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The UK budget 2016 has exposed convincingly the grim reality of 'dementia friendliness'

The most significant aspect of yesterday’s Budget was that UK growth is revised down last year, this year, and indeed every year it’s forecast. But it was the day last orders were given – failure to meet most targets, and more borrowing and national debt. The current Government boasts that it is only with a strong economy it can deliver on aspects of life, many of which are relevant to people living with dementia and all types of carers. But it is clear that the UK economy is still inherently weak. The concept of the ‘dementia friendly communities’ has been to the financial benefit of many people without dementia, but the key question remains about its license to operate from the perspective of people living with dementia and their significant others.

 

Instead, as a question of priorities, corporation tax has been cut and billions being handed out in tax cuts to the very wealthy. This is unlikely to be exhibited in any significant improvement in dementia friendliness by multi-nationals and high street chains.

 

It is right that the Chancellor has recognised the funding pressures facing councils and local services over the next few years and has not announced any more cuts to local government.

 

But it is indeed disappointing that the Conservative Chancellor has not accepted calls by councils, the NHS, care providers and the voluntary sector to bring forward the £700 million of new money in the Better Care Fund by 2019/20 to this year. The failure to do so means vulnerable members of the community still face an uncertain future where the dignified care and support they deserve, such as help getting dressed, fed or getting out and about, remains at risk. This is the grim reality of what is marketed as ‘dementia friendly communities’ has come to in the UK, a concept which still continues to benefit some rather than others. This is at a time when the Government is known to be shifting priorities from dementia to diabetes, to which instruments such as the ‘sugar tax’ and obesity strategy might more directly speak to. The morale of people expected to deliver high quality care, including junior doctors and nurses, is at the lowest it has been for quite some time.

 

Vital social care services are relevant to protecting and enable people in society, not just in relieving the massive problem of delayed discharges in the NHS. The threat of a care home crisis is still disturbing. The deficit in the NHS has risen to its highest level ever on record. Waiting times are up, the NHS is in a critical condition, hospital after hospital faces serious financial problems. The NHS should have the resources to concentrate on the health needs of the people, not do budgetary acrobatics to survive. With a distinct lack of influential people speaking truth to power, dementia policy in the UK is in a dire state.

 

At a time when the Public Accounts Committee have only just reported that NHS finances have deteriorated at a severe and rapid pace, we do not just need gimmicks from charities loyal to Government of ‘fixing dementia care’.

 

The whole system needs proper resource allocation so that people living with dementia can have their health and wellbeing enhanced, whatever the care setting. Mistakes here are compounded in a double lock from serious mistakes by Government civil servants in dementia. The recent Implementation Plan for the Department of Health 2020 document on dementia did very little to prioritise the importance of skilled workforce such as clinical specialist nurses in care pathways, and indeed was generally bereft of meeting the needs of people with dementia and carers in clinical settings.

 

We have also seen devastating cuts to public health budgets and mental health budgets, further having a devastating impact on English dementia policy. Previous governments have touted the use of these tools as promoting ‘choice and control’, and yet the rhetoric is clearly mismatched to reality. Earlier this month the Government forced through a £30 per week cut to disabled ESA claimants. As dementia is a disability both under domestic and international legislation, it is hard to see how the UK wishes to promote international policy of sustainable communities and independent living for people living with dementia under the lens of disability rights.

 

Finally, the UK needs to value and acknowledge the social capital of the huge army of upaid carers, as well as paid carers many of whom are afflicted by under-employment and insecurity. Security comes from knowing where your income is and knowing where your job is. We need to value all carers if the rhetoric of ‘dementia friendly communities’ is to have any substance.

 

All in all the UK budget exposed the grim reality of “dementia friendly communities”, and the stark impotence of key individuals now to speak truth to power.

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Changing the story will change minds

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The fundamental concern, not true, about many innovative initiatives in dementia care and support, such as engagement and ‘friendly communities’, is the unintended consequence that they act as a sticking plaster, but very little else. Proponents of sticking plasters will be the first to point out that they’re better than nothing.

