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Kate Swaffer is admitted onto the World Dementia Council

KS

 

Late on Wednesday it was announced that the decision has been taken to admit Kate Swaffer to the World Dementia Council.

Kate Swaffer is Chair of Dementia Alliance International (“DAI”), which is a leading non-profit group of people with dementia from all around the world that seek to represent, support, and educate others living with the disease. DAI is an organisation that will provide a unified voice of strength, advocacy and support in the fight for individual autonomy and improved quality of life.

 

Kate, from Adelaide in South Australia, was diagnosed with semantic dementia – a form of fronto-temporal dementia – in 2008 at the age of 49.

Since getting her diagnosis Kate has become a campaigner, speaker and accomplished writer on dementia issues. In January 2016, her book ‘What the hell happened to my brain?” was published, and has rapidly become a landmark contribution of a detailed account of a lived experience with dementia.

In this excerpt from her first book about dementia, What the hell happened to my brain, Kate Swaffer has written this:

Subsequent to my being diagnosed with younger onset dementia at the age of 49, health care professionals and service providers all told me the same thing: “to give up work, give up study and go home and live for the time I had left.” On the way, it was also suggested I put my end-of-life affairs in order – even though at no time was I told dementia is a terminal illness. I was also told to get acquainted with aged care, including selecting a respite day care and residential care facility, sooner rather than later, so I could become used to it. My husband was told he would soon have to give up work to become a full-time family carer.  

Very quickly I termed this Prescribed Disengagement™, and thankfully I eventually chose to ignore it. Because Prescribed Disengagement™’ is a term I came up with, I was advised to trademark it before someone else did, and hence have done so.

Kate last year was awarded a distinction in her Master of Science in dementia care from the University of Wollongong.

 

The statement from the Dementia Alliance International reads as follows.

Dementia Alliance International (DAI) Chair Kate Swaffer from Australia has today officially become a member of the World Dementia Council, the second person with dementia to join this council. This is an important and significant appointment for DAI, and for people with dementia globally.  She joins another DAI member, who is also Vice Chair of the European Dementia Working Group, Hilary Doxford from the UK.”

Established by the last UK government, the World Dementia Council has the stated mission to champion dementia research and development and unlock investment around the world.

 

The membership of the Council is currently wide-ranging, but includes senior figures in dementia policy internationally.

On 16 October 2014, I wrote an open letter to DAI members which was indeed published on the official DAI blog, establishing my wish for the World Dementia Council to have members who are currently living with dementia. At the time, there were no such members, despite there being 47.5 million people estimated to be currently living with dementia in the world.

 

Kate’s admission to the World Dementia Council is a highly significant event.

DAI has been working towards full access for people with dementia to the United Nations Convention on the Rights of Persons with Disabilities (CRPD), which is a global tool for achieving social change, this second appointment is particularly significant. Article 19 of the Convention is the right to live independently and to be included in the community. Indeed, Prof Peter Mittler is due to be presenting on this, on behalf of DAI, at the Alzheimer’s International Conference in Hungary in April 2016.

Article 29 on “participation in public and political life” enshrines an obligation for State Parties “to persons with disabilities political rights and the opportunity to enjoy them on an equal basis with others, and shall undertake to ensure that persons with disabilities can effectively and fully participate in political and public life on an equal basis with others.”

 

The four major prongs of the World Dementia Council’s work currently are integrated development, “optimising the path of medicines from research through to market by reducing barriers & encouraging regulatory flexibility”; finance and incentives – “looking at ways to increase the relatively low investment in funding dementia innovation by exploring new types of funding product”; open science – “unleashing the potential of open science for sharing information and knowledge to accelerate progress in developing new treatments and care approaches”; and public health/prevention – “The Council is also beginning an evidence review into existing research on how risk factors such as diabetes and heart disease relate to dementia, as well as looking into public health messaging on lifestyle and prevention.”

Even with the development of new drugs to delay the progression of the dementias, the leading cause of which is Alzheimer’s disease in the world, the need for prevention of progression of diseases through both cognitive and non-cognitive therapies will be essential. Kate’s input as a person living with dementia and as an accomplished student of dementia herself will be unique.

 

 

 

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Kate Swaffer is clearly a world class ambassador for living beyond dementia

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Err… since this photo was taken in the Hotel Adina, opposite the conference centre hosting the Alzheimer’s Disease International (ADI) conference for 2014, I have lost a lot of weight (I wish.)

