There’s something about 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.


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.

Why I love dementia research

First of all, I should not actually ‘love dementia research’ if only because I’ve been doing it discontinuously since my finals in neuroscience at Cambridge in 1995-6. Familiary breeds contempt, and all that.

I think meeting three people in the last year really turbo-boosted my interest in research into dementia. And I think if you compare the contents and style of my two books in dementia, published last year and this year, I feel the second book, as Steve Hilton might put it, is ‘more human’.

The three people are Wendy Mitchell, Chris Roberts and Hilary Doxford – of all these three, I know Chris by far the best, but I find the eagerness of all three to promote dementia research awesome.

Chris Roberts, living with a mixed vascular and Alzheimer’s dementia (not uncommon a combo), managed to do two interviews on the BBC last week, “Victoria Live” and “BBC World”, managing to get a plug in for ‘Join Dementia Research’.

Join Dementia Research’ (@beatdementia) is an initiative anyone can join in to take part in dementia research. It’s sort of like a different sort of dating agency – one where you paired up to the research project most suitable to you. You don’t have to be living with dementia to participate.

When I  tweeted this picture earlier today, I did not actually realise Chris Roberts and Jayne Goodrick were standing on the far right (where they are not politically.) Hilary’s on the far left (not politically either, to my knowledge) and Wendy’s in the eye-catching red jacket (not a political statement either, I think.)


Chris here explains his own experience of dementia, and explains the need for research in his BBC World interview. Any person with dementia becomes an expert in his or her own condition in time and place.

But having thought about it a lot recently, in light of national policy, I’ve concluded that I like research into dementia a lot. I enjoy reading about it all the successes and failures. I like doing my work, even though it does not consume any expensive resources. I’ve so far got a chance to present my findings, which have not cost anything at all, at two international conferences: Alzheimer’s Europe and Alzheimer’s Disease International.

I think I would strongly recommend anyone living with dementia or closest to such a person to think about even doing research for himself or herself, and publishing the research. Once you get involved with the research bug, it’s a great way to meet people, and talk effortlessly with people who share your interests. I’m invariably impressed by medics who’ve had the time, opportunity or resources to pursue research of some sort, not least because they’re furthering the knowledge and reputation of the profession. It also tells me that “they’re not one trick ponies”.

I don’t think of a primary goal of a researcher should be gainful paid employment. The people I’ve found who excel at research are the ones who are genuinely passionate about it. It’s a great privilege I feel to be able to study a topic in detail, and to take on contemporary challenges. As a person, I feel philosophically that nothing goes to waste, so for me even ‘negative findings’ have value.

Whilst I do not share in the hyperbole surrounding the drug trials research presented last week in Washington at the Alzheimer’s Association conference, I think any development which overall increases our understanding, however small or incremental, is to be welcomed. The advantage of well designed trials, even if they do not throw up the ‘clean results’ many would like to see, not least for a ‘return on investment’, is that they provide something people in the future can rely on. Money we spend on research is literally investing in hope. A love of knowledge I suspect would get a widespread democratic mandate, as would a greater understanding of human experience. All of this helps the NHS in our jurisdiction to offer a better care and support environment, with colleagues in social care, in theory and hopefully in practice.

I don’t feel it’s a just but lost cause, like any good Jacobite would, although I’ve been in love with lost causes since I became a supporter of Tottenham Hotspur, or a book called ‘Jude the Obscure’ (St Jude was apparently the Patron Saint of Lost Causes).

Possibly even there’s no such thing as satisfaction. In “The Dawn”, the 19th century philosopher Friedrich Nietzsche claimed that that which is erroneously called ‘pity’ is not selfless but actually self-motivated. Am I motivated by negative emotions such as ‘pride and satisfaction’ in doing research into dementia? Am I ‘taking control of biology’? Possibly.

I published my paper in 1999 with Prof John Hodges and various others for a reason. This was because they were patients turning up in cognitive neurology clinic, query the behavioural variant of frontemporal dementia, whose tests appeared at first blush entirely normal. And yet these tended to be people in their 50s or 60s with quite profound changes in personality which had been noticed by their closest. I provided an explanation for why this paradox exists in this paper which is now cited in the current Oxford Textbook of Medicine. I argued it’s because the part of the brain which is affected, a part of the brain near the front of the head towards the eye, is hard to investigate.

The vast majority of my colleagues in research have confirmed this finding, which brings me onto my final point. It is incredibly rewarding when someone you’ve never met before claims to agree with you and have taken your results further. And it’s wonderful when somebody you’ve never met before knows your research and likes it – this happened to me when I met Prof Brendan Boeve from the Mayo at the Alzheimers Association conference last year in Copenhagen.

“Alive inside: the story of music and memory”. A film screening in Brighton on March 20th.

I always tell anyone I can meet, “Anything can happen to anyone at any time”.  I believe in persons not patients; I believe in looking at what people can do rather than what people cannot do; I believe repair is important, but so is care.

2 Shibley

Don’t let anyone fool you into thinking that the human brain is anything other than complex. There’s about 1 000 000 000 000 000 different nerve cells, some of which are connected w’ith other, but some aren’t.

“Alive inside: the  story of music and memory” is a film which charts a one-man mission of Dan Cohen to bring music to residents of residential nursing homes.

I am honoured to have been invited yesterday to introduce this film at St George’s Church, Brighton, to an audience of about 100-120 members of the community.

3 Before

I am truly grateful to Lucy Frost, a clinical nursing specialist in Brighton, and Rachel Mortimer, from “Engage and Create”, a social enterprise which promotes wellbeing in an evidence-based way.

1 Lucy Frost

Music is a remarkable cultural phenomenon. Whatever side of your political fence, it’s true that the whole is more than the sum of the individual parts.

Music, as correctly observed by Prof Oliver Sacks, is in an unique position to involve numerous distributed neuronal networks involved in auditory perception, emotions, and attention. But what is also special about music is that it can raise powerful personal emotions, including ‘chills’ down your spine, and can compel you into voluntary movement and coordination.

Furthermore, it can bring back powerful personal memories from your autobiography. It is not uncommon for someone to tell you that they can vividly recollect the first time they heard a particular song.

Henry in his 90s, in a nursing home in a slumped posture in a chair, becomes ‘awakened’ when he hears music. But the remarkable thing is that this phenomenon is replicable.

I don’t feel ‘awakening’ is a hyperbolic word to use in this context.

I remember when I would put a horizontal cane in front of a person with Wilson’s disease, a rare copper metabolism problem; and who was ‘stuck’ in movement, like someone with Parkinson’s disease. The year was 1998, and the city was Warsaw as I was doing a study on cognition for my Ph.D.