But is it actually true that they’re better than nothing?

Take for example the scenario of someone being invited along to give a talk in response to a new Government/charity document, and that person has been given a diagnosis of dementia. Imagine, if after four years of intense ‘awareness’ raising and innovative initiatives into ‘friendliness’, including from some of the biggest names in the business, that person was accidentally left off the scheduled programme.

A concern has been for me is that engagement and involvement serves more of a marketing function, as a printing press for grant raising, rather than genuine involvement. That is, rubber stamp tick box ways of working. You can quite simply have a pathological culture and have the semblance of quasi-involvement.

Look past how that document from Government/charity might have been produced. At first, I have been encouraged to think of this as ‘who’s in the room..’ after Alison Cameron educated me on the ‘no more throwaway’ work of Prof Edgar Cahn, and the co-production workstreams from Nef and Nesta. Alison is totally correct. And it’s essential to add ‘…and who’s also listening to those people in the room.’

I am worried that this document would have been produced by the usual ‘big names’ in the third sector; few from people working in this area with a daily understanding of good professional practice and evidence; and not more than one or two living with dementia or carers. And you see this pattern repeated time and time again, say in the formation of “clinical excellence” guidelines.

And it at once becomes perfectly understandable how a person living beyond a diagnosis of dementia, to use Kate Swaffer’s succinct term, could have got left off the timetable. Shocking but not surprising. Whatever the explanation, the emotional effect has been made, but it is time for all of us to move on – until the next time that is.

Time and time again people with dementia or carers, if at all, are given a small slot, more often than not at the end of the day’s programme, exist as an afterthought for event organisers, with other speakers not aware of the defect. Exceptions though exist; a friend of mine living with dementia was given a slot in the morning in an excellent research conference, and was specifically told to take his time even if the government minister overran.

A lot of faith is put into the rules of the game. But sometimes the rules of the game need changing. There needs to be a fundamental change of culture. People with dementia have been advocating for their rights, but this is as useful as the issue of who is listening. A third friend of mine is about to set out the case for human rights and disability for people with dementia in Geneva; but will the relevant non-governmental organisations listen and act?

Like a dog sitting on the word ‘no’ in the phrase ‘no dogs allowed’, we have to concede Apartheid is no longer the law in South Africa. It is not acceptable to have a sign in a B&B saying ‘No Irish, no blacks, no dogs’. There is normally a lag between a moral outrage, and a change in behaviour. I hope that this will happen too in a change in narrative away from the prejudices of society about dementia.

 

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There's something about tau

Tau

Alzheimer’s disease is the most prevalent type of dementia globally, and therefore traditionally gets the most focus. However, there are other neurodegenerative conditions of note which are of massive importance. For example, neurodegeneration with brain iron accumulation (NBIA) is a group of disorders characterized by dystonia, parkinsonism and spasticity. Models of Alzheimer’s disease, frontotemporal dementia, Parkinson’s disease and Huntington’s disease show some striking similarities to the corresponding human pathologies in terms of axonal transport disruption, protein aggregation, synapse loss and some behavioural phenotypes (Gilley, Adalbert and Coleman, 2011). In early stages of Alzheimer’s disease, neurofibrillary tangles (NFT) are largely restricted to the entorhinal cortex and medial temporal lobe. At later stages, when clinical symptoms generally occur, NFT involve widespread limbic and association cortices. At this point in the disease, amyloid plaques are also abundantly distributed in the cortex.

Induced pluripotent stem cells (also known as iPS cells or iPSCs) are a type of pluripotent stem cell that can be generated directly from adult cells. The iPSC technology was pioneered by Shinya Yamanaka’s lab in Kyoto, Japan, who showed in 2006 that the introduction of four specific genes encoding transcription factors could convert adult cells into pluripotent stem cells. He was awarded the 2012 Nobel Prize along with Sir John Gurdon “for the discovery that mature cells can be reprogrammed to become pluripotent.”

