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Are we there yet? The road to the dementia cure is paved with biomarkers.

This was the CORRECT entrance – the Eastern entrance.

If you come to the ExCeL centre in anything other than a black cab, you will be circling the complex for hours before you set foot in an entrance.



Make no mistake – this particular conference was intensely scientific. But it was nice to sink one’s teeth into the something other than the dividend-producing engagement and empowerment of the dementia industry.




Being a card-carrying academic, I personally think there is a lot to boast about in terms of the quality of neuroscience being done globally for dementia. Unfortunately, the genuine advances in the socio-economic-legal policy are dwarfed by a vocal minority of people with massive egos, who have a pathological addiction to introducing themselves to members of their inner circle.

But the good guys were there in force – mainly my Specialist Registrars from 2002 who had now become Professors in dementia at Queen Square.

Take Jonathan Schott.



Or Huw Morris.

(I was especially glad to hear there is now a palliative nurse specialist in the progressive supra nuclear palsy service.)


Prof Martin Rossor – our boss – in fact tapped me on the shoulder as I was walking along one morning. I thought it was a security guard at first!



So there are many reasons to be cheerful.



#AAIC17 for me was total heaven. The enthusiasm of the researchers was authentic and deep, and the camaraderie was inspiring. I still think this was one of the best slides in the whole conference, presented by Prof Philip Scheltens.



The mild cognitive impairment (MCI) continues to be rather fraudulently in my opinion as a ‘staging post’ to dementia, and there indeed to be some professionals who cannot even tell the difference between MCI and dementia. This is rather worrying.



The narrative of the ‘conversion’ has been far too overblown – with nearly hyperbolic remarks on its importance in the lifecourse trajectory in the Lancet Commission which emerged at the end of the conference. The Commission curiously contained a reference to mild behavioural impairment – legitimising of course the self-entitled pronouncements of the medical profession of ‘what is normal’ when it comes to behaviour or cognition.

I agree with the Aunt Sally argument that there is some behaviour which is clearly abnormal (though in Cambridge it was hard to tell as there were indeed some people who had won the Nobel Prize more than once).  But one has definitely to be worried about human beings being drugged up to the eyeballs for being a ‘bit apathetic’ or a ‘bit depressed’, on the off chance he or she might develop dementia one day.

I found the Conference quite relaxing, like some package holiday one had been waiting patiently for for months.



My questions at the poster sessions ranged from ‘Where do you park your car at Addenbrooke’s?’ to ‘How long does it take you to do a lumbar puncture?’ Unfortunately, the young postdoc had no idea how long lumbar punctures took, despite her poster being all about CSF TDP43 markers and diagnosis – but she knew the junior doctor had done them all for her.

This is in a sense how idealised and pie-in-the-sky some of the international research has become – the need to focus on a chemically accurate diagnosis, whatever the symptoms are.

Like everyone else, I was there to flog something – my book in fact – available from all good bookshops, but possibly not from the Big Charity in dementia as yet.


And this person is a genuine ‘consumer’ of books of mine and Kate Swaffer, who sits on the World Dementia Council and is CEO of ‘Dementia Alliance International’ – the largest stakeholder group of people living with dementia in the world, the partner organisation of Alzheimer’s Disease International.



It was great to see Kiki from Kenya, who is doing great work on the World Dementia Council – and also a friend of ours.






Everyone knows that the current state of the amyloid hypothesis is a mess – for example, “the drugs don’t work” and there are people around who have loads of amyloid plaques and better cognition than you or me. But why spoil a good story? The feel good factor, like you get in a Billy Graham convention, is of course what conference goers in dementia lap up.



It was nice to see the Lewy Body Society – they have ALWAYS supported my work, and included me. And I am interested very much in Lewy body dementia, and I think Prof Ian McKeith is great.




The members of the Alzheimer’s Research UK team were fun all week – and it was great to see Hilary Evans (and George).

The work being funded by ARUK in neuroscience is of course a complete contrast to the lack of good neuroscience, apart from on cholinesterase inhibitors, which emerged in the Lancet Commission on dementia. The Lancet Commission on dementia seemed to confuse seamlessly whether the authors were discussing Alzheimer’s disease only at one minute, or >100 different types of dementia at another minute. But then again – for some researchers – the Alzheimerisation of dementia was complete long ago.

There was barely any sensible comment on the neurobiology of sleep in dementia, for example, the mechanism by which sensory impairment might lead to Alzheimer’s disease or any other form of dementia, or any meaningful biological mechanism of ‘cognitive reserve’ even though discussed at some length.



But I really  should’ve been concentrating on the basics – as for half of the week, I entered the ExCeL centre through the wrong entrance.



This was, however, one of my favourite posters. There is much to be said about how genes, prominent in the development of the human central nervous system, behave in dementia. I know notch-3 because of its rôle in vascular cognitive impairment, specifically CADASIL, but I found Lavinia Alberi Auber’s work as a PI brilliant.


Lavinia was extremely knowledgeable about notch (and Wnt and wingless) as you’d expect her to be.



This was another amazing poster by Kirsty McAleese.