This is reminiscent of the ‘Awakenings’ captured later in the famous film to do with the magical effect of a dopamine chemical medication on people with Parkinson’s disease symptoms, as following the outbreak of encephalitis lethargica.

Medical breakthroughs always come from the weirdest of places.

I think unlocking movement through a physical obstacle is akin to unlocking thinking through music.

In other words, I think the human brain responds well to external triggers when it cannot generate the computer program itself. I think the human brain has a form of human metronome which enables this response to physical obstacles and music in different contexts.

The late (and great) Prof Sir Richard Doll, after a lecture at Cambridge, said to me how he’d been told that, “serendipity is like looking for a needle in a haystack, and finding the farmer’s daughter.”

Numerous previous research studies have showed that your wellbeing is improved if you improve the wellbeing of others. Also, the effect of the musical ‘intervention’ is quite longlasting, in improving someone’s quality of life, or enhancing temporarily memory.

In this target-driven culture, where all outcomes have to be identified in meticulous detail, it is quite remarkable that music used this way has very few risks (e.g. it does not cause physical disease, it is not intensely costly if you have an inexpensive mp3 player which has relevant playlists.)

I managed to do a bit of ‘product placement’ for my own iPod Nano, even.

4 photo with iPod

And the potential benefits are enormous. Historically, it has been far too easy for certain professionals to abuse their power to prescribe antipsychotic medications as a ‘chemical cosh’ to “turn off” residents with dementia in homes.

The whole project forces us to justify whether the money put into prescribing medications which often very have modest effects on cognition and wellbeing, and have no proven effect on disease progression, is justified.

If Pharma did not have such a policy strangehold through corporate and regulatory capture, social prescribing, where doctors could prescribe a mp3 player, would be the norm not the exception. “Nesta”, the innovation hothouse, found in their report that most people want it but most people aren’t offered it.

As Kate Swaffer, Co-Chair of the ‘Dementia Alliance International’, a peak body representing people with dementia, emphasised last week addressing dignatories in Geneva for the World Health Organization, we need more effort to be put into research into living well with dementia.

“It is possible to live well with dementia” is in a way the first amendment of the Alzheimer’s Disease International. Bringing music back into some people’s lives might be a good start.

I was much more open about where I thought our English dementia policy has gone wrong, in a small pub in Brighton round the corner from the venue. Elated by my Diet Pepsi, I explained how we could be in a better place – but that’s for another day.

5 after


Meet Norman and Terry: two people living with a dementia in different ways

“Dementia is not just about sitting in a bathroom all day, staring at the walls.”

So speaks Norman McNamara in his recent BBC Devon interview this week.

Norman McNamara

This may seem like a silly thing to say, but the perception of some of “people living  with dementia” can be engulfed with huge assumptions and immense negativity.

The concept of ‘living well with dementia’ has therefore threatened some people’s framing of a person who happens to have one of the hundred or so diagnoses with dementia.

It’s possible memory might not be massively involved for someone who has been diagnosed with a dementia.

Or as “Dementia Friends” put it, “Dementia is not just about memory loss.”

Norman McNamara and Sir Terry Pratchett are people who are testament to this.

“If you made a mistake, would you laugh it off to yourself and say ‘Ha, ha, maybe it’s because I have dementia.””

If somebody else made a mistake, would you laugh at that person and say ‘Ha, ha, maybe it’s because you have dementia.” Definitely not.

There are about a hundred different underlying causes of dementia.

“Dementia” is as helpful a word as “cancer”, embracing a number of different conditions tending to affect different people of different ages, with some similarities in each condition which part of the brain tend to be affected.

These parts of the brain, tending to be affected, means it can be predicted what a person with a medical type of dementia might experience at some stage.

This can be helpful in that the emergence of such symptoms don’t come as much of a shock to the people living with them.

Elaine, his wife, noticed Norman was doing “weird and wonderful things”.

Norman says “my spatial awareness was awful”, and “I was stumbling and falling”.

Norman, furthermore, was putting “red hot tea in the fridge”, and “shower gel, instead of toothpaste, in [my] mouth”.

Dementia with Lewy bodies (DLB) is a type of dementia that shares symptoms with both Alzheimer’s disease and Parkinson’s disease. It may account for around 10 per cent of all cases of dementia. It is not a rare condition.

It is thought to affect an estimated 1.3 million individuals and their families in the United States.

Problems in recognising 3-D objects, “agnosia”, can happen.

Lewy bodies, named after the doctor who first identified them, are tiny deposits of protein in nerve cells.

See for example this report in this literature.

“Night terrors” have long been recognised in diffuse lewy Body disease.

“The hallucinations are terrific”

The core features tend to be fluctuating levels of ability to think successfully, with pronounced variations in attention and alertness and recurrent complex visual hallucinations, typically well formed and detailed.  

See for example this account.

For Norman, it was ‘prevalent in his family’.

Other than age, there are few risk factors (medical, lifestyle or environmental) which are known to increase a person’s chances of developing DLB.

Most people who develop DLB have no clear family history of the disease. A few families do seem to have genetic mutations which are linked to inherited Lewy body disease, but these mutations are very rare.

Monogenetic forms of Lewy body disorders, where a patient inherited the disease from one parent, are rare and comprise about 10% of cases. These familial variants are more common in persons with an earlier age of disease onset.

The patterns of blood flow can help to confirm an underlying diagnosis (see this helpful review).

Also, in this particular ‘type of dementia’, it can be helpful for medical physicians to avoid certain medications (which people with this condition can do very badly with). So therefore while personhood is important here an understanding of medicine is also helpful in avoiding doing harm to a person living with dementia.

However, Norman has been tirelessly campaigning: he, for example, describes how hundreds of businesses in the Torbay-area of Devon have signed up for ‘dementia awareness.”

And, as Norman says, “When you’ve met one person with dementia, you’ve met one person with dementia.”

Sir Terry Pratchett is another person living with dementia.

Sir Terry Pratchett described on Tuesday 13th May 2014 the following phenomenon bhe had noticed:

“That nagging voice in their head willing them to understand the difference between a 5p piece and £1 and yet their brain refusing to help them. Or they might lose patience with friends or family, struggling to follow conversations.”


“Astereognosis” is a feature of ‘posterior cortical atrophy’ (“PCA”).

A good review on the condition of PCA is here.

Sir Terry Pratchett has written a personal reflection on society’s response to dementia and his own experience of Alzheimer’s to launch a new blog for Alzheimer’s Research UK:

Sir Terry became a patron of Alzheimer’s Research UK in 2008, shortly after announcing his diagnosis with posterior cortical atrophy, a rare variant of Alzheimer’s disease affecting vision.