Pluripotent stem cells hold great promise in the field of regenerative medicine. Because they can propagate indefinitely, as well as give rise to every other cell type in the body (such as neurons, heart, pancreatic, and liver cells), they represent a single source of cells that could be used to replace those lost to damage or disease.

According to Wray and Fox (2016),

“It is the use of stem cells as disease models that perhaps has the most to offer in terms of immediate gain, and the most exciting development is the potential to assay potential therapeutics with induced pluripotent stem cells (iPSCs).”

But Wray and Fox (2016) later comment:

“Of particular relevance to Alzheimer’s disease is the fi ending that the expression profile of tau remains feral-like in iPSC-derived neurons until 1 year in culture. Even in cases of familial disease with the earliest onset, the disease only manifests clinically several decades after the onset of pathology and structural changes—how effectively will iPSCs recapitulate the full time course of disease-associated molecular changes?”

Tau proteins (or τ proteins, after the Greek letter by that name) are proteins that stabilise parts of the cell called “microtubules”. They are abundant in neurons of the central nervous system and are less common elsewhere, but are also expressed at very low levels in CNS astrocytes and oligodendrocytes. Pathologies and dementias of the nervous system such as Alzheimer’s disease are associated with tau proteins that have become defective and no longer stabilise microtubules properly.

The tau hypothesis of Alzheimer’s disease states that excessive or abnormal phosphorylation of tau results in the transformation of normal adult tau into PHF-tau (paired helical filament) and NFTs (neurofibrillary tangles). But it is clearly more complicated than that. Deposition of highly phosphorylated tau in the brain is the most significant neuropathological and biochemical characteristic of the group of neurodegenerative disorders termed the tauopathies. Pathological hyperphosphorylation of the microtubule-associated protein tau is characteristic of Alzheimer’s disease and the associated tauopathies. The reciprocal relationship between phosphorylation and O-GlcNAc modification of tau and reductions in O-GlcNAc levels on tau in AD brain offers motivation for the generation of potent and selective inhibitors that can effectively enhance O-GlcNAc in vertebrate brain (Yuzwa et al., 2008).

The discovery of tau fragments in these diseases suggests that tau cleavage and tau phosphorylation, both of which induce conformational changes in tau, could each have roles in disease pathogenesis. As Hanger and Wray (2010) note, the identities of the proteases responsible for degrading tau, resulting in the appearance of truncated tau species in physiological and pathological conditions, are not known.

The Bavarian psychiatrist Alois Alzheimer is traditionally credited with the first description of the most characteristic pathological brain change—neurofibrillary tangles (NFT)—of a yet-unnamed disease in a 51-year-old woman from Frankfurt am Main, who had developed dementia.

During the 1990s, the significance of tau pathology for neurodegenerative diseases, in particular for dementia of the Alzheimer Type, remained in the shadow of the amyloid based approaches. However, as the distribution pattern and overall quantity of amyloid turned out to be of limited significance for pathological staging of AD progression and symptom severity, and after detailed studies of the maturation and distribution of NFTs showing correlation with degree of cognitive decline and memory impairment in Alzheimer’s disease, Braak and Braak proposed a neuropathological staging of the gradual deposition of abnormal tau within vulnerable neurons in brain areas in the form of either NFT or neuropil threads. Post-mortem Braak staging of neurofibrillary tau tangle topographical distribution is one of the core neuropathological criteria for the diagnosis of Alzheimer’s disease.

Based on the biochemically diverse range of pathological tau proteins, Šimić and colleagues (2006) have recently reviewed a number of different approaches which have been proposed to develop new potential therapeutics. Here we discuss some of the most promising ones: inhibition of tau phosphorylation, proteolysis and aggregation, promotion of intra- and extracellular tau clearance, and stabilization of microtubules.

