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Comparative Research Budgets (charity and government resources) for the four major diseases in the UK



Research Budget (government and charity)

£  per Sufferer per Year



£5.5 million




£58.4  million




£188.5  million




£9.1 million



NB The cost of caring for someone with Alzheimer's disease is more than double that of caring for someone with one of the three other major diseases in the UK.

Research News


There has been more exciting news on the anti-amyloid vaccine from Elan Corporation. Edinburgh University has designed a new maze for mice with Alzheimer’s which has been able to demonstrate their short term memory ability – something that it has not been easy to do previously. Mice with Alzheimer’s given the vaccine over a number of months have improved in their ability to remember the maze. This is remarkable because it seems to demonstrate that perhaps a vaccine which stops the build up of amyloid (one of the pathologies of the disease) is not only preventing the symptoms appearing but that in breaking down the plaques it may be reversing the effects of the disease so that mice are again able to learn and remember.

This vaccine does not affect at all the other pathology of the disease – the tau tangles – and still nobody is sure about the affects of this protein.

If all of the stages of subsequent testing works, general availability of the vaccine is still some four or five years away, but it has given a huge boost to researchers, and has made the Trust’s funding of a project on early and definitive diagnosis even more important.


· Researchers in Illinois and Arizona have found that patients taking the statin class of cholesterol lowering drugs may reduce their risk of developing Alzheimer’s disease. They had a 70% lower prevalence of AD than a control group of the over 60s.

· Cardiff University has succeeded in growing human brain cells in the laboratory giving a potentially endless supply of specialised brain cells that could in future perhaps be used to replace cells lost in Alzheimer’s, Parkinson’s and Huntington’s diseases. Previous work has relied on large numbers of aborted foetuses, but after the initial phase using a single foetus, this technique would mean it was no longer necessary to do this.

· Cloning of human embryos up to 14 days old has been passed by Parliament. This will allow stem cells (non-specific cells which can turn into any type of cell wanted) to be extracted from them for use in treating diseases such as Alzheimer’s by enabling the dying brain cells to be replaced.


We are often asked about the various forms of dementia and how their symptoms differ. Dementia is the progressive loss of the faculties of the brain, affecting functions like memory, language, personality and the ability to cope with everyday activities, such as dressing and eating. Most cases are late-onset, ie over 65 years, though there are some tragic sufferers in their 40s and 50s.

Here’s a short guide to the most common forms:

ALZHEIMER'S DISEASE (AD) (early and late-onset)

Alzheimer’s disease is the most common type of both early and late-onset dementia, accounting for about 2/3 of all patients, or over half a million people in Britain. At the moment, definitive diagnosis is only possible in a post mortem, when the main feature is large numbers of “neuritic plaques” in the cortex, the vital outer layers of the brain. These plaques are deposits of b amyloid and other proteins, containing damaged nerve cells or neurones. Often there are also clumps of tangled threads inside neurones, which eventually kill the cell. These tangles and plaques are sometimes found in the brains of healthy old people, but don’t normally have the diseased neurites. But it’s the loss of neurones, and especially their connections, that is thought to cause the dementia of AD. An early sign of AD is memory loss, followed by disorientation and behavioural changes. Some sufferers become emotionally disturbed and may wander or suffer hallucinations or become agitated and aggressive.


In FTD (Pick’s disease is one type) the pathology and the cell death is especially in the frontal and temporal parts (ie the front and the sides) of the brain. Brain scans can help to diagnose the patient, and the symptoms differ from AD, with behavioural changes, eg apathy, stereotyped behaviour (such as repeated washing) and/or poor speech, preceding loss of memory. There is a spectrum of related dementias, stretching from FTD to dementia with motor neurone disease.


DLB has similar neuronal inclusions (“blobs” within the brain cells) to those found in Parkinson’s disease (PD) – “Lewy bodies”. But, whereas in PD Lewy bodies are mainly in the brainstem, or base of the brain, in DLB they are also seen in the cortex, the outer layers. DLB patients suffer from visual hallucinations, from PD-like movement problems and from fluctuating mental abilities (though PD sufferers are also prone to dementia). Over half of DLB cases have AD pathology – ie the plaques and tangles - as well.


Vascular dementia is dementia due to cerebrovascular disease, ie diseased blood vessels in the brain. But even this simple definition is a problem. For one thing, AD also often involves cerebrovascular damage. For another, the two diseases may be hard for doctors to distinguish, though some signs, such as walking problems, are more typical of vascular dementia. There are several subtypes of vascular dementia, including multi-infarct dementia (due to mini strokes), various types of damage to small blood vessels and white matter (brain tissue) damage. There seems to be a spectrum of diseases, including cerebrovascular disease without dementia, several types of vascular dementia, ‘mixed’ dementia (ie AD plus vascular) and ‘pure’ AD.

Apart from these and other brain diseases, such as CJD, dementia can also be due to causes such as alcohol abuse, vitamin B12 deficiency or benign tumours that are potentially reversible; so early diagnosis is crucial. Where dementia is diagnosed, treatment is at present limited, alleviating some symptoms, but not preventing the disease’s progress.


There is still no way of detecting the characteristic amyloid plaques and neurofibrillary tangles of Alzheimer’s disease in the brain in life. If these aggregates of insoluble proteins could be detected in living people, then it would be possible to diagnose AD with certainty and to follow the progression of the disease. A report from Duke University, USA has been hailed in the press as a big step towards this goal. These researchers showed that they could detect the amyloid plaques in a piece of brain taken after death by a method they called ‘magnetic resonance microscopy’. The piece of brain was placed in a small magnetic resonance coil and exposed to a high magