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The David and Goliath problems of the English Dementia Charities

To be clear, I think the work of the Alzheimer’s Society is fantastic.

Since their restructuring, with the support of the Department of Health, they have done really important work in activities to do with dementia, not just Alzheimer’s disease.

Goliath (Hebrew: גָּלְיָת,) is a a giant Philistine warrior defeated by the young David, the future king of Israel, in the Bible’s Books of Samuel (1 Samuel 17).

Britain’s energy market is said to be dominated by the Big Six gas and electricity suppliers. All markets need competition to function effectively, with genuine choice for consumers.

Mentions of the Alzheimer’s Society are extensive.

This is for example Hazel Blears on 16 December 2013:

Blears Hansard

And here is the recruitment drive of Jeremy Hunt, four minutes in into his speech at the G8 Summit in December 2013:

It really has become a gigantuan operation for smaller charities to compete also in the social media:

David and Goliath tweet

Last week, it was announced that staff at Marks & Spencer, Argos, Homebase, Lloyds Bank and Lloyds Pharmacy will attend special sessions to help them understand the needs of customers with dementia and support them better.

The Alzheimer’s Society makes clear that the drive towards ‘Dementia Friends’ forms part of the six-month progress report on the Prime Minister’s Challenge on Dementia.

And it has been a success we can all be proud of. Norman McNamara is also soldiering on with his “Dementia Friendly” Torbay initiatives.

As a result of commitments from  various businesses regarding “Dementia Friends”, over 190,000 staff will become Dementia Friends – 60,000 from M&S, 70,000 from Lloyds Pharmacy, 50,000 from the Home Retail Group, which owns Argos and Homebase, and 11,500 from Lloyds Bank.

And yet ‘dementia friendship’ is a global initiative.

Supportive communities are well known in Japan.  For example, Fureai kippu (in Japanese ふれあい切符 :Caring Relationship Tickets) is a Japanese currency created in 1995 by the Sawayaka Welfare Foundation so that people could earn credits helping seniors in their  community.

An initiative from another charity, the Joseph Rowntreee Foundation,  “York Dementia Without Walls” project looked into what’s needed to make York a good place to live for people with dementia and their carers.

They found that dementia-friendly communities can better support people in the early stages of their illness, maintaining confidence and boosting their ability to manage everyday life.

There are various reasons why it is so easy for the Alzheimer’s Society to ‘clean up’ in the dementia charity market in England.

These are helpfully summarised in this summary slide, derived from the work of Michael Porter, Bishop William Lawrence University Professor of Business Management at the Harvard Business School, USA.

Porter

The Alzheimer’s Society have protected their visual mark for “Dementia Friends” on the trademark register for the IPO, as trademark UK00002640312. It is protected under various categories. This is across various classes, including ‘gymnastic and sporting articles’.

picture 3

It would have cost a lot for the Alzheimer’s Society plus the cost of instructing their lawyers, which are cited here as the big commercial/corporate law firm DLA Piper in Leeds. It’s simply impossible for smaller charities to compete resource-wise over this arm of intellectual property.

Currently, according to the UK trademark office, it costs £170 to apply to register a UK trade Mark if you apply on-line (£30 discount applies for on-line filings). This includes one class of goods or services. It is a further £50 for every other class you apply for.

And the pattern of news stories about dementia has now reached a consistent homogeneous pattern. For example, this story about Prunella Scales being diagnosed with dementia has a standard line with the word ‘suffering’ (“Fawlty Towers star Prunella Scales is suffering from dementia – but is determined not to let it stop her performing, her actor husband Timothy West has revealed.”)

But the language is not one of ‘living well with dementia’, consistent with other metaphors such as ‘timebomb’, ‘explosion’, ‘flood’ and ‘tide’.

And crucially it is very rare to have any other dementia charity named apart from the Alzheimer’s Society because of their strong brand presence inter alia.

There are other dementia charities in England, however.

BRACE is a registered charity that funds research into Alzheimer’s disease and other forms of dementia. Their role is to help medical science understand the causes of dementia, find ways of diagnosing it earlier and more accurately, and develop more effective treatments.

Dementia UK is a national charity, committed to improving quality of life for all people affected by dementia. They provide mental health nurses specialising in dementia care, called Admiral Nurses. And yet there have been cuts to the Admiral Nurses service.

On December 13th 2013, the Dementia Advocacy Network reported that they would be closing after 12 years of supporting independent advocates (this is the current link to their website.)

DAN closure

An article in the European Journal of Marketing (Vol. 29 No. 10, 1995, pp. 6-26), entitled “The market positioning of British medical charities” by Sally Ann Hibbert from Department of Marketing, University of Stirling, Stirling, Scotland, does throw some light on this issue.

