Photo of Claire Miriam Allen, mother of Becky Allen. Artwork by Laura Pannack.
It is hard to say when Mum was first affected by dementia. She had trouble remembering some people’s names. She was less confident going out and about and making decisions. She argued more with me and Dad. Words: Becky Allen.
But Mum was fit and active, endlessly interested in people and great company.
Then, last summer, things changed. She was agitated, angry, called an ambulance three times in a week. The GP telephoned to tell me she wanted to section Mum, but by the time she was admitted to hospital, she was delirious.
What I had thought were the signs of worsening dementia were the resultof a urinary tract infection. Its assault on an aged and unwell brain were catastrophic, and there was no way back. After six weeks in hospital, Mum could no longer walk or stand. Coaxing her to eat even tiny morsels of foods she had once found irresistible was impossible. Three months, one live-in carer and two nursing homes later, she died.
Today, I wonder: where is the hope, rather than hype? When will we have better treatments? And in the meantime, how can we better care for people with dementia – and their families?
Closer to effective treatments
As a science journalist based in Cambridge, I speak to the University’s dementia research community regularly. I wanted to know what they – the fundamental scientists, the clinicians, the epidemiologists – thought about the future for dementia care.
I start with Chris Dobson, Professor of Chemical and Structural Biology at the Centre for Misfolding Diseases, who works on the fundamental science underlying Alzheimer’s and Parkinson’s. I interviewed Chris four years ago. Then he was circumspect about when work in the lab would translate into practical treatments for patients; today, he’s excited. Curing dementias remains a very challenging long term goal, he says, but we are much closer to effective treatments.
Over the past 10 years, Professor Dobson’s team has been examining what happens when proteins – the complex molecules that do most of the work in our cells – fail to fold into the correct shape. Misfolded proteins can’t function properly. Instead, they form toxic clumps or aggregates that underlie many diseases from Alzheimer’s to diabetes.
Two things excite him most. The first is that we now understand protein misfolding well enough to search for molecules that can interrupt the aggregation process. The second is that several of the molecules that seem to do this effectively in the lab in model organisms such as nematodes are drugs already licensed for other diseases.
“We’ve realised that if you understand the basic mechanisms, then you can be rational about designing molecules that will be therapeutic,” he says. “The research suggests that mechanistically, it is these aggregation processes that are the crucial issue, and if we can interrupt those we’re in a strong position. And if we can repurpose drugs, developing new therapies should be faster.”
Claire Miriam Allen (née Plaut) was born in Berlin in 1925, escaping to England with her parents in 1938 – the rest of her family were murdered in concentration camps. Colourful and unconventional, she spent much of the war in Oxford as an art student where she became friends with Philip Larkin – she is thought to have been the inspiration for the character of Katherine in A Girl in Winter. Miriam died in 2014, leaving behind her husband John, daughter Becky and many friends.
Growing research community
As Professor Dobson hints, Cambridge’s dementia research community is growing in size and strength. For this piece, I spoke to Professor John O’Brien about his work on biomarkers (ways of identifying the pathology of dementia earlier than at autopsy) and about new UK clinical trials in dementia, including a study of amlodipine (a high blood pressure medicine) in vascular dementia. I spoke to Professor David Rubinsztein about the new Alzheimer’s Research UK Drug Discovery Institute, whose researchers will be able to bridge the gap between academia and industry, and about his own research on making cells better at disposing of aggregated proteins. I spoke to Professor Carol Brayne about what her epidemiological studies reveal about the impact of education and preventive health measures on dementia rates, and to Dr Stephen Barclay, whose research and teaching on palliative care will help GPs provide better end-of-life care. They gave me some comfort that, in the future, doctors may have more to offer people with dementia.
But what about the patients who are being diagnosed today? I meet clinician Professor Roger Barker in an exam room at the Centre for Brain Repair. Next to a couch and scales sits a colourful, plastic model of the brain, which I guess he uses to explain things to his patients and their families. Barker has worked on Parkinson’s and Huntington’s diseases for the past 20 years and is intimately acquainted with dementia. His father was developing an early dementia when he died and the vast majority of people with Parkinson’s and Huntington’s will develop dementia. “After Alzheimer’s Disease, Parkinson’s is the second commonest cause of dementia in the UK,” he says, “and the thing patients fear the most.”