The recent development of candidate PET imaging tracers targeting aggregated tau (now enables not only the brain burden but also the anatomical distribution of tau pathology to be mapped directly in living subjects. One such PET tracer, 18F-AV-1451 (also known as 18F-T807), has been shown to bind selectively to paired-helical filament (PHF) tau, and to exhibit favourable kinetics, low non-specific binding and differential uptake in Alzheimer’s disease versus healthy control subjects. It has been very recently been reported that in vivo 18F-AV-1451 positron emission tomography images across the Alzheimer’s disease spectrum can be classified into patterns similar to those prescribed by Braak neuropathological staging of tau pathology (Schwarz et al., 2016).

But there’s more to tau than Alzheimer’s disease. In NBIA, iron accumulates in the basal ganglia and may be accompanied by Lewy bodies, axonal swellings and hyperphosphorylated tau depending on NBIA subtype (Arber et al., 2015). And there’s more to Alzheimer’s disease than tau. For example, results from Pooler and colleagues (Pooler et al., 2015) strongly support the hypothesis that cortical amyloid accelerates the spread of tangles throughout the cortex and amplifies tangle-associated neural system failure in AD. The story is gradually though unravelling.

Talk

Dr Selina Wray will be giving a presentation at 4 pm today in session 11 of the Alzheimer’s Research UK Research Conference entitled “Modelling tauopathy in patient-derived neutrons: good things come to those who wait?” (link here).

Recommended reading

Arber CE, Li A, Houlden H, Wray S. Insights into molecular mechanisms of disease in neurodegeneration with brain iron accumulation: unifying theories. Neuropathol Appl Neurobiol. 2015 Apr 14. doi: 10.1111/nan.12242. [Epub ahead of print].

Gilley J, Adalbert R, Coleman MP. Modelling early responses to neurodegenerative mutations in mice. Biochem Soc Trans. 2011 Aug;39(4):933-8. doi: 10.1042/BST0390933.

Hanger DP, Wray S. Tau cleavage and tau aggregation in neurodegenerative disease. Biochem Soc Trans. 2010 Aug;38(4):1016-20. doi: 10.1042/BST0381016.

Schwarz AJ, Yu P, Miller BB, Shcherbinin S, Dickson J, Navitsky M, Joshi AD, Devous MD Sr, Mintun MS Regional profiles of the candidate tau PET ligand 18F-AV-1451 recapitulate key features of Braak histopathological stages. Brain. 2016 Mar 2. pii: aww023. [Epub ahead of print].

Šimić G, Babić Leko M, Wray S, Harrington C, Delalle I, Jovanov-Milošević N, Bažadona D, Buée L, de Silva R, Di Giovanni G, Wischik C, Hof PR. Tau Protein Hyperphosphorylation and Aggregation in Alzheimer’s Disease and Other Tauopathies, and Possible Neuroprotective Strategies. Biomolecules. 2016 Jan 6;6(1). pii: E6. doi: 10.3390/biom6010006.

Wray S, Fox NC. Stem cell therapy for Alzheimer’s disease: hope or hype? Lancet Neurol. 2015 Dec 15. pii: S1474-4422(15)00382-8. doi: 10.1016/S1474-4422(15)00382-8. [Epub ahead of print].

Yuzwa SA, Macauley MS, Heinonen JE, Shan X, Dennis RJ, He Y, Whitworth GE, Stubbs KA, McEachern EJ, Davies GJ, Vocadlo DJ.29. A potent mechanism-inspired O-GlcNAcase inhibitor that blocks phosphorylation of tau in vivo. Nat Chem Biol. 2008 Aug;4(8):483-90. doi: 10.1038/nchembio.96. Epub 2008 Jun.

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It's the diagnosis and research stupid, but don't forget about care

drugs

Anyone linked to the UK government would prefer you not to talk about the crisis in social care. This gets in the way of shimmering spin about current dementia press releases.