He went on to make a personal donation of $1 million to the charity, and has subsequently campaigned for greater research funding, including delivering a major petition to No.10 and countless media appearances.

Terry Pratchett Dementia Friends campaign

In his inaugural post for the blog, Sir Terry Pratchett writes: “There isn’t one kind of dementia. There aren’t a dozen kinds. There are hundreds of thousands. Each person who lives with one of these diseases will be affected in uniquely destructive ways. I, for one, am the only person suffering from Terry Pratchett’s posterior cortical atrophy which, for some unknown reason, still leaves me able to write – with the help of my computer and friend – bestselling novels.”

Posterior cortical atrophy (PCA) refers to gradual and progressive degeneration of the outer layer of the brain (the cortex) in the part of the brain located in the back of the head (posterior).

The symptoms of PCA can vary from one person to the next and can change as the condition progresses. The most common symptoms are consistent with damage to the posterior cortex of the brain, an area responsible for processing visual information.

Consistent with this neurological damage are slowly developing difficulties with visual tasks such as reading a line of text, judging distances, and distinguishing between moving objects and stationary objects.

Other issues might be an inability to perceive more than one object at a time, disorientation, and difficulty maneuvering, identifying, and using tools or common objects.

Some persons experience difficulty performing mathematical calculations or spelling, and many people with PCA experience anxiety, possibly because they know something is wrong. In the early stages of PCA, most people do not have markedly reduced memory, but memory can be affected in later stages.

Astereognosis (or tactile agnosia if only one hand is affected) is the inability to identify an object by active touch of the hands without other sensory input.

An individual with astereognosis is unable to identify objects by handling them, despite intact sensation. With the absence of vision (i.e. eyes closed), an individual with astereognosis is unable to identify what is placed in their hand. As opposed to agnosia, when the object is observed visually, one should be able to successfully identify the object.

Living well with dementia means different things to different people.

Pratchett further writes:

“For me, living with posterior cortical atrophy began when I noticed the precision of my touch-typing getting progressively worse and my spelling starting to slip. For an author, what could be worse? And so I sought help, and will always be the loud and proud type to speak my mind and admit I’m having trouble. But there are many people with dementia too worried about failing with simple tasks in public to even step out of the house. I believe this is because simple displays of kindness often elude the best of us in these manic modern days of ours.”

As we better understand what dementia is, our response as a society can be more sophisticated. I’ve found one of the most potent factors for encouraging stigma and discrimination is in fact total ignorance.

Both Norman and Terry demonstrate wonderfully: it’s not what a person cannot do, it’s what they CAN DO, that counts.

This is ‘degree level’ “Dementia Friends” stuff, but I hope you found it interesting.


The difficulties of the delayed diagnosis for dementia in primary care

If a surgery appointment is booked for someone over 65, a ‘participating GP’,  might be incentivised to ask about memory problems in a patient at risk of dementia due to heart disease, stroke or diabetes.

There is a concern that some people are missing out on a timely diagnosis of dementia.

It is claimed that some people go undiagnosed for around ten years even, and a large proportion of persons with dementia have never received a formal diagnosis of a dementia.

A further worry is that certain people with much lesser degrees of memory impairment will be plugged into the dementia care pathways, according to Dr John Cosgrove.

At worst, this policy, where individuals are said to be ‘ambushed’ in the video above, may put people from going to see their GPs about other problems.

The risk factors, heart disease, stroke or diabetes, are not known to be risk factors for many types of dementia, although they are certainly treatable risk factors for the ‘vascular dementias’.

There is a concern about what then happens to those people who then receive a possible diagnosis of dementia.

It is known that many of these individuals do not actually want further investigations. In fact, for some, they will not even turn out to have a dementia at all.

A probable diagnosis of dementia is certainly ‘life changing’, and it can mean that a person has access to support services.

But a full work-up of a dementia, ideally, needs more than a quick chat over memory problems.

In one type of dementia, frontal dementia, common in the younger age group (that is, below the age of sixty), memory problems are not even prominent. This type of dementia is characterised by an insidious change in behaviour and personality, often noticed first by those closest to the person with that type of dementia.

And dementia is not the cause of all memory problems: depression in the older age group is an important cause of memory problems.

It is not entirely clear what the medical model offers for dementia; many of the drugs for memory have modest effect if that in Alzheimer’s disease, the commonest form of dementia worldwide.

In fact, Prof Sube Banerjee last week in the Brighton and Sussex Medical School as the new Chair of Dementia there voiced concerns about the relative ineffectiveness that antidepressants can have in dementia; this comes on top of previous concerns that antipsychotics may be relatively contraindicated in some patients particularly, and might even lower the objective quality of life of an individual with dementia.

It’s impossible also to ignore the effects that a diagnosis of dementia might potentially have on the ability of a person to drive a motor vehicle.

And a diagnosis of dementia might put pressure on well informed people concerning financial considerations through ‘lasting power of attorney’.

One wonders how the drive for diagnosis in primary care can enable a balanced discussion of all these powerful issues, against the background of this government policy to improve diagnosis rates of dementia.

At the tail end of Cathy Jones‘ excellent Channel 5 report, the lack of adequate funding of social care is raised.

Further details of Dr Cosgrove’s concerns are described clearly in this blogpost.

This policy as it stands could do much more damage than good,with many unintended consequences arising from false diagnoses.

But there are pressures at play which might give this policy a sustainable momentum for the timebeing.

Concerns about the paired associates learning test for dementia

To begin to understand how a cathode-ray TV set works, I could remove one component called the “transistor”, and the picture disappears. It would be an incorrect conclusion to say that the purpose of that transistor is to produce the picture. However, I could argue correctly that the transistor was somehow part of the system required to produce the picture.

If I showed the transistor was particularly “hot” while the TV set was on, producing a picture, it might be reasonable for me to conclude the transistor was involved in producing the picture.

This is the sort of basic approach still used to work out what is going on in the brains and minds of people with Alzheimer’s disease, typical presentations of which might be memory problems. You can see whether removing parts of the brain in humans produces similar effects to the problems in thinking found in Alzheimer’s disease. Or alternatively, you could just try to look at the system of components in the brain which might be contributing to memory in brains working normally.

TV set

Whatever, it’s a puzzle. In this particular case, it’s a puzzle to solve correctly.

An innovation culture in the diagnosis of Alzheimer’s disease

David Cameron praised Cambridge Cognition’s work in developing new innovative tests for Alzheimer’s disease in the G8 summit held towards the end of last year.