But actually literally seconds before this snap was taken, Kate had said ‘you goose!’ in utter surprise when I suggested to Kate she should turn her roaming charges off. We were, of course, both in Australia, and the country of habitual residence of Kate is also Australia.

I have many happy memories of that conference, though overall I tend to be antagonistic of conferences. Most of the plenary speakers tend to be overwhelmingly underwhelming.

There are of course some exceptional speakers. I always enjoy the updates on Prof Martin Prince on epidemiology of dementia, with a focus on low and middle income countries. I know this is a complicated area, as I am sure Prof Carol Brayne from my alma mater will demonstrate in Budapest for this year’s ADI conference.

Many of the pervasive issues internationally about living with dementia also relate very much to domestic jurisdictions: including research, drug therapies, timely diagnosis, care and support, enhancing health, and dying well.

Sometimes it can be all too easy to become an innocent pawn in massive corporate agendas, which sometimes tragically reveal themselves in slick ads from ‘big charity’, raising money, but pushing stigma of dementia to do so.

I first spoke with Kate over a rather greasy lamb moussaka. Beth was there. Beth and Kate took a mutual interest in what the restaurant had to offer.

I showed Kate the manuscript of my first book expecting her to be wholly uninterested in it: actually, the opposite was the case.

Kate’s background is not straightforward. A devoted mother and wife, haute cuisine chef (trained with the best people in this field), a distinction in dementia care from a world famous University, nurse specialist in operating theatres, volunteer in bereavement counselling, and, of course, keen international speaker on dementia.

I think Kate manages to update her blog every day, and has introduced an unique term called ‘living beyond dementia‘, which sums up a positive and flourishing approach – novel and original – setting aside the negative aspects of the impact of the medical profession in imparting a diagnosis.

Kate was the first person in the world to coin the term ‘prescribed disengagement‘ which was a huge impact in the field of dementia.

As Kate says, “This Prescribed Dis-engagement(TM) sets up a chain reaction of defeat and fear, which negatively impacts a person’s ability to be positive, resilient and proactive.”

“Dementia is the only disease or condition and the only terminal illness that I know of where patients are told to go home and give up their pre-diagnosis lives, rather than to ‘fight for their lives’.”

It is all too easy to become ageist about dementia, but it is the case that dementia encompasses conditions of the age which can affect people below the age of 65. Particular considerations for the so-called ‘young onset dementia’ might include how the diagnosis is arrived at, as well as subsequent impact on real lives such as family or employment.

I personally don’t think that academics can have the moral integrity to present the full picture, when what is truly valuable and a scarce commodity is the expertise and lived experience of people living with dementia.

I think it goes further than ‘working with not for’ in fact: it is more of a question of ‘who’s in the room’ at all. I think of the co-production imperative as ensuring there are ‘no more throw away people’ as per Prof Edgar Cahn. This, as Prof Peter Mittler reminded me recently, has a parallel in the inclusivity literature as ‘No one left behind’.

And above all – it is clear people having had a diagnosis of dementia feel great comfort from the experiences of other people in similar circumstances who have reconfigured their lives accordingly. Indeed this should be the analogous to how people with physical disability are given ‘reasonable adjustments’. Whilst reasonable adjustments is a rather legalistic clunky term, it is an aspect which has been seriously lacking in the drug-focused medical model of dementia.

Kate Swaffer, not just living with a dementia, has an important narrative to tell, which is continually evolving. It is totally unsurprising that her being Chair of Dementia Alliance International (DAI), an international stakeholder group for people with dementia, has been welcomed as a huge success by Alzheimer’s Disease International.

It always seems like a marathon not a sprint, and a long one at that. I thought it was unbelievably clumsy that the World Dementia Council, a steering group on world dementia work, did not have a single representative living with dementia currently.

I indeed wrote an open letter on October 13 2014, which is on the DAI website here. I was of course ecstatic when Hilary Doxford, a mutual friend and colleague, was appointed onto the WDC, as documented here.

Kate is a world-class advocate for people with dementia, and, take it from me, a force to be reckoned with.

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Once bitten, twice shy? No – we should remain cheerful about dementia research.

The idiom “Once bitten, twice shy” is well known to all of us: “When something or someone has hurt you once, you tend to avoid that thing or person. ”

There are 47 million people living in the world with dementia.