But we know that the patient experience of people with dementia and carers is often destroyed by delayed discharges. If your train is late, it’s inappropriate for you to be labelled ‘a platform blocker’. This government, like the previous one, is failing to get on top of this problem.

If you’d believe the grass is greener on the dementia diagnosis front you’d be wrong. People languishing without a formal diagnosis is not right. But if we want high quality prompt diagnoses we should be able to pay for them.

Jeremy Hunt mysteriously views dementia as the ‘jewel in his crown’, but in fact there is a shared ethos between the NHS and English dementia strategy. That is, a stench of the ‘something for nothing’ culture – like paying #juniordoctors to stretch their work to seven days for the same money.

The Dementia Discovery Fund, launched today at the Alzheimer’s Research UK conference in Manchester by Jane Ellison MP, will pay for the development of new drugs for dementia. The announcement is seek to confirm that some of the world’s largest pharmaceutical companies have joined forces to seek new treatments for a group of brain diseases affecting 850,000 people in the UK.

They include Biogen, GlaxoSmithKline, Johnson and Johnson, Lilly, Pfizer and Takeda. The giant firms have signed up with Alzheimer’s Research UK to form a ground-breaking public-private partnership.

This is highly reminiscent of the approach which was taken for the development of drugs for HIV. Some time ago, ater spending a few years laying a foundation to streamline clinical testing and drug development, leaders from the US Food and Drug Administration body (“FDA”) took their Critical Path Initiative (CPI) from concept to implementation.

There remained public concerns about drug safety, dangerous imports, and rising pharmaceutical costs, much like today here in the UK for dementia. But here the UK taxpayer is in effect helping to underwrite drug development costs for these blockbuster revenue companies. Whilst political leaders use the limp mantra ‘you shouldn’t have to choose between cure and care’, in effect the choice has been made. Care is on its knees.

The famous political saying from Carville is of course ‘it’s the economy stupid, but don’t forget about healthcare.’ With the current Government’s growing economy, there is little joy from the people who can deliver potentially high quality professional care – nurses and doctors – who are unanimously demoralised and destroyed by Jeremy Hunt and his colleagues, wherever they may be.

The shambolic state of the English dementia policy could not have been made clearer by the lack of discussion of care pathways and clinical specialist nurses in dementia. What resulted was a underwhelming appalling document known as the ‘Implementation Plan’ for Dementia 2020 from the Department of Health.

The fluffy ‘health MOTs’ for people in their 40s is not evidence based at all. It is the pipedream of a non-clinical policy wonk, wishing to ensnare the ‘worried well’ into the lare of the private insurance industry, as I describe here. Nobody is of course objecting to true professional health promotion, but there are limitations to promoting ‘brain health’ – in the same ways to improve a healthy leg has limitations for you dealing with a dislocated hip or fractured neck of femur.

The relative lack of substantial professional clinical input really shone through in many areas, such as the lack of discussion of co-morbidities. Many of the ideas are gimmicks which have been recycled ad infinitum in various guises. The aim had been to assess ‘the lessons learnt’ from the only ever English dementia strategy, “Living well with dementia”, in 2009, but clearly the Department of Health cannot even been bothered to do that, not wishing perhaps to scrutinise the appalling state of social care or the high number of inappropriate referrals to memory clinic.

Or maybe the Department of Health do not want to discuss why primary care is not well placed to deliver on dementia diagnosis, when that arm of the profession is suffering a recruitment crisis, overwhelmed by bureaucracy and regulation, and is relatively grossly underfunded.

If the rest of English dementia policy were in a fit state, then a Drug Discovery Fund would be something to shout about. But the fact that there were 101 spectacular failures in drug development for dementia between 1998 and 2012 is also a fact.

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None of us know what the future will bring. To be prepared is half the victory.

Ayres Rock Chris Shibley

 

 

Through public awareness initiatives such as “Share the orange” from the Alzheimer’s Research UK charity, slowly more and more people in the general public are cottoning onto the idea that dementia is not a normal part of ageing.