Hibbert notes that clusters of people who donate to charities exist overall.

“Following on, the next highest scores are revealed for cancer and deaf charities, the former investing notably in education and research for cures, the latter focusing largely on treating the effects of deafness to improve the quality of life for people affected. This trend from preventive approaches to care services can be traced down through the charities on the vertical dimension to hospices, which are primarily carers.”

In the absence of a reliable marker through scans or psychology before symptoms, and in the absence of good treatments of dementia which stop the condition “in its tracks“, it was hard to make the pitch for molecular biology research and treatments. The industry was described as “ailing“.

That’s why it was so crucial to compare dementia to AIDS (see video above).

There is a legitimate concern that driving policy towards limited angles in this way could obscure the need for funding a grossly under-resourced community care services for dementia.

And living well with dementia is an appropriate policy plan for persons currently with dementia and their caregivers.

But specialist groups of people with dementia are beginning to emerge. For example, the “Dementia Action Alliance” is a non-profit dedicated to improving the quality of life for people living with the effects of dementia.

The DAA Carers Action (@DAACarers) also do incredible work .

Like the Government has been to provide an “equal playing field” for any qualified provider of NHS services, it is impossible to think that the playing field for raising money for dementia through charities and people such as the Purple Angels is anything like an “equal playing field”.

This is a major flaw in current policy, and could mean that there are some losers and some winners. This ‘zero sum gain’, simply, is not on I feel.

It is deeply concerning that “might is right”. We should try to work together.

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Is the drug industry "stopping dementia in its tracks" or in actual fact "running out of steam"?

Sometimes you have to trust people to get on with things.

That’s why headlines saying fracking under homes could go ahead without permission don’t help.

And the reported assimilation of ‘caredata’ into the NHS information “borg”, without clear valid consent, is running into problems.

We cannot sign off every single decision about how each £ is spent in the ‘fight against dementia’ as it’s called. But the issues about care vs cure in dementia is running into the same problems with imbalance in information as fracking and care data. This threatens seriously to undermine trust in policy leaders supposedly working on behalf of us in tackling dementia.

The origins of the phrase “stopping dementia in its tracks” are obscure. Stopping something in its tracks may be somehow related to the phrase “running out of steam” for nineteenth century railway trains “running out of steam”, or coming to a sudden end when travelling. Is the drug industry “stopping dementia in its tracks” or in actual fact “running out of steam”?

To stop something in its tracks, nonetheless, is a popular metaphor, as it tags along with the combattive ‘war’ and ‘fight’ against dementia theme.

Tracks

While there’s been a need to focus on bringing value to lives with dementia, much of the fundraising has involved painfully pointing out the costs. A study conducted by RAND Corp. for the federal government earlier in 2013 found that nearly 15% of people ages 71 or older, or about 3.8 million people, now have dementia. Each case costs $41,000 to $56,000 a year, the study found. By comparison, direct expenses in the same year for heart disease were $102 billion. The study also tried to get a handle on the cost of informal care, which is often provided by family members in their homes. It pegged that cost at a range of $50 billion to $106 billion a year.

In a press release dated 24 January 2014, the Alzheimer’s Society and Alzheimer’s Drug Discovery Foundation (ADDF) are reported in their “Drug Discovery Programme” as offering up to $1.5 million to new research projects which could speed up developing treatments for Alzheimer’s disease (AD) and dementia. It is hoped that international collaboration could help make the hope of finding effective dementia treatments within the next ten years a reality. This call is open for research looking at all forms of dementia including Alzheimer’s disease. This international call for research proposals comes just weeks after the G8 Dementia Summit in London called for more global collaboration in dementia research in order to develop effective treatments by 2025.

It is described in this promotional video as “halting dementia in its tracks”. To “halt something in its tracks” literally means “stop (dead) in something tracks to suddenly it stop moving or doing something”.

A previous research grant from the Alzheimer’s Society looked at fruit flies. It was for Dr Onyinkan Sofola at University College London for £208,277. It started on October 2007 and was completed on September 2010. The researchers developed a fruit-fly model of Alzheimer’s disease where the flies accumulated amyloid, and investigated the involvement of “GSK-3” on the behaviour of the flies. It was hoped that dialing down GSK-3 in healthy flies also did no harm suggesting this approach could work as a safe therapy for Alzheimer’s disease in humans.

Ahead of the G8 Dementia Summit in London last year (11 December 2013), Professor Simon Lovestone, Institute of Psychiatry, but soon to be at Oxford, set out what he hopes the Summit will achieve, the challenges of developing new therapies for dementia, and the real possibilities of one day preventing this devastating disease. The Summit was supposed to bring together Health Ministers from across the G8, the private sector and key international institutions to advance thinking on dementia research and identify opportunities for more international collaboration, with the ultimate aim of improving life and care for people with dementia and their families.