Alzheimer’s disease is the most common cause of dementia around the world. It inevitably takes up the ‘lion’s share’ of interest, but it’s important to note that there are many other people living with other types of dementia, for example, frontotemporal dementia, we have to meet the needs of as well.

Let me lay my cards on the table.

I think it’s possible to create an environment such that people living with various dementias can be at their best, whether in work or not. I feel the emphasis must be on acknowledging dementia as a disability; and, from this, arises a mature conversation about reablement and rehabilitation.

But likewise I don’t think we should be subsumed with previous failures in neuropharmacology for us to ‘give up’ on medications which might ‘stabilise’ any underlying disease processes in dementia. I don’t think we should subject them to hyperbole either, but when there are glimpses of hope we should not be in the business of extinguishing hope.

I think one of my greatest privileges of all time was a chance to sit next to César Milstein at dinner in Cambridge.

The story of monoclonal antibodies is also well known.

Monoclonal antibodies were pivotal in medically treating a person who’d contracted Ebola.

Monoclonal antibodies are proteins that recognise and fight “aliens”, such as bacteria or viruses. Since the early twentieth century scientists had been keen to produce large amounts of antibodies specific to a particular target for research or clinical purpose, but with no success.

However, in 1975 César Milstein and his colleague Georges Köhler at the MRC Laboratory of Molecular Biology in Cambridge developed a way to produce monoclonal antibodies by fusing myeloma cells — a type of cancerous immune cell — with mouse spleen cells that had been exposed to a target. As well as creating a research tool for investigating the immune system and the pathways of disease, this innovative research also laid the foundations for the production of antibody-based drugs against specific diseases.

Cesar

But this initial success has inevitably caused others to raise their game.

First identified by Alois Alzheimer in 1906, Alzheimer’s disease is an irreversible, progressive brain disease that slowly destroys memory and cognitive skills (Alzheimer, 1096).

Accumulation of Aβ (“beta-amyloid”)in the brain, manifesting as β-sheet rich plaques, is a hallmark of Alzheimer’s disease. Attacking amyloid plaques in symptomatic patients is sometimes referred to as ‘too little, too late’.  (However, it has also been suggested that plaques may be the body’s way of sequestering the toxic Aβ oligomers.)

I first became interested in amyloid because of its effects all over the body, but its effects in the brain are extremely noteworthy.

Eli Lilly & Co.’s drug solanezumab, and bapineuzumab – a drug developed jointly by Pfizer Inc., Johnson & Johnson and Elan Corp. – had also targeted amyloid plaques.

The prediction that “immunotherapies” targeting soluble Aβ oligomers will elicit clinical benefit is supported by studies of human Aβ autoantibodies, of which only a subset appears to be ‘disease-protective’ (in particular, the subset that preferentially recognizes Aβ oligomers) (see papers by Dodel et al., 2011; Moir et al., 2005).

Thus, immunotherapeutics with high selectivity for soluble Aβ oligomers, which resemble these protective auto-antibodies, might be expected to deliver a clinical advantage compared with the non-selective immunotherapies in clinical development?

One important caveat when considering the activity of Aβ assemblies is the dynamic nature of the aggregation process.

Initial studies clearly demonstrated that aggregation of Aβ was essential for toxicity, but characterisation of the assemblies used was limited and it was assumed that, because amyloid fibrils were detectable, it was fibrils that mediated the observed toxicity.

Yet, this appeared inconsistent with a finding that there might be actually a relatively weak correlation between the severity of dementia and the density of fibrillar amyloid (Terry et al., 1991).

In contrast, robust correlations between the levels of soluble Aβ and the extent of synaptic loss and severity of cognitive impairment have been fairly consistently demonstrated (e.g. Lue et al., 1999; McLean et al., 1999) – the term soluble Aβ refers to all forms of Aβ that remain in aqueous solution following high speed centrifugation of brain extracts.

It has been critical, some argue, to re-ignite the interest in finding a pharmacological means of stabilising dementia of the Alzheimer type, in light of recent clinical failures of several high-profile experimental therapeutics for dementia of the Alzheimer type, and the high risks and costs of such development endeavours.

The work of Dr Dennis Gillings and colleagues at the World Dementia Council has definitely kept a show on a road.

The recent clinical failures also have intensified scrutiny of the ‘amyloid cascade hypothesis’, which spawned many of the recent experimental drugs for dementia of the Alzheimer type, targeting the amyloid-beta (Aβ) peptide.