There has been concern that some individuals with Alzheimer’s disease do not receive their diagnoses in a particularly fast way. A number of explanations for this have been offered, including medical personnel not being able to spot the symptoms of Alzheimer’s disease easily.

It is also helpful to understand what an “innovation” is. An innovation might be a product which enables you do something much more easily, and depends for its success popular uptake by the user. Strictly speaking, paper was an innovation too. However, the rise in cost of diagnosing Alzheimer’s disease, arguably, is an intriguing example of “Baumol’s cost disease“.

Individuals with Alzheimer’s disease have memory problems which are typically not thought to be qualitatively similar to those found in ageing elderly individuals. Often such people have real problems in navigating around environments. It is clearly a very laudable aim to have a bedside test which might be able to alert a physician to an underlying memory problem in Alzheimer’s disease.

The benefits and concerns, and my passing involvement

There are a number of important caveats here. Not all dementias are Alzheimer’s disease. There are in fact hundreds of dementias, some of which are reversible. Whatever test is used, the test should be sensitive enough to identify reliably a genuine thinking problem in Alzheimer’s disease, but should not be so ‘broad brush’ the test also misattributes memory problems, say found in the ‘mild cognitive impairment’ or even depression, to Alzheimer’s disease. Such mislabelling can perceivably cause distress, and cause people to be caught up in the medical system for further lengthy tests when they should not have been in the first place. On the other hand, it is of concern that the diagnosis might be missed in some people, and hence the drive from the Department of Health and the Alzheimer’s Society in “The Prime Minister’s Dementia Challenge”.

I wish Cambridge Cognition well, not least because I have worked with CANTAB whilst a graduate student at the University of Cambridge. In fact, some of my papers are cited in their bibliography. Their search facility is here.


The CANTABmobile “paired associates learning” test

To explain the “paired associates learning” test from first principles, and I’m not using actual screenshots, imagine me presenting you with a number of blank boxes dotted around the screen.

Fig 1

And I open each box in turn and reveal a shape to you. I can present the problem with a varying number of shapes.

Fig 3     Fig 2

After showing you all the shapes, I then present to you a shape and ask you to identify the box in which it was first presented.

Fig 4

Cambridge Cognition in welcoming the Draft National Plan to Address Alzheimer’s disease in my opinion set out entirely correctly the advantages of this computerised testing battery; including fast, not culturally biased, not heavily loading on language, norm-referenced, culturally unbiased, and easy-to-use.

The reasoning behind it being sensitive to early Alzheimer’s disease – but what about mild cognitive impairment?

To understand why the narrative for the test being so attractive in early Alzheimer’s disease, you have to understand that this test has been found to be sensitive to functions of particular brain areas. If you chop out bits of the brain near the front of the head (frontal cortex) or near the ear (temporal cortex), performance on this task is impaired, as Prof Adrian Owen showed when he was a post-doctoral fellow (paper here). With hindsight, perhaps Owen should have looked at the effects of other brain areas further back in the brain, such as the parietal cortex, which are also now thought to be important in memory for spatial cues.

A consistent finding has been loss of brain cells in the “entorhinal cortex”, in the temporal cortex, early in Alzheimer’s disease (see for example here). Therefore, that the paired associates learning test should identify memory problems in early Alzheimer’s disease immediately makes intuitive sense.

But the issues I feel are much more complicated, and I wish Cambridge Cognition well in clarifying them.

If it’s not Alzheimer’s disease, what else could be causing the memory problems?

One possibility is “mild cognitive impairment”. It is described, for example on the authoritative Mayo Clinic website, that:

“Mild cognitive impairment (MCI) is an intermediate stage between the expected cognitive decline of normal aging and the more serious decline of dementia. It can involve problems with memory, language, thinking and judgment that are greater than normal age-related changes. If you have mild cognitive impairment, you may be aware that your memory or mental function has “slipped.””

David Hart, Senior Business Development Manager of Cambridge Cognition, kindly sent Dr Peter Gordon the rationale for the use of the CANTAB task by Dr Andrew Blackwell, their Chief Scientific Officer (as produced on Peter’s blog here).

Cambridge Cognition concede that distinguishing between MCI and Alzheimer’s Disease “is difficult”, but this is a distinction that must be arrived at otherwise a test potentially will give “false positives” – but no test is perfection, and it basically is impossible to strive for perfection. What we all trying avoid is where a test for possible dementia itself is expensive followed by a further expensive investigation to show the original result was a false positive – or as the Express euphemistically called it recently, “Dementia diagnosis proved wrong by new super scanner”.  (It is important to state clearly here that no details are given how a diagnosis had been arrived at previously for Ros Davies.)

To give them credit, Cambridge Cognition cite the Chandler et al. (2008) paper, but the full citation of this is “Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association Volume 4, Issue 4, Supplement , Pages T551-T552, July 2008″ – i.e. it is a supplement of abstracts not full papers. This particular abstract can be viewed here.

It is hoped that this full study will have been published elsewhere, and if so Cambridge Cognition will need to update their website with the full paper. Notwithstanding this, the numbers of individuals in each group are disappointingly low: there are seventeen with putative MCI and twelve with putative Alzheimer’s disease.

Is this task actually sensitive and specific?

However, the discussion by Dr Andrew Blackwell and colleagues in his 2004 paper is useful. I have more than a passing interest in that paper as the main author on that paper was one of my PhD supervisors at Cambridge, Prof John Hodges. John has also kindly written one of my three Forewords for my book, “Living well with dementia” to be published on January 14th 2014.

Blackwell remarks correctly that this task has been used to distinguish between unipolar depression and Alzheimer’s disease in Rachel Swainson’s study. But is this enough? I looked to the previous Beats study in “geriatric depressive”, and there was nothing forthcoming there. How confident can one be that only early patients with Alzheimer’s disease, and not those severely depressed or with an underactive thyroid, will perform abnormally on the PAL? Personally, I’m not at all confident yet, despite the Swainson study, but these fears can easily be allayed with a sensitivity/specificity study of much higher power.

Blackwell is however correct in citing my study with Dr Andy Lee in that patients with semantic dementia and behavioural variant frontotemporal dementia are relatively unimpaired, though the clinical presentations of the frontotemporal dementias can be quite clearly different in the clinic from Alzheimer’s disease. Completing the double dissociation, I did find that the behavioural variant of frontotemporal dementia did present with rather specific risk-taking decision-making of its own.

But in the meantime the comparison with frontotemporal dementias is useful.


Nonetheless, this approach is being rolled out.