Improving care for all
Yet Barker believes that when it comes to improving care, talking to carers and giving patients and their families more information are key. “Families need to know what’s likely to happen, and how to cope with things when they go awry,” he says. “People need to know more about infections. The nature of dementias is that they get slowly worse; if they get suddenly worse, something else has happened and the commonest thing is an infection. That’s what I tell my patients.”
His words are hard to hear, because with more information, I might have made different decisions. Most were made in haste or in crisis, and – apart from one brief discharge meeting at the hospital – without help from experts. I wish Mum’s doctor had been more like Roger Barker. Or Professor James Rowe, who wears a yellow lanyard that says ‘dementia champion’, and has just been appointed to Cambridge’s new chair in cognitive neurology (aka dementia).
Rowe works in the Herchel Smith Building, which houses researchers from Neurology and Psychiatry, the MRC Cognition and Brain Sciences Unit plus NHS memory clinics. “This building represents the best integration of psychiatry and neurology when it comes to the brain and the mind, and how that translates into dementia and dementia care,” he says.
“My research relates to the impact of these illnesses on people – how they think, how they behave, how they manage. I’m interested in how you can treat symptoms and identify changes in people’s bodies and brains even before they get unwell,” Rowe says. “If we could identify and alter the course in that window of opportunity you’d radically alter the outcome of dementia for many people.”
My research relates to the impact of these illnesses on people – how they think, how they behave, how they manage.
None of the researchers I speak to talk yet in terms of cure. However, halting or slowing the disease early enough would have a similar effect because most dementias are slowly progressive diseases of the brain. “In those who we believe the change is already under way, if we could slow those changes, push their dementia back by 20 or 30 years, then for that family we’d be close to solving the problem,” he says.
Rowe, like the others, thinks delaying the disease is a realistic goal, and that Cambridge will play a key role. There is a critical mass of world-class researchers here and major investment in facilities like the new PET-MRI machine and a new ultra-high field MRI – one of the strongest scanners in the world. “It’s making junior researchers excited about dementia research; that’s totally different from 10 or 15 years ago. It’s now a priority area for people from many backgrounds: typical disciplines like neurology, psychiatry and psychology, but also computing, informatics and engineering,” he says.
Good for researchers and patients too is the high rate of patient participation. Around 80 per cent of patients are involved in dementia studies at Cambridge. “That’s phenomenal,” says Rowe. “It’s part of the active engagement between clinicians, patients and their families, and it gives people a way of taking charge of their illness, rather than being tossed to the four winds by it.”
Looking to the future
But until science and drug trials deliver better therapies, how can people with dementia – and their carers – get better care? Part of the answer must lie in reintegrating health and social care. But part lies in more research on dementia care, so my final conversation is with Dr Eneida Mioshi. Born and brought up in Brazil, where she trained as an occupational therapist and worked in geriatrics, she came to Cambridge to do a PhD on frontotemporal dementia.
People with different dementias may struggle with the same everyday tasks, such as cooking – but the reasons they struggle vary according to the disease. “This matters because otherwise we can’t teach the family – or change the environment – to address the tasks they need help with,” Mioshi explains. Working with patients in Australia, Japan and Brazil, she has adapted an intensive, 15-week carers’ programme to equip them with tools to tackle the problems more effectively.
“Carers learn what they can change and improve, and what they can’t alter and therefore need to accept,” she says. Mioshi is now working on a four-year project on functional ability and says that the research is crucially for families, because until better therapies arrive, they still have to manage.
Managing is hard. While a great deal more investment is needed – for every six cancer researchers, only one is working on dementia – Cambridge’s dementia researchers gave me more hope about the therapies there will be in 10 or 20 years’ time. They showed me what good dementia care could look like. And they impressed me with their compassion and commitment. As Professor Dobson says: “Once people start to put their minds and techniques to this, then one can be optimistic that things can develop rapidly. We need to plug into these developments to enable progress to be as fast as possible.”
Article by Becky Allen. The images of Claire Allen on this page appear with the kind permission of her family. The artwork was created by Laura Pannack. Becky is donating her fee for this article to the Alzheimer’s Society and Marie Curie.
This article first appeared in CAM - the Cambridge Alumni Magazine, edition 76. Find out how to receive CAM.