The G8dementia summit was described as a response thus by the BBC website:

BBC

Drugs currently used to treat Alzheimer’s Disease have limited therapeutic value and do not affect the main neuropathological hallmarks of the disease, i.e., senile plaques and neurofibrillar tangles. Senile plaques are mainly formed of beta-amyloid (Abeta), a 42-aminoacid peptide. Neurofibrillar tangles are composed of paired helical filaments of hyperphosphorylated tau protein.

New, potentially disease-modifying, therapeutic approaches are targeting Abeta and tau protein. Drugs directed against Abeta include active and passive immunisation, that have been found to accelerate Abeta clearance from the brain. The most developmentally advanced monoclonal antibody directly targeting Abeta is bapineuzumab, now being studied in a large Phase III clinical trial.

In the 1980s, the amyloid cascade hypothesis emerged, and it was the most long considered theory. It is based on the β-amyloid overproduction as responsible for the senile plaque formation and for the neurotoxicity that leads to the progressive neuronal death. However, controversial data about if β-amyloid is the cause of the disease or one of the main risk factors for AD are reported.

A further postulated theory at the end of the past century was the tau-based hypothesis. It is based on aberrant tau protein, a microtubule-associated protein that stabilizes the neuronal cytoskeleton, as the origin of Alzheimer’s pathology. There have been two phase IIb clinical trials with two different compounds, tideglusib and methylene blue. Both compounds have reported some positive results in the increase of cognitive level of AD patients after the first treatments on phase IIa clinical trials.

In the meanwhile, intensive research on the physiology and pathology of tau protein leads to the discovery of two kinases responsible for its posttranslational aberrant modifications. After cloning, these kinases were identified more than ten years ago, including the now well-known glycogen synthase kinase 3 (GSK-3).

The excitement of this “GSK3 hypothesis of Alzheimer’s disease” is described here in this paper with Professor Simon Lovestone as last author.

But all may not be as well as it first appears.

GSK-3 inhibition may be associated with significant mechanism-based toxicities, potentially ranging from hypoglycemia to promoting tumour growth. But encouragingly, at therapeutic doses, lithium is estimated to inhibit approximately a 25% of total GSK-3 activity, and this inhibition degree has not been associated with hypoglycemia, increased levels of tumorigenesis, or deaths from cancer. Currently it’s hoped, in pathological conditions, the GSK-3 inhibitor would be able to decrease the upregulation of the enzyme and, in the case that this treatment would slow down the GSK-3 physiological levels, other compensatory mechanisms of action would play the restorative function.

Therapeutic approaches directed against tau protein include inhibitors of glycogen synthase kinase- 3 (GSK-3), the enzyme responsible for tau phosphorylation and tau protein aggregation inhibitors. NP-12, a promising GSK-3 inhibitor, is being tested in a Phase II study, and methylthioninium chloride, a tau protein aggregation inhibitor, has given initial encouraging results in a 50-week study.  Fingers crossed.

Another important challenge for a GSK-3 inhibitor as an AD treatment is its specific brain distribution. The drug needs to cross the blood-brain barrier to exert its action in the regulation of exacerbated GSK-3 brain levels. Usually this is not an easy task for any kind of drug, moreover when oral bioavailability is the preferred administration route for chronic dementia treatment.

And once it gets into the brain, it has to to go to the right parts where GSK-3 needs to be targeted, not absolutely everywhere, it can be argued.

Nonetheless, the enthusiasm about the approach of drug treatments is described on Prof Simon Lovestone’s page for the Alzheimer’s Society.

However, Professor Lovestone’s research group has run into problems when trying to demonstrate their findings in mice, an important step in the research process. The problem is that mice do not naturally develop Alzheimer’s disease, and it is even difficult to experimentally cause Alzheimer’s disease in mice.

We may soon have to face up to the concept, with the current NHS having to do ‘more with less’, and ‘with no money left’, ‘we can’t go on like this’. It would be incredibly wonderful if you could give an individual a medication which could literally ‘stop dementia in its tracks’. But even note the scientific research above is for Alzheimer’s disease, one of the hundred causes of dementia, albeit the most common one. Or we may have to stop this relentless spend on finding the “magic bullet” in its tracks, and think about practical ways of enhancing the quality of life or wellbeing of those currently living with dementia. Nobody reasonable wishes to snuff out hope for prevention or cure of the dementias, but, for a moral debate, the facts have to be on the table and clear. Every money we spend on investigating magic bullets which don’t work could have been spent in giving a person living with dementia adequate signage for his environment, or a ‘memory phone’ with photographs of common contacts. But the drug industry, and the people who work with them, never wish to admit they’re running out of steam.

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