries.

Throughout this past year, funds raised through sharing these stories have served two primary purposes:

  1. Supplementing PhD students’ salaries. The top-up to their stipend means students don’t need to find a second (part-time) job just to survive. As future innovators and leaders in brain and nervous system research, it’s critically important that they focus on their work – not on how they’re going to pay the bills.
  2. Providing funds for the Sydney Brain Bank. The Sydney Brain Bank is a vital resource that prepares, stores and distributes brain tissue to research groups at NeuRA and other research organisations in Australia and around the world.

This way of distributing your donations means they have the potential to make an impact across the whole of NeuRA.

How you can get involved

Admittedly, when I started at NeuRA, I was surprised at the numerous ways people could support our research. In addition to one-off or regular donations, you can:

Michael Cartwright, who raised over $16,000 for NeuRA's research into Alzheimer’s disease

Michael Cartwright, who raised over $16,000 for NeuRA’s research into Alzheimer’s disease

  • challenge yourself like Michael Cartwright (pictured) and run to Queensland! Ok, you don’t have to go that far, but you could enter a fun run, climb Mt Kosciuszko or go without social media for a month… and ask people to sponsor you for it.
  • celebrate a milestone (birthdays, wedding anniversaries, retirement parties) by asking people to donate to NeuRA what they otherwise would have spent on a gift.
  • consider a bequest in your Will. Leaving a gift to NeuRA is a great way to support our research. It doesn’t cost you anything now, and it’s a simple and powerful way to support our work into the future.
  • get involved with NeuRA’s annual Bridge for Brains Research Challenge and Books for Brains events.
  • ask people to donate to NeuRA in lieu of flowers at the passing of a loved one.

A final word from carer Wendy Smith

Wendy Smith, holding a picture of her husband George

Wendy Smith, holding a picture of her husband George

You may have read the story about George and Wendy Smith (pictured), who featured in our summer letter (missed it? read it here).

Wendy’s words are straight from the heart:

“When he was diagnosed with frontotemporal dementia, George said we had to help research as much as we could and try to get a breakthrough. With so many types of dementia, we need discoveries or cures so that other families do not have to go through what we had to.”

So, this Christmas, we say thank you to our donors for their loyal support. You are contributing to future breakthroughs and discoveries that we hope will dramatically change the outcomes for people, like George, who suffer from either degenerative brain and nervous system diseases or other chronic illnesses.

Uncomfortably numb: Nerve damage after cancer treatment

Dr Susanna Park is working on ways to prevent one of the lesser known side effects of chemotherapy: nerve damage.

One hundred years ago cancer was invariably fatal. Over the past century, however, we’ve made such huge advances in cancer treatment that today, more than two in three patients diagnosed with cancer will survive their cancer for five years or more. As a researcher, I regularly see patients complete treatment and go on to live their lives cancer free.

One thing I see often, however, as a direct result of more people surviving cancer and cancer treatment, is the long-term side effects of chemotherapy. While nausea and fatigue are well-known to patients, these other side effects seem to take people by surprise. One in particular, nerve damage, is the focus of my research.

Nerve damage first appears in the hands and feet as tingling, numbness and loss of sensation. This damage, known as chemotherapy-induced peripheral neuropathy, is caused by chemotherapy drugs used to treat a number of different cancer types, including colorectal, breast, ovarian and blood cancers.

We don’t yet understand the mechanisms underlying this damage and there is currently no known treatment or cure. The damage can be irreversible and limits the amount of treatment that patients can receive. Unfortunately, nerve damage sometimes develops late in treatment or even after the chemotherapy has stopped, making it harder to identify and treat.

Dr Susanna Park

Living with nerve damage

Neuropathy can become such a significant problem that patients have trouble with everyday activities such as walking and handling objects.

For example, one patient told me that during treatment she couldn’t hold a pen to write. She said her legs felt like they didn’t belong to her and she still has difficulty walking months after her chemotherapy treatment ended.