On 28 June 2013, the use of CANTABmobile was described as follows:

“The Guildford and Waverley Clinical Commissioning Group (CCG) is leading the use of an innovative new iPad-based memory assessment  system as part of a national push to decrease dementia diagnosis waiting times and streamline the referral process.   Accessed through NHS medical professionals, CANTABmobile enables GPs to test a patient’s episodic memory through an easy to use and administer 10-minute cognitive assessment.”

The CANTAB paired associates learning test is pictured under the heading “intuitive touchscreen interface”. if you go to “download information” on this page.

It was covered in the national media here: for example Victoria MacDonald’s report (this page provides a criticism of another report by Victoria MacDonald this time over Prof Brian Jarman’s proposed HSMR data by NHS Consultant, Dr Jacky Davis).

So what does this task test?

In understanding how the task works in reality, I found a paper where Prof Ed Bullmore and colleagues put individuals with Alzheimer’s disease and control subjects performing the task into a scanner really helpful.  Bullmore and colleagues frontloaded their discussion with the following comment:

“Independent of the level of difficulty, the majority of subjects in both groups activated a network of brain regions, including the anterior cingulate, lateral, and medial occipitoparietal and frontal cortices, during successful encoding and retrieval.”

This is interesting as it doesn’t point to the usual suspects of the narrative, i.e. the entorhinal cortex and other parts of temporal lobe. Even Andrew Blackwell had described how the damage to the entorhinal cortex might possibly account dor deficits on the paired associates task:

“The transentorhinal region is a complex transitional area located between the entorhinal region proper and the adjacent temporal isocortex. It has been suggested that damage to this site in early [Alzheimer’s disease] disrupts reciprocal connections with the hippocampal formation and that this disruption underlies deficits in episodic memory.”

But on reflection is this wholly a surprise? Ed Bullmore and colleagues from their results, also from Cambridge, discuss that the lateral parietal activations reported during episodic memory tasks are thought to reflect recognition processes and retrieval processing of spatial information. Medial parietal activity has been proposed to underlie imagery and retrieval success.

I don’t feel it’s altogether surprising given what is known about the build-up of pathology in Alzheimer’s disease, either. The authors of one study looking at this report that:

“[18F]FDDNP-PET signal was significantly higher across widespread cortical regions in subjects with poorer neuropsychological test performances. Strong correlations were seen in the entorhinal, orbitofrontal, and lateral temporal cortices, temporoparietal and perisylvian language areas, parietal association cortices, and much of the dorsolateral prefrontal cortex.”

But the Sahakian lab elsewhere did find something was up with the parts in “the hippocampus and associated structures”, i.e. the structures in the temporal lobe, in this task.

But that study was only comparing MCI with normal controls. It did not include patients with Alzheimer’s disease. This is relevant, if you happen to believe that MCI ‘predates’ Alzheimer’s disease, as the authors of that study clearly do:

“Later in the course of the transition from MCI to clinical Alzheimer’s disease, functioning of the MTL deteriorates further to an extent that such compensatory activity is no longer possible. The hyperactivity in early MCI might then represent a possible predictor or biomarker of the progression to Alzheimer’s disease.”

But in the real world this is far from clear.

However, the evidence of progression of MCI (mild cognitive impairment) to DAT is currently weak. It might be attractive to think that MCI is a preclinical form of dementia of Alzheimer Type, but unfortunately the evidence is not there to back this claim up at present: most people with MCI will not progress to dementia even after ten years of follow-up (Mitchell and Shiri-Feshki, 2009). Drug companies have been trying hard to push the identification of “biomarkers”, possibly subtle psychological ‘deficits’, scan results or changes in substances in the fluid surrounding the brain (or cerebrospinal fluid). It is no accident that psychological testing and biomarkers were heavily promoted in David Cameron’s G8 dementia speech in Lancaster House at the end of last year.

In summary, I don’t think it can be taken as red that entorhinal cortex problems are causing the observed deficits in the CANTABmobile paired associates learning task.


Overall, my personal view is that the deficits on the CANTAB paired associates learning task are real in early Alzheimer’s disease, but possibly not for the reasons felt by some in their groups. Above all, I don’t care as such, as long as greater numbers of people benefit from a correct diagnosis of Alzhemer’s disease, but I do feel that the logic in their reasoning has gone a bit awry.

My academic viewpoint is utterly irrelevant actually, as above all I wish the whole of the medical profession well in their “war against dementia”.

I’d be the first to admit I’ve got it wrong. I am simply raising the issues in a constructive way that I hope is beneficial for the public interest.

But Dr Mitul Mehta, Reader in Neuroimaging at the IoP, does have his concerns.

Blurred lines in English dementia policy – privatisation in all but name

In case you don’t like the soundtrack, here are the slides.

To some extent, Europe resolved our dispute about whether we should aspire to an ‘early diagnosis’, or ‘timely diagnosis’ for dementia. The overall consensus from the European ALCOVE project was that a diagnosis should be timely, in keeping with the needs of the person with a dementia, his friends, his family or his carers.

This was an extremely helpful move in English policy, although the road had not been that clear.

One blurred line in the public was how dementia so massively became conflated with all memory problems in the elderly. Whilst it was argued that the memory problems in Alzheimer’s disease should no longer be passed off as ageing (and indeed there are strong cultural pressures elsewhere for calling dementia ageing), there was some concern from GPs that older people thought their memory problems were dementia because of the widespread media campaign. Many of these individuals were later to arrive at a diagnosis of minor cognitive impairment, underactive thyroid, or depression. Given that there are hundreds of different causes of dementia which can affect any part of the brain and brainstem (though they all tend to start off in different areas), it’s not altogether surprising that some of the dementias don’t present with memory problems at all.

The drive to make the diagnosis is almost certainly going to be affected by the policy from NHS England to achieve ‘ambitions’ for increasing dementia diagnosis rates. The evidence from the MRC study at Cambridge has demonstrated that this prevalence has in fact been falling over some decades, so there is serious concern that a drive to increase dementia rates will lead to a large number of false diagnoses in 2014. This is definitely one to watch, as a false diagnosis can lead to very serious harmful repercussions. Nonetheless, the number of people who have a MMSE in the region of 10-15 on initial diagnosis is, arguably, staggering, and blatant lack of diagnoses of more obvious presentations of diagnosis most people would agree is unacceptable.

The spotlight in G8, and certainly the presence of corporates there, will lead to increased scrutiny of those people who financially have much to gain from an early diagnosis. An early diagnosis may indeed lead to someone ‘accessing care’, even that care results from a personal health budget with treatments which are not proven clinically from the evidence. The direction of this particular plan depends how far individualised consumer choice is pushed in the name of personalisation. Genetics, neuropsychologists, and pharmaceutical private sector companies wishing to monitor the modest effects of their drugs on substances in the brain all stand to capitalise on dementia in 2014, much of which out of the NHS tax-funded budget. This of course is privatisation of the NHS dementia policy in all but name. One thing this Government has learnt though is how to make a privatisation of health policy appear popular.