Nevertheless, the causal linkage between Aβ and dementia of the Alzheimer type appears to remain strong and appears to be supported by numerous different studies spanning the past two decades (e.g. Ferreira and Klein, 2011).

Let me know turn to BiiB037, which is Aducanumab.

I think there is cause to be extremely cheerful about this novel agent, though we need to be cautious: once bitten, twice shy.

Aducanumab is a human IgG1 monoclonal antibody derived from a patient with AD by using reverse translational medicine methodology (the background to this is described here in “World Intellectual Property Organization International Publication Number WO 2008/081008 A1”). The overall rationale was that these donors’ immune systems had successfully resisted Alzheimer’s disease and that the operative antibodies could be turned into therapeutics by a process called “reverse translational medicine”: these agents target ‘neb-epitopes’ in the jargon.

A Phase 1 safety and pharmacokinetics study began with a single-ascending-dose trial of 0.3 mg/kg to 30 mg/kg intravenous BIIB037 in 56 people with “mild to moderate dementia of the Alzheimer type”. Participants were assessed at 10 time points up to two years after dosing.

It seems that, according to the available data, BiiB037 binds soluble Aβ oligomers and fibrillar Aβ with high affinity and binds monomeric Aβ with low affinity.

But the next stage of the drug development process inevitably has to turn to safety and efficacy, and I am positive that Biogen will be open in discussing their data with peers in due course.

Amyloid-related imaging abnormalities (ARIAs) have been reported in clinical trials of monoclonal antibodies in the dementia of the Alzheimer type.

Concerns raised by the US Food and Drug Administration regarding MRI abnormalities observed associated with amyloid-modifying therapy in patients with the dementia of the Alzheimer type prompted the Alzheimer’s Association to convene a work group (Sperling et al., 2011).

The work group coined the phrase ARIA (amyloid-related imaging abnormalities) to describe a spectrum of MRI findings that include sulcal effusion and parenchymal edema (ARIA-E) and haemosiderin deposition (ARIA-H). Specifically, ARIA-H refers to areas of hypointensity on gradient echo MRI that are believed to represent deposits of iron in the form of haemosiderin.

Animal models currently appear to indicate that anti-amyloid β treatment removes vascular amyloid with a corresponding compromise of the integrity of the vascular wall and leakage of blood resulting in microhaemorrhages and haemosiderin deposition (Zago et al., 2013).

The aetiology of ARIA remains unclear but the prevailing data support vascular amyloid as a common pathophysiological mechanism leading to increased vascular permeability. In the phase 2 bapineuzumab trial, dose-related vasogenic oedema (ARIA-E) had been observed (Salloway et al., 2009). Twelve cases of vasogenic oedema were reported, all in treated patients, and all resolved over time. But it seems that ARIA does not seem to be associated with all monoclonal antibodies?

As reported elsewhere, PRIME is an ongoing Phase 1b randomised, double-blind, placebo-controlled, multiple-dose study evaluating the safety, tolerability, pharmacokinetics and pharmacodynamics of aducanumab in patients with prodromal or mild AD.

This interim analysis of PRIME reflects data for 166 patients, up to week 54 in the placebo (n=40), 1 mg/kg (n=31), 3 mg/kg (n=33) and 10 mg/kg (n=32) dose arms, and up to week 30 data for the 6 mg/kg (n=30) dose arm.

On March 20 2015, it was reported that:

“CAMBRIDGE, Mass.–(BUSINESS WIRE)–Today Biogen Idec (NASDAQ:BIIB) announced data from a pre-specified interim analysis of PRIME, the Phase 1b study of aducanumab (BIIB037), in which aducanumab demonstrated an acceptable safety profile and positive results on radiologic and clinical measurements in patients with prodromal or mild Alzheimer’s disease (AD). These data are being presented today at the 12th International Conference on Alzheimer’s and Parkinson’s Diseases and Related Neurological Disorders in Nice, France.

Treatment with aducanumab produced a dose- and time-dependent reduction of amyloid plaque in the brain. Amyloid plaque is believed to play a key role in the development of the symptoms of AD. In exploratory analyses, a dose-dependent, statistically significant effect of slowing clinical decline was observed on the Mini Mental State Examination (MMSE) and Clinical Dementia Rating (CDR) scales.”

The safety observations are particularly interesting.