Another patient told me that he cut his finger on a razor but only noticed when he saw the blood on his finger.

One patient’s feet ached all the time and she couldn’t stand the pressure of shoes and socks.

I’ve also seen patients who have difficulties with typing, buttoning clothes, and many often report stumbling and tripping. The unfortunate reality is that these effects can continue for years after the completion of chemotherapy treatment.

Preventing nerve damage

As there is currently no way of reversing nerve damage, our research team at NeuRA and the Prince of Wales Hospital focus on prevention; we have recently developed a nerve assessment technique to detect and measure early signs of nerve damage, enabling clinicians to identify patients at risk of severe nerve damage early in their treatment. Up until now, clinicians have had to rely on patients reporting symptoms, by which point a great deal of nerve damage may have already occurred.

While this technique is promising, we still need to determine exactly how nerve damage affects the everyday lives of patients. We are only just now starting to look at improving quality of life after cancer; and as a result, the impact of nerve damage on patient function and daily life has been largely underestimated.

I’m currently looking at these day-to-day problems and how we can quantify the difficulties that patients experience. By developing these assessment tools, we will be able to better identify and measure nerve damage, which will hopefully lead to improved outcomes for cancer survivors following chemotherapy treatment in the future.

“I was dizzy for over ten years…”

In 2002, Lydia Volek had a sudden onset of dizziness and was told she would probably never get better. After learning to live with it for over a decade, Lydia stumbled upon a study to treat dizziness at NeuRA. As our guest blogger this week, Lydia tells us how participating in this research turned her life around in just a few short minutes.

Lydia: My dizziness appeared suddenly and was extremely unpleasant. I couldn’t look up without everything spinning and when I bent down I felt like I was going to fall on my head. It’s not very pleasant, I can tell you that much. I had to be really careful getting in the bath or on the bus; I had to watch my steps and not do anything too quickly.

Dizziness can be physically debilitating and extremely distressing.

Dizziness can be physically debilitating and extremely distressing.

I was really frustrated to begin with and then I became worried about what it might mean. The specialist told me my condition was benign and probably wouldn’t get worse – but also may not get better. The treatment I received didn’t really help that much and so I started to learn to live with it. When you know that you don’t have a choice, you just wipe it from your mind and keep going – that’s all you can do.

I felt dizzy on and off for over 10 years – probably more on than off. This was how I lived until I heard about the study at NeuRA and thought ‘Ah! This might be the way for me!’

Lydia was assessed by the study team from the Falls and Balance Research Group at NeuRA. They recorded her medical history and levels of anxiety and depression; they tested her vision, strength and balance and measured her cardiovascular health, including blood pressure, and inner ear function. 

The team determined that the cause of Lydia’s dizziness was a displacement of calcium crystals in her inner ear – a condition called Benign Paroxysmal Positional Vertigo. She was offered physiotherapy to remove the dislodged particles.

Lydia: The treatment I received was very easy and simple; the physiotherapist rolled my head in a certain way and was finished in a few minutes. I felt very good straight away; I could turn around with my eyes closed and not feel like falling. I was so surprised! To tell you the truth, in that moment I thought, my goodness, why didn’t anyone tell me about this before? But I suppose that’s why they’re doing this research.

Now, a few weeks later, my vertigo is still gone. I can look at the sky and see the birds in the tops of the trees and not feel like I’m going to fall over. It’s little things like this that make a big difference to my life. From now on, if I meet someone who’s been told to live with dizziness, I’m going to tell them to go and get treated. There is life beyond this!

We are still seeking volunteers for our study, so if you would like to participate, please contact Mayna from the Dizziness Research Team on (02) 9399 1255 or at m.ratanapongleka@neura.edu.au.

 §

A comment from the NeuRA study team: We believe that Lydia’s condition was not properly treated when she first experienced symptoms. What probably happened was the dislodged particles in her ear canals were not completely removed, which led to a continuation of her symptoms.