An ignorance of what to expect in dementia can be very distressing. Forewarned is forearmed.

I am generally not in favour of aggressive war analogies in the context of dementia, by, say, when you’re overcoming flu, your immune system does launch an attack on a foreign species. You talk about ‘fighting the flu’. Therefore, you can defeat flu.

The problem with the analogy for dementia, however, is that you rarely hear of people who have won their fight against dementia. Defeating a type of dementia is not an unworthy aim, though.

If you do, however, decide to extend the military metaphor for dementia, then there’s no doubt for me that, as attributed to Miguel de Cervantes, “to be prepared is half the victory”.

About 16 years ago to the day, I started my Ph.D. up in Cambridge. I would visit families with dementia all around East Anglia, and do some specialised psychological assessments of areas such as memory or planning in people living with the then-called ‘frontal variant’ of frontotemporal dementia.

I came to focus on decision-making, and I found that risk taking was a much under-recognised feature of people with a type of dementia known as the behavioural variant of frontotemporal dementia, whose calling sign is quite an insidious change in behaviour and personality. This is highly relevant to personal budgets in social care, and also development of therapeutic targets (taking in work in the related area of impulsivity.)

Now, it is known, not thanks to me but thanks to a handful of specialised laboratories around the world, that your genetic blueprint you’re born with can be traced to various well defined categories of frontotemporal dementia, a type of dementia that affects the frontal and temporal bits of your brain. (They’re the parts of the brain right at the front and near your ear respectively.)

Bring the clock forward to 2016, and we now have quite a good idea of tiny parts of the cell, the basic unit of the human body, called “ribonucleosides” which seem to act funny in some of the frontotemporal dementias. This is, of course, significant as this gives us leverage to attack the dementia process – like looking for the weakest link in the enemy army.

I didn’t go to Cambridge last year. In fact, I had not been to Cambridge for a decade until recently when I was invited to give a talk on risk and dementia at one of the Cambridge Colleges.

I instead went to Australia with Chris Roberts, his wife Jayne Goodrick, and one of their daughters. Chris is presently living with a mixture of vascular dementia and Alzheimer’s dementia. Visiting Ayres Rock was my personal highlight.

Again, it’s the case that very bright researchers have worked out that changes to the blood flow around the brain can somehow lead to a process of dementia. It’s well known vascular changes in the human body can be brought about by a whole host of factors such as diet and smoking – this again gives a means of preventing the rate of progression of an enemy army.

neuroanatomy

[source here].

Knowing the plumbing of the human brain can therefore very relevant to working out how to stop the rate of decline in dementia. How well blood flows in the brain is closely linked to the health of the brain through a process called “neurovascular coupling”.

When you think of the size of the numbers of people around the world living with dementia, close to 50 million, this leaves you with two options. One is to give up altogether; the other is to build up bit by bit a detailed working knowledge of the dementias.

I know Chris, living with dementia to the best of his ability, and in an environment which can be optimised as ‘dementia friendly’ as possible, works relentlessly to campaign for recruitment into research in dementia (“Join Dementia Research”).

Working out how factors in the circulation might be progressing in Chris’ dementia would be a wonderful thing to know, and provide much greater precision for a possible therapy one day for people who have the type of dementia Chris has.

The aim of research into dementias is to gather this detailed knowledge, pool it together and share it, and think about how best it can be used to promote and protect the health of citizens. Research is an investment which is inevitably very costly due to manpower and consumables.

Nonetheless, the next step is to make sure the right mood music (and money) is in place to convert this knowledge into something meaningful for a person living with dementia. The regulatory infrastructure of course around the world needs to be able to responsive and responsible to such innovations.

I wish Chris well as he helps to launch next week’s Research Conference for Alzheimer’s Research UK up in Manchester, where other brilliant initiatives such as ‘Dementia United’ providing devolved joined up health and care services for dementia are also afoot.