“Aducanumab demonstrated an acceptable safety and tolerability profile in this analysis. The most frequently reported treatment-related serious adverse event (SAE) and adverse event (AE) was ARIA (amyloid-related imaging abnormalities). Based on MRI scans, the incidence of ARIA-E (edema) was dose- and apolipoprotein E4-(ApoE4) status-dependent. In general, the onset of ARIA-E was observed early in the course of treatment and was asymptomatic or with mild, transient symptoms. The majority of patients with ARIA-E continued treatment and did so at a lower dose.”

It will be helpful if there is more research into characterising ARIA.

I was struck by one line in the abstract of the paper by Zago and colleagues (2013), in particular:

“These data suggest that vascular leakage events, such as microhemorrhage, may be related to the removal of vascular Aβ. With continued treatment, this initial susceptibility period is followed by restoration of vascular morphology and reduced vulnerability to further vascular leakage events. The data collectively suggested a vascular amyloid clearance model of ARIA, which accounts for the currently known risk factors for the incidence of ARIA in clinical studies.”

All of this makes you wonder whether we are to be cheerful or cautious?

I think both, and I keep reminding myself that we have come an extremely long way.

Reason to be cautious? Yes. Reason to be cheerful? As long as we don’t neglect the 47 million people living in the world with dementia, yes.

 

 

Selected readings

Alzheimer A. Über einen eigenartigen schweren Erkrankungsprozeß der Hirnrinde. Neurologisches Zentralblatt. 1906;23:1129–36.

Dodel R, Balakrishnan K, Keyvani K, Deuster O, Neff F, Andrei-Selmer L-C, Röskam S, Stüer C, Al-Abed Y, Noelker C, Balzer-Geldsetzer M, Oertel W, Du Y, Bacher M. Naturally occurring autoantibodies against β-amyloid: investigating their role in transgenic animal and in vitro models of Alzheimer’s disease. J Neurosci. 2011;31:5847–5854.

Ferreira ST, Klein WL. The Aβ oligomer hypothesis for synapse failure and memory loss in Alzheimer’s disease. Neurobiol Learn Mem. 2011;96:529–543.

Lue LF, Kuo YM, Roher AE, Brachova L, Shen Y, Sue L, Beach T, Kurth JH, Rydel RE, Rogers J. Soluble amyloid beta peptide concentration as a predictor of synaptic change in Alzheimer’s disease. Am J Pathol. 1999;155:853–62.

McLean CA, Cherny RA, Fraser FW, Fuller SJ, Smith MJ, Beyreuther K, Bush AI, Masters CL. Soluble pool of Abeta amyloid as a determinant of severity of neurodegeneration in Alzheimer’s disease. Ann Neurol. 1999;46:860–6.

Moir RD, Tseitlin KA, Soscia S, Hyman BT, Irizarry MC, Tanzi RE. Autoantibodies to redox-modified oligomeric Aβ are attenuated in the plasma of Alzheimer’s disease patients. J Biol Chem. 2005;280:17458–17463.

Salloway S, Sperling R, Gilman S, Fox NC, Blennow K, Raskind M, Sabbagh M, Honig LS, Doody R, van Dyck CH, Mulnard R, Barakos J, Gregg KM, Liu E, Lieberburg I, Schenk D, Black R, Grundman M. Bapineuzumab 201 Clinical Trial Investigators. A phase 2 multiple ascending dose trial of bapineuzumab in mild to moderate Alzheimer disease. Neurology. 2009;5:2061–2070.

Sperling RA, Jack CR, Black SE, Frosch MP, Greenberg SM, Hyman BT, Scheltens P, Carrillo MC, Thies W, Bednar MM, Black RS, Brashear HR, Grundman M, Siemers ER, Feldman HH, Schindler RJ. Amyloid-related imaging abnormalities in amyloid-modifying therapeutic trials: recommendations from the Alzheimer’s Association Research Roundtable Workgroup. Alzheimers Dement. 2011;5:367–385.

Terry RD, Masliah E, Salmon DP, Butters N, DeTeresa R, Hill R, Hansen LA, Katzman R. Physical basis of cognitive alterations in Alzheimer’s disease: synapse loss is the major correlate of cognitive impairment. Ann Neurol. 1991;30:572–80.