Dizziness can be physically debilitating and extremely distressing. Despite being relatively common in middle-aged and older people, we don’t fully understand its causes and, as a result, sufferers often receive a wrong diagnosis or inappropriate treatment, with little or no relief of their symptoms.

Dr Jasmine Menant measures a patient's blood pressure

Study leader Dr Jasmine Menant measures a patient’s blood pressure.

With this study, we hope to come to a better understanding of the causes of dizziness. We are also assessing the effectiveness of individually tailored treatment plans that include one or more therapies; currently, many patients are offered only one of these therapies and continue to experience symptoms because their dizziness has not been completely treated.

The therapies we offer the participants in our study, depending on their assessment, are:

  • vestibular rehabilitation for peripheral vestibular (inner ear) conditions, administered by a physiotherapist;
  • a home exercise program for balance, strength and walking impairments;
  • cognitive-behavioural therapy for those people experiencing anxiety and depression;
  • a comprehensive medical and medication assessment by a clinician for those people with other medical conditions, such as low blood pressure, or those experiencing side-effects from medication.

We hope that by improving how we diagnose the causes of dizziness, and by offering an individualised selection of treatments, we can improve the quality of life for the many Australians like Lydia who have been told that they just have to learn to live with the condition.

Read more about the study here on Australian Ageing Agenda.

 

 

Read the summer edition of the NeuRA Magazine!

Aside

The NeuRA Magazine Issue 7

The NeuRA Magazine Issue 7

 

We’ve just published the summer edition of the NeuRA Magazine – find it online here.

Inside, read about our new guidelines to keep kids safer in cars, how alcohol affects the developing teenage brain, and how we may be able to use readings of electrical activity in the brain to diagnose schizophrenia.

If, in future, you’d like us to email or post you a copy of the NeuRA Magazine, subscribe here.

Enjoy!

Of squiggly lines and schizophrenia

Dr Jason Bruggemann is investigating new ways of identifying children at risk of developing schizophrenia.

I am relatively new to schizophrenia research, so I was surprised by the sheer diversity of people I have met who have schizophrenia – men and women from a wide variety of backgrounds with distinct personalities who don’t conform to any particular stereotype. While the disease affects them in different ways, however, they have all described the significant challenges that schizophrenia has posed for them and their families.

Schizophrenia is a neurodevelopmental disorder that typically begins during late adolescence or early adulthood. Healthy development during adolescence involves large-scale reorganisation and restructuring of the brain, including changes to the delicate excitatory/inhibitory balance of the brain’s neurotransmitter systems and underlying brain structure. This process seems to go awry for people with schizophrenia. Environmental factors like stress also appear to contribute to the onset of the disease.

Dr Jason Bruggemann

Dr Jason Bruggemann holds an EEG ‘net’, made up of wires and electrodes.

We know that early diagnosis and treatment can significantly improve long-term outcomes and help minimise the damaging effects of schizophrenia. Hence, current research is focused on potential ways of identifying children at risk of developing schizophrenia. Our colleague Dr Kristin Laurens and her team from Kings College London are currently evaluating a combination of factors as potential early markers, including subtle peculiarities of speech and movement, lower IQ and poorer academic achievement, disturbances in social, emotional, and behavioural functioning, and subclinical psychotic-like experiences such as occasionally hearing voices that nobody else can hear.

At NeuRA, we are conducting research into another potential marker of schizophrenia risk called the mismatch negativity (MMN). The MMN is an index of the brain’s electrical response to changing patterns of sounds. It’s derived from a measure of the electrical activity of the brain called the electroencephalograph (EEG), more commonly known as ‘brainwaves’. The raw EEG signal may look like just a bunch of squiggly lines running across the computer screen but, once analysed, the resulting data can help us better understand patterns of normal and abnormal brain function.

An example of a raw EEG

The squiggly lines of a raw EEG read out.