Despite corners being cut, and the drive to do ‘more for less’, it will be quite impossible to avoid making a correct diagnosis in individuals thought to have a dementia in the right hands. A full work-up, though the dementia of the Alzheimer type, is the most common necessitates a history of the individual, a history from a friend, an examination (e.g. twitching could be associated with the motor neurone disease variant found in one of the frontotemporal dementias), brain scan (CT/MRI/PET), brain waves (EEG), brain fluid (cerebrospinal fluid), bedside psychology, formal cognitive psychological assessment, and even in some rarely a brain biopsy (for example for variant Creutzfeld-Jacob or a cerebral inflammatory vasculitis).

Analysis by paralysis is clearly not desirable either, but the sticking point, and a blurred line, is how England wishes to combine increasing diagnostic rates; and making resources available for post-diagnosis support; making resources available for the diagnosis process itself including counselling if advised. As the name itself ‘dementia’ changes to ‘neurocognitive impairment’ under the diagnostic manual DSM in 2015, the number of people ‘with the label’ is likely to increase, and this will be ‘good news’ for people who can capitalise on dementia. The label itself ‘neurocognitive impairment’ itself introduces a level of blur to the diagnosis of dementia itself.

The general direction of travel has been an acceleration of privatisation of dementia efforts, but this to be fair is entirely in keeping with the general direction of the Health and Social Care Act (2012). A major question for 2014 is whether this horse has now truly bolted?

When we know when “the war against dementia” is over?


In writing this article, I have no intention of ‘sanitising’ dementia. I’m mindful of two recent comments which fell in my path indirectly: “Dementia is such a cruel disease” (by a daughter of someone living with dementia), and “I don’t know of anyone who doesn’t suffer something as a result of his or her dementia”. The purpose of this article is just to review common motifs in dementia media communications.

When will know when the “war against dementia” is over? This is not an altogether frivolous question, as a MP once famously asked Tony Blair in Prime Minister’s Questions, “When will the war against terrorism be over?”

On 28 November 2013, about dementia, Jeremy Hunt wrote in the Telegraph: “It is a truly horrible disease“.

This set the ‘mood music’ for some of the G8 dementia conference, but the G8 conference was indeed a very positive occasion.

Recently, in “The Loss of Sadness”, Horwitz and Wakefield (2007) wrote that, while depressive disorder can certainly be a devastating condition warranting medical attention, the apparent “epidemic” in modern culture reflects the way the psychiatric profession (perhaps under the influence of pharmaceutical companies looking to widen markets) has understood and reclassified normal human sadness in the DSM-IV as a largely abnormal experience.

The popular metaphorical framing of dementia seems to operate on two levels. It is generalised as a vast, natural or monstrous force that we must “fight”, and it is also located as a very specific condition that affects individuals in extreme ways. In both cases, the effect is to make us feel both terrified and relatively powerless. As Terry Pratchett, who is reported in the public media as having a condition akin to posterior cortical atrophy, viewed: “People seem to think of Alzheimer’s as something rather terrible and dreadful, almost as if witchcraft is involved”

Literally meaning ‘‘away’’ or ‘‘out’’ of ‘‘mind’’ or ‘‘reason’’ in Latin, the actual term ‘‘dementia’’ entered the English language from the French ‘‘de ́mence’’ via the French psychiatrist Philippe Pinel, who made notable contributions to the categorisation of mental disorders in the late 18th and early 19th centuries. Over the centuries, the phenomenology of dementia has been causally associated with witchcraft, moral degeneracy, bad blood and a dissipation of vital energy from the brain, among other factors.

The Wordie for David Cameron’s speech at the G8 summit is indeed interesting, and to be fair in the vast majority is largely upbeat and positive. Whilst there is no recording of the speech on YouTube, the full text of the speech at the ‘G8 dementia summit’ at Lancaster House on 11 December 2013 is available here.


The opening to this speech was pretty chilling, however:

“It doesn’t matter whether you’re in London or Los Angeles, in rural India or urban Japan – this disease steals lives; it wrecks families; it breaks hearts and that is why all of us here are so utterly determined to beat it.”

What exactly is this “it”? What kind of creature is it which steals, wrecks and breaks? This is the fundamental problem. Dementia is not a creature, it’s not an alien, it’s not a mega monster even. It’s an umbrella term covering about 200 different conditions where parts of the brain lost structure and function, leading to problems for that individual; however certain functions remain in the earlier stages, which is why it is potentially unfair to use such graphic language.

It is therefore with some irony Jeremy Hunt had concluded his piece in the Telegraph thus:

“With advances in medical science, the commitment of governments across the world and a willingness from everyone to change attitudes, we truly can be the generation that beats dementia.”

And it’s not the first time David Cameron had used this turn of phrase. In his keynote speech about increasing funding for dementia, the U.K. Prime Minister talked about “the quiet crisis, one that steals at lives and tears at the heart of families” (March 26, 2012). As was noted at the time, this language echoes descriptions of primeval monsters such as Grendel in the Anglo Saxon poem “Beowulf”. Dementia becomes an invader or evil monster that creeps up on people and steals them from themselves. Correspondingly, people living with dementia correspondingly become “victims”.


Noticeably, the Wordie includes “malaria” and “AIDS”. This is because of the following line:

“In generations past, the world came together to take on the great killers. We stood against malaria, cancer, HIV and AIDS and we are just as resolute today.”

Jeremy Hunt in the Telegraph had written:

“In the Sixties people were too scared to talk about cancer. In the Eighties the same happened with HIV/Aids. After a long and painful journey, we are now much more open about both – and better able to tackle them.”

It seems that this parallel with HIV/AIDS and cancer has been very carefully choreographed. There are indeed some successful treatments for many cancers, but cancer like dementia is an umbrella term covering a wide variety of conditions. A “cure for dementia” is meaningless as a term, as the frontotemporal dementias particularly common in the younger age group are a different pathological entity to the most common type, the dementia of the Alzheimer type.

And how exactly has cancer done?  According to the world statistics from WCRF, there were an estimated 12.7 million cancer cases around the world in 2008, of these 6.6 million cases were in men and 6.0 million in women. This number is expected to increase to 21 million by 2030. How is a similar “war” against HIV/AIDS doing? According to AmfAR, more than 35 million people now live with HIV/AIDS, 3.3 million of them are under the age of 15; in 2012, an estimated 2.3 million people were newly infected with HIV, and 260,000 were under the age of 15. Every day nearly 6,300 people contract HIV—nearly 262 every hour.