Zago W, Schroeter S, Guido T, Khan K, Seubert P, Yednock T, Schenk D, Gregg KM, Games D, Bard F, Kinney GG. Vascular alterations in PDAPP mice after anti-Aβ immunotherapy: Implications for amyloid-related imaging abnormalities. Alzheimers Dement. 2013 Oct;9(5 Suppl):S105-15. doi: 10.1016/j.jalz.2012.11.010.

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The World Dementia Council will be much stronger from democratic representation from leaders living with dementia

There is no doubt the ‘World Dementia Council’ (WDC) is a very good thing. It contains some very strong people in global dementia policy, and will be a real ‘force for change’, I feel. But recently the Dementia Alliance International (DAI) have voiced concerns about lack of representation of people with dementia on the WDC itself.  You can follow progress of this here. I totally support the DAI over their concerns for the reasons given below.

“Change” can be a very politically sensitive issue. I remember going to a meeting recently where Prof. Terence Stephenson, later to become the Chair of the General Medical Council, urged the audience that it was better to change things from within rather than to try to effect change by hectoring from the outside.

Benjamin Franklin is widely quoted as saying that the only certainties are death and taxes. I am looking forward to seeing ‘The Cherry Orchard” which will run at the Young Vic from 10 October 2014. Of course, I did six months of studying it like all good diligent students for my own MBA.

I really sympathise with the talented leaders on the World Dementia Council, but I strongly feel that global policy in dementia needs to acknowledge people living with dementia as equals. This can be lost even in the well meant phrase ‘dementia friendly communities’.

Change can be intimidating, as it challenges “vested interests”. Both the left and right abhor vested interests, but they also have a strong dislike for abuse of power.

I don’t mean simply ‘involving’ people with dementia in some namby pamby way, say circulating a report from people with dementia, at meetings, or enveloping them in flowery language of them being part of ‘networks’. Incredibly, there is no leader from a group of caregivers in dementia; there are probably about one million unpaid caregivers in dementia in the UK alone, and the current direction of travel for the UK is ultimately to involve caregivers in the development of personalised care plans. It might be mooted that no one person living with dementia can ever be a ‘representative’ of people living with dementia; but none of the people currently on the panel are individually sole representatives either.

I am not accusing the World Dementia Council of abusing their power. Far from it, they have hardly begun to meet yet. And I have high hopes they will help to nurture an innovation culture, which has already started in Europe through various funded initiatives such as the EU Ambient Assisted Living Joint Programmes (“ALLADIN”).

I had the pleasure of working with Prof Roger Orpwood in developing my chapters on innovation in my book “Living well with dementia”. Roger is in fact one of the easiest people I’ve ever worked with. Roger has had a long and distinguished career in medical engineering at the University of Bath, and even appeared before the Baroness Sally Greengross in a House of Lords Select Committee on the subject in 2004. Baroness Greengross is leading the All Party Parliamentary Group on dementia, and is involved with the development of the English dementia strategy to commence next year hopefully.

Roger was keen to emphasise to me that you must listen to the views of people with dementia in developing innovations. He has written at length about the implementation of ‘user groups’ in the development of designs for assistive technologies. Here’s one of his papers.

My Twitter timeline is full of missives about or from ‘patient leaders’. I feel one can split hairs about what a ‘person’ is and what a ‘patient’ is, and ‘person-centred care’ is fundamentally different to ‘patient-centred care’. I am hoping to meet Helga Rohra next week at the Alzheimer’s Europe conference in Glasgow; Helga is someone I’ve respected for ages, not least in her rôle at the Chair of the European Persons with Dementia group.

Kate Swaffer is a friend of mine and colleague. Kate, also an individual living with dementia, is in fact one of the “keynote speakers” at the Alzheimer’s Disease International conference next year in Perth. I am actually on the ‘international advisory board’ for that conference, and I am hoping to trawl through research submissions from next month for the conference.

I really do wish the World Dementia Council well. But, likewise, I strongly feel that not having a leader from the community of people living with dementia or from a large body of caregivers for dementia on that World Dementia Council is a basic failure of democratic representation, sending out a dire signal about inclusivity, equality and diversity; but it is also not in the interests of development of good innovations from either research or commercial application perspectives. And we know, as well, it is a massive PR fail on the part of the people promoting the World Dementia Council.

I have written an open letter to the World Dementia Council which you can view here: Open letter to WDC.

I am hopeful that the World Dementia Council will respond constructively to our concerns in due course. And I strongly recommend you read the recent blogposts on the Dementia Alliance International website here.

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