In adults with schizophrenia, the size of the MMN has been related to disease severity, ability to function in the wider-community (functional outcome), and grey matter volume loss in the frontal and temporal brain regions. The MMN is usually smaller in adults with chronic schizophrenia compared with typical individuals. In light of this, we recently investigated whether a group of children who may be at increased risk of schizophrenia (based on having some of the risk factors described above or having a first-degree relative with schizophrenia) also have a smaller MMN relative to typically developing children.

Our results showed that although the MMN exhibited by the children at risk of schizophrenia was unlike that of their typically developing peers, it also differed from the smaller MMN observed in adults with schizophrenia. In fact, we found a relative increase in the MMN over the frontal brain region, rather than a decrease!

“If we can reliably identify at-risk children then perhaps we can reduce the burden of schizophrenia for future generations.”

It was difficult for us to interpret this result in the context of what we know about MMN in adults with chronic schizophrenia. We looked at MRI data from an overlapping sample of children, which revealed differences in grey and white matter volume in the same brain regions that produce the electrical activity seen in the MMN. Also, the developmental literature indicates that the MMN tends to be larger in young children compared to adults. This has led us to speculate that perhaps the ‘at-risk’ children are on a different developmental trajectory than their peers. It is possible that this unusual MMN result may reflect the complex interplay between developmental changes and the factors placing these children at higher risk of developing schizophrenia.

It’s essential to conduct long-term follow-up of these potentially at-risk children to establish who goes on to develop schizophrenia and how their MMN changes as they mature. This follow-up work, being completed by our colleague Dr Kristen Laurens, will tell us whether the increased MMN we found in this study may indeed be a useful way of identifying children at risk of developing schizophrenia.

The unique people with schizophrenia that I have met currently live their lives as best they can despite the challenges raised by this condition. If we can reliably identify at-risk children then, with appropriate early treatment, perhaps we can reduce the burden of schizophrenia for future generations.

Is high cholesterol putting your brain at risk?

If you want to reduce your risk of Alzheimer’s disease, says Dr Scott Kim, be mindful of your cholesterol levels.

Notwithstanding the recent debate in the media, most of us understand that high cholesterol is harmful to your health because it can negatively affect your heart and arteries.

What you may not know, however, is that high cholesterol can also affect your brain; specifically, there’s growing evidence leading neuroscientists like me to suspect that high cholesterol may increase your risk of developing Alzheimer’s disease.

NeuRA's Dr Scott Kim is investigating the role of cholesterol in Alzheimer's disease

NeuRA’s Dr Scott Kim is investigating the role of cholesterol in Alzheimer’s disease

The growing evidence

Why do we suspect this? Firstly, we know that factors that increase your risk of developing heart disease – specifically, high blood cholesterol levels but also high blood pressure and a history of stroke and diabetes – also increase your risk of developing Alzheimer’s disease. Furthermore, there’s evidence that taking cholesterol-lowering drugs, called statins, decreases your likelihood of developing Alzheimer’s disease.

Another red flag is data from several animal studies suggesting a link between cholesterol and the production of amyloid-beta, the protein that accumulates abnormally in the brains of people with Alzheimer’s disease.

So how is it that high cholesterol increases your risk of Alzheimer’s disease? At NeuRA, we are trying to answer that question.

Cholesterol in the brain

Cholesterol is abundant in our brains; although the brain makes up only two per cent of body’s weight, it contains nearly a quarter of all the body’s cholesterol stores. Cholesterol has important jobs in the brain such as storing energy, acting as a structural component of the cell membrane and acting as a signalling (communication) molecule.

Cholesterol is transported out of cells by transporter proteins, and it’s these proteins – known as ABC transporters – that are the main focus of our research.