Dementia has replaced cancer as the “scourge of modern times”. The discourses of the scientific community reinforce this pervasive sense of horror about the dementias. For example, the prevalence of dementias is described in dramatic terms as an “epidemic”. The prevalence of dementia in the UK has in fact thought to be falling in recent times (hence explaining the formidable Prof Burns’ relative unease about dementia being called a ‘timebomb’ by Emily Maitlis on BBC News, a ‘timebomb’ which crucially scientists have failed to address.)

In 2011 in an article entitled “Dementia crusade’s £20m breakthrough”, the Care Services Minister at the time announced a multi-million pound boost in funding for the fight against dementia. The word “crusade” achieves an interesting multiplicity of effects, including an emphasis on faith and battle and on something that not only is metaphysical but can also be “won.” The overall impression is of dementia as huge and ancient, and of massive significance. It appears beyond our grasp and can only be understood through reference to massive natural phenomena (usually disasters) or in biblical/mythical terms.

Flooding is a particular popular literary turn. The danger of flooding has long been associated with dementia. A 1982 UK report was entitled: “The rising tide: Developing services for mental illness in old age“. Rising tides continue to inform the language of contemporary politicians when discussing dementia.

Cameron likes it too, apparently. He referred to the need for Britain to change its attitude to the “rising tide of people suffering with dementia” (May 26, 2012). Alistair Burn’s article “The number of people with dementia in England: turning the tide – Alistair Burns” continued this “tide” theme.

The press and television documentaries abound in “personal” stories about dementia and in tales of cures that are imminent or preventative measures that can be taken to ward it off. Classifying the hundreds of different types of dementia has also been politically powerful. It has undoubtedly facilitated funding and research into diseases for which it is implied that there will eventually be a cure. Ultimately, this broad brush approach is now being used to argue for a “one glove does not fit all” approach: the big corporate winner of personalised medicine, as explained by Cameron thus:

Take just one initiative – Bio Bank. More than half a million people have volunteered to take part in this providing blood samples, getting their vital signs checked, so we can see how diseases like dementia get signalled. The plan is to use Bio Bank to take brain scans of up to 100,000 people – allowing us to see the earliest stages of Alzheimer’s and other diseases. That is the kind of ambition we’re seeing here in the UK ambition that should give hope to people right around the world.

There’s something subtle at work here with the words “ambition” and “ambitious”. Of particular concern to those worried about overmedicalisation is that some experts are now arguing for treating asymptomatic (‘‘normal’’) people with ‘‘abnormal’’ imaging and cerebrospinal fluid biomarker profiles with long-term preventative therapies. This is exactly what seems to be happening here with Cameron’s comment. In a sign of desperation of Pharma wishing to resurrect an ‘ailing industry‘, multi-national Big Pharma believes that early treatment is key to finally achieving a treatment success of any meaningful magnitude.

There are some expected financial memes: like “economy”, “genomics” and “reinvest”. Whilst the spokesmen officially don’t officially promote particular ‘brands’, the speech explicitly mentions UK life sciences companies, like Ixico, Cambridge Cognition, Psychology Online and Proteome Sciences, in developing new tests for Alzheimer’s Disease. As such dementia can’t be seen as “wealth creating”, so the need to promote private markets and innovation is a delicate one to take. However, David Cameron has increasingly appeared giving speeches in the manner of CEO wishing for corporate investment. As such, ‘cure’, not ‘care’, is where the money is at possibly. Cure’s in the wordie; care is not.

“Fight” is THE BIG prominent word. This recurring linguistic device in the cultural framing of dementia is the reliance on military and war-like metaphors. Cameron has been fighting for some time, it’s a wonder he himself isn’t exhausted. On March 26, 2012, he proclaimed rather triumphantly: “We need an all-out fight-back against this disease; one that cuts across society.”

The dementia “time bomb” crops up frequently in U.K. broadsheets and other tabloids. Time bombs are devices that could go off at any time; their most common use has been in politically motivated terrorism. The association of dementia with terrorist tactics is fascinating, invoking the sense of a threat. So when will we know when the war against dementia is over..?

Now listen carefully. As sure as night follows day, academics won’t be able to fight these horrible journalists, destroying the ambitions of people trying to live with dementia in a positive light. Whilst the electoral timebomb continues to tick tock, we can find a cure for this government and their partners trying to demonise those people currently trying to live with dementia. While the war will be long, we can turn the tide on the Pharma companies destroying minds with their false promises, and encourage a new dawn after this crisis where wellbeing interventions are treated seriously at last.

See what I did there?

Why I wrote ‘Living well with dementia’


Living well with dementia: the importance of the person and the environment for wellbeing” is my book to be published in the UK on January 14th 2014. I have written it on my own, but I have drawn on the published work a number of Professors working in the field of dementia have sent me. I hope the advantage of having an overview of their research programmes has been to put together with one voice where exactly this approach might be heading using the most contemporary published papers. I am enormously grateful that these busy Professors were able to supply me with their recent papers.

I was asked by my publishers to provide pointers about what a “marketing strategy” for this book might be. I can honestly say that, having given considerable time to thinking about this issue, I have no intention of pursuing a conventional promotion of my book. I don’t intend to do nothing, but I can confidently say that this book will be widely read. I have no intention of flogging it to commissioners, who will have their own understanding of what health or wellbeing is in the modern construct of NHS England’s policy.

I do, however, have every intention of addressing what I think is a major shortfall in the medical profession in their approach to dementia. Their emphasis has been, where done well, the exact diagnosis of dementia through an accurate history and examination of a patient, with appropriate investigations to boot (such as a CT scan, MRI, lumbar puncture, EEG or cognitive psychology). The combined efforts of Big Pharma and medics have produced limited medications for the symptomatic treatment of memory and attention in some dementias, but it would simply be a lie to say that they have a big effect in the majority of patients, or that they reverse the underlying the disease process consistently and robustly.

But that’s the medical model, and certainly the ambition for a ‘cure’ is a laudable one. I found the recent G8 dementia summit inspiring, but a bit of a distraction from providing properly funded solutions for people currently living with one of the hundreds of dementias. Many of us in the academic community have had healthy collaborations for some time; see for example one of the Forewords to my book by Prof Facundo Manes, Chair of Research of the World Federation of Neurology (Dementia and aphasia). To say it was a ‘front’ for Big Pharma would be unnecessarily aggressive, but it has been openly admitted in the media that a purpose of the summit was to assist ‘an ailing industry’.