Anyone involved in research knows it’s a marathon not a sprint; and most researchers I know know they’re in it for the long haul. But we can only get more detailed knowledge as, in other areas, we have a strong, high capacity, workforce making use of all available specialist talent.

You see, none of us know what the future will bring. Anything can happen to anyone at any time.

The UK, being the sixth richest country in the world, is an unique position to do this. The travesty is that social care is on its knees, and this is a painful truth for many people trying to live with dementia presently. And this needs correcting.

The future, on the other hand, might be brighter, if not necessarily orange.

 

 

 

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You need to ask the right questions to get the right answers

Idea concept with row of light bulbs and glowing bulb
Idea concept with row of light bulbs and glowing bulb

I think the worst aspect of the term ‘innovation’ is the term itself. For me, it more often than not conjures images of gimmicks and the snake oil salesmen of these gimmicks.

But there’s a certainly a place for ways in which people can be motivated to take an interest in his or her own health. There needs to be, nonetheless, an informed debate; for example, a healthy “health check” is no guarantee that you won’t succumb to some malady within a few years time.

I’ve known people to run a full distance on a cardiac treadmill in a hospital, with no monitored changes in heart function, only to drop dead seconds later in the hospital car park.

Nonetheless, most definitions of innovations are quite broad, and are generally doing things differently or doing different things.

It’s often said by physicians that the vast majority of a reliable diagnosis can be taken from a good history of symptoms. That I believe to be supremely the case for dementia.

I am not going to bombard you with the predicted million people living with dementia in the UK, as quite frankly if it’s your mum living with dementia that should be good enough for you to take an interest.

The question, “Have you had trouble with your memory?”, is likely to engender a lot of false positive responses as a diagnostic screening tool for dementia. A better one would be possibly, “Have you had trouble with memory but feel that your mood has been quite good?” But even this question would not be ‘fool proof’ as people can live with both dementia and depression.

There is a good ‘push’ argument against supporting a status quo in the current approach to dementia. That is, it is overly reliant on a medication solution, when the vast majority of drug research work in this area has resulted in failure. This ‘promissory hope’, of “one last push”, is needed to keep the general public engaged with this mission, and certainly helps the surpluses and profits in the short term.

Indeed, many of the arguments for ‘barriers to innovation’ can cut both ways. For example, it might be the case that in these economic challenging the times the last thing you’d want to do is to take a massive punt on redesigning diagnostic care services for dementia. Or, on the other hand, you might take the view that there’s nothing to lose.

The need for innovations to be ethical and accountable has become increasingly important under the umbrella term ‘responsible innovation’. Not all dementia is Alzheimer’s disease, and yet we are led down the Alzheimer’s path continually by the media. If there were a ‘biomarker’ for Alzheimer’s disease which was very specific and sensitive, and inexpensive to get the results of, would this information help you?

The answer is possibly – but if this were coupled with a private insurance system, you could also find your insurance premiums going through the roof, even if you were to have forty years of healthy living ahead of you.

Certainly the more expensive the investigation doesn’t make it more fool-proof. I’ve known patients with a clear diagnosis of frontal dementia who’ve had plum normal investigations including state of the art MRI scans. And likewise people with radiological atrophy on MRI who don’t have dementia.

I see innovations in dementia as a tool in dementia diagnosis, support and care, but only if used responsibly. Otherwise more noise can be added to the signal, as was clearly the case for incentivising primary care to run case finding tests for dementia. The very predictable unintended consequences that the number of false positive diagnoses of dementia also shot up, although ignorance is possibly worse than fear.

Ask any corporate strategist about the future and he or she will always tell you some of it is about turning threats into opportunities. For me, if you cut through the shill and waffle, an intelligent way to redesigning dementia care isn’t a bad idea, even if I would not necessarily start from here.

 

 

 

This is the talk I will be giving for #WHIS16, the World Health Innovation Summit in Cumbria, on innovation as a societal response to dementia.

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