Our work has shown that ABC transporters are key regulators of how much cholesterol is inside brain cells. Just recently, we demonstrated that deleting a specific ABC transporter, called ABCA7, in a mouse model of Alzheimer’s disease caused significant increases in amyloid-beta levels. We suspect that the ABCA7 transporter facilitates the clearing of amyloid-beta from the brain. This is direct evidence that ABCA7 is crucial in the development of Alzheimer’s disease.

It’s important to understand what’s happening at a molecular level in Alzheimer’s disease so that we can discover new targets for drug treatments. By understanding the role of ABCA7, we may be able to learn how to inhibit the build-up of amyloid-beta protein and therefore provide potential therapeutic avenues for the treatment of Alzheimer’s disease.

In the meantime…

In the meantime, what can you do in terms of cholesterol to decrease your risk of developing Alzheimer’s disease?

Although controlling cholesterol levels in the brain by altering what you eat is generally very difficult, you can lead a healthy lifestyle and reduce foods in your diet that contain high levels of saturated fat. This will help to reduce the risk factors associated with Alzheimer’s disease that I mentioned earlier on.

Apart from healthy eating and regular exercise, keeping your brain active is also helpful. If playing games, writing a letter or simply interacting with others sounds easy (and it is!), then don’t delay – as the saying goes, ‘use it or lose it’!

Are you smiling or frowning?

The inability to understand facial expressions can have a profound effect on the lives of people with dementia and their families, says Dr Fiona Kumfor.

Recently I met a lady who, despite only being in her 50s, was suspected of having dementia. Susan* and her family had come to the dementia clinic at NeuRA (where I conduct research) to get help with a diagnosis.

Susan wasn’t forgetting things; in this sense, her mind was very sharp. But in the last year she had become far less socially engaged and caring, even towards her teenage children. For example, she had started telling private things about her children to people outside the family; she didn’t seem to recognise that it was embarrassing for her children. This was very distressing for her family, even though Susan herself felt that nothing was wrong.

Dr Fiona Kumfor studies how dementia can disrupt a person’s ability to understand emotions.

While this may not sound like the dementia you’re familiar with, the effects of this disease are in fact much broader than the confusion and memory problems of Alzheimer’s disease. People with the type of dementia we saw in Susan, called frontotemporal dementia, show profound changes in their behaviour and personality. One of the most difficult changes that families must cope with is a loss of empathy that occurs, at least in part, because of an inability to interpret facial expressions.

Understanding what a frown means

For a healthy adult, interpreting facial expressions happens automatically and rapidly. Our research focuses on how this complex skill is affected in patients with frontotemporal dementia. Our research has revealed that people with this disease are unable to distinguish between facial expressions very well at all. Because they might mistake a sad expression for an angry one, they also have difficulty understanding how other people are feeling and responding appropriately.

So what happens in the brain to cause this change? Importantly, our study has revealed for the first time that shrinkage in the frontal and temporal parts of the brain, in regions called the amygdala and insula in particular, is responsible for this loss of emotional understanding. Previous studies have shown that these regions activate in healthy people when they view emotional faces.

The image on the left is an MRI scan of a person with frontotemporal dementia. The black areas show the frontal regions of the brain that have shrunk due to dementia. The scan on the right shows a healthy adult of the same age.

This loss of emotional understanding undoubtedly makes interacting with others challenging; people with frontotemporal dementia are no longer able to understand the subtle social cues that healthy people take for granted. It can cause conflict if they misinterpret their friends and family’s emotional expressions. This was certainly the case for Susan; her family told us that she didn’t seem to understand when they were feeling upset or frustrated anymore.

Improving quality of life

Unfortunately at present no cure exists for frontotemporal dementia. We do hope, however, that our findings will help in the development of techniques to improve the quality of life for people with this disease and their families.

In fact, we’ve already had some heartening results. A second study we conducted showed that, in some cases, exaggerating the emotional expression improved how well patients recognised the emotion. For me, this finding is particularly encouraging because it suggests that even simple techniques may have a direct and positive impact on how people with frontotemporal dementia and their families can continue to communicate and connect.

*name changed