I think to emphasise what might be done for future patients of dementia would be to fail to maximise the living of people with dementia NOW. By this, I mean a correct and timely diagnosis of an individual, the suggestion of appropriate assistive technologies and innovations, appropriate leisure activities, and the proper design of a positive environment (whether that be a ward, a house or external environment).

My book is strongly footed in current research, but I openly admit that research does not have all the answers. I should like there to be a strong emphasis also in non-pharmacological approaches, such as the benefits of life story and reminiscence, art or dancing. Lack of current research certainly does not make these approaches automatically invalid, particularly when you consider the real reports of people with dementia who have reported benefit.

The main reason is that I do not wish to organise attendance in a series of workshops or conferences about dementia is that I do not wish to be perceived as selling a book. I am more than happy to talk about the work if anyone should so desire. A number of my friends are very well-known newspaper journalists, and I deliberately have not approached any of them as I consider this might be taking advantage of my friendship. I haven’t approached dementia campaigners, or other dementia charities, as I don’t wish to get involved in some sort of competition for other people’s attention. I haven’t sought the ‘celebrity backing’ of some senior practitioners in dementia, although Prof John Hodges (a world expert particularly in the frontotemporal dementias) kindly wrote one of my Forewords. If people wish to discuss the issues in a collaborative manner to take English policy further, I’d be delighted.

At the centre of this book is what an individual with dementia CAN do rather what they cannot do. If you’re looking for a cogent report into the medical deficits of people with dementia, you’ll be sorely disappointed. I spent about 10 years of medical training at undergraduate and postgraduate levels, without having heard of personhood or Tom Kitwood’s work once. I think this a travesty. As a person who is physically disabled himself, the need to understand the whole person is of massive personal significance to me. I think that, beyond doubt, future training of anyone in the caring professions, including medicine, will have to start with understanding the whole person, rather than seeing a patient with a series of problems to be cured or symptomatically addressed.

No academic, practitioner, or charity can have a monopoly of ideas, which is why I hope my book will be sincerely treated with an open mind. People have different motivations for why they get involved in dementia; for example, a corporate wishing to be part of a ‘dementia friendly community’ through a charity might have a different guiding principle to an academic at a University wishing to research from scratch some of the fundamental principles of a dementia friendly community. Despite all the “big players”, nobody can match up to THAT individual who happens to be living with  dementia; that person is entitled to the utmost dignity and respect, as brilliantly expressed by Sally Marciano in her powerful Foreword.

I am hoping very much to meet up with some personal friends that I’ve met in the #dementiachallengers community on January 18th 2014, and this is as close as I’ll get to the book launch. But I hope you will find the book readable. I don’t feel that there’s any other book currently available which bridges these two totemic topics (dementia and wellbeing); but I hope there are other good reasons for reading it!


The G8 dementia Summit: the comparison with the botched NHS reforms is striking

frail hands

This week,  to great fanfare, the G8 hosted its summit on dementia. Indeed, that the G8 were discussing a single condition was indeed remarkable. That they were joining forces to consider working together on this inspired hope.

What was unforgiveable was the sheer volume of myths about dementia which were pedalled though by the media. Prof Alistair Burns to his credit gave an answer in an interview by Emily Maitlis explaining how dementia prevalence rates appeared to be falling, in response to the backdrop set up by media memes such as ‘timebomb’. Many were left extremely angry on account of the lack of balance, completely distorting the picture such that any idea of someone ‘living well with dementia’ became a rarity.

What was not expected was a sanitisation of advanced dementia, but even there there was not a discussion of end of life care. In fact, there generally was no discussion of a minimum safe level of health and social care in any of the countries. The media pushed hard ‘a cure for dementia by 2025′, which major Alzheimer’s societies had signed up to. The claim is complete and utter rubbish, as there are over a hundred different types of dementia; the public were unashamedly being sold a pup.

The English health system, the National Health Service, has an obsession with ‘efficiency’. So much so it will happily fork out to pay one for one junior doctor covering all the general medical hospital every night for a week, and that junior doctor doesn’t stop all night. Sometimes that junior doctor will be expected to cover the wards too. Cover by nurses can be equally ‘lean’ during the weekends too.

The obsession with measuring ‘I want good care’ and regulation is akin to a teacher who has forgotten to teach but can set regular assessments. When the system is set up to run everything with much less doing a lot more, it’s possible something has got to give. And this is of course precisely what happened at Mid Staffs.

And yet out of the blue there appeared a 493 page document ultimately called the Health and Social Care Act (2012) which had nothing to do with this most important point about patient safety. There is not even a single clause to do with patient safety (unless  you include the clause abolishing the National Patient Safety Agency). The medical Royal Colleges were not involved. The BMA was not involved. And yet the Act of parliament, outsourcing and privatising the NHS, is just what the Corporate ordered.

This is what is known in the (business) trade as an ‘opportunity cost’ where money and efforts could have been better spent elsewhere. In this particular case, despite a promise of ‘no top reorganisation’, there was a £3bn reorganisation.

When attending a medical ward, you have to go to the sick patient first. You have to prioritise. If there had to be an unannounced reform of the NHS, outsourcing it was not the priority. The latest survey even shows that the public don’t especially like private providers doing NHS work.

Likewise, the priority for dementia care should have been investment in the social capital of caring. Too often carers are embattled with the biological, financial and legal considerations of caring. Many carers are themselves on zero-hours contracts. The G8 dementia summit was a great opportunity to confront that.

It didn’t. Instead, with alarming synchrony, the G8 leaders came together to sing off the corporate script. Vivienne Parry with effortless ease choreographed a seemingly spontaneous discussion about well rehearsed arguments for the need for ‘big data’, global data sharing, genomics, and personalised medicine, for much of the day. Prevention was of course discussed, but this is of course intimately wound up with the collection of information about the person, and the use of that other pet subject, biomarkers.

And more research is not better research, in the same way bigger information is not better information. If research monies are diverted into data analysis, genomics and personalised medicine, these monies will be diverted away from research into caring for example. One wonders whither the ‘cure for dementia’ will actually go, unless they have another fifteen years to look at slowing the progression of Alzheimer’s disease. The evidence that cholinesterase inhibitors, a class of drugs used to treat symptomatically memory and attention problems in Alzheimer’s disease, has a beneficial effect on slowing disease progression is as low as it possibly can be after nearly 20 years of expensive research in this area.

The G8 summit, like the Health and Social Care Act, was ‘corporate capture’ at its best, so if you’re angry, well done, that is the appropriate emotional reaction!  If you were wondering if you’d accidentally missed the discussion of carers and how they would be involved until 2025, don’t worry, you hadn’t. They weren’t there.