Definitely a star in neuroscience for the future.


The importance of the poster for people interested in how the parietal cortex goes wrong in posterior cortical atrophy cannot be overstated.



I’m a huge fan of the work of Prof Seb Crutch – so I was immediately drawn to these striking results on the neural substrates of posterior cortical atrophy.



Kieran presented his brilliant work on the factors affecting the prescription of anti-psychotics.



The content and tones varied a lot – so one minute it was Kirsty’s poster, and then it was Assoc. Prof. Lee Fay-Low with a sensational talk on dementia policy.

Seeing Prof Henry Brodaty walking around was exciting as seeing Bob Dylan in person.


It was great to see some familiar friends, and now good friends, like Prof Dawn Brooker.

Dawn promised to help me with the parts of my new book ‘Essentials of dementia’ I’m doing with Prof Rob Howard that Dawn proposed herself – like “The VIPS model”. We ended up having quite a relaxing chin-wag about Namaste care and the issues of ‘process consent’ (but how Prof Jan Dewing’s work had helped a lot.)



I looked carefully at Barbara’s poster on behalf of some geriatricians who strongly support the bedside ‘clock drawing test’ for dementia.



With the ‘greater awareness’ of dementia (however-so defined), there is going to be a varying perception of risk.

I’ve always liked Dr Richard Milne since we first met in Newnham College in Cambridge for a mini-conference on dementia.


And his poster was a crowd puller – as well as really important work if we want to get people interested in slowing the progression of dementia in those people who’ve been newly diagnosed with it.



One hopes that the urge to publish something ‘big’ on dementia during #AAC17 was not primarily due to the lack of progress on novel neuropsychopharmacological cognitive/behavioural interventions (and a big Phase III trial result) – but of course I would never be so cynical.



It makes intuitive sense that dementia develops long before the existence of symptoms. In other words, brain changes which lead to dementia are already setting foot in people when they are young.

But the problem with framing it as ‘this can prevent you from getting dementia’ argument is precisely what somebody living with Lewy body dementia once told me – “Shibley, I did none of that, and I still have dementia.” It is far better to frame the approach as risk reduction.

Baroness Thatcher and Harold Wilson were both highly educated Prime Ministers, having gone to a University called Oxford University.

And they both developed dementia.








There will be people who live ‘virtuous lives’ and who still go onto develop dementia.



Quite amazingly, there is no mention of “determinants” in the main body of the text – and inequalities is only mentioned once in the text of the Lancet commission. This is simply not acceptable if one is taking seriously a life course analysis.

I was left genuinely wondering whether this Venn diagram from the Lancet Dementia Commission could’ve been easily adapted for frailty – but this thought is an artefact of the Commission consisting of the ‘great and good’ in that particular disease operating in rigid silos.
















For example, there as a huge amount on abuse in the Lancet Commission but nothing on deprivation of liberty safeguards. Academics work too in their own silos, promoting their own research grants too much, meaning that the work can too easily distorted and biased.

There is never any discussion of how the Wishlist for statistical analysis is derived (except the statement “We sought to calculate a combined PAF for known modifiable risk factors for dementia. We decided which risk factors to include by identifying those listed in the UK National Institute of Health and Care Excellence (NICE) and US National Institutes of Health (NIH) guidelines” is bordering on the too whimsical.)

There is never any discussion of the degree of independence of the factors (e.g. diet and diabetes), so consequently the results and discussion appear much more precise than they deserve.





Prof Rob Howard’s talk was exceptionally useful – given how thorough and methodologically sound it was. But the acoustics were terrible.




And the lack of sensible discussion in the talk and the paper on the factors affecting ‘social vulnerability’, such as the effects of poverty, poorly organised health and social care systems – genuinely troubled me. One of the questions in the audience alluded to whether the report was too medical – and I wonder about this too.


Even though the panel discussion of social vulnerability in the launch was poor in response to my question generally, Prof Alistair Burns correctly referred to the section of the paper which does indeed refer to social vulnerability – that is, of course, depression. (This impacts on social networks, loneliness and inclusion, discussed elsewhere in the paper.)


There is no mention of “advance decisions” or the “United Nations Convention on Rights of Persons with Disability”, and only a mention of human rights in relation to abuse, which lead to me to conclude that the The Lancet Dementia Commission did not understand at all the legal field of substituted decision-making and the full importance of autonomy.  But having said that the discussion of advance care planning, and the importance of palliative care/end of life, was exemplary in my view.






If you’re genuinely interested in research, this conference is really for you. I had a thoroughly enjoyable and all too brief chat with Prof Ken Rockwood. Ken’s work is extremely well known to me – and I am particularly looking forward to discussing the work of Ken and of colleagues in Dalhousie University, Nova Scotia, in my book ‘Frailty: from assets and deficits to resilience’ for next year (Prof Ken Rockwood and Prof Adam Gordon are doing the forewords.)



It was great to meet people I’d never met before – including Dr Joe Kane, a SpR in psychiatry with an interest in Lewy body dementia.


Some people transcend all whinges I have – because they’re such decent people.

Chris Roberts is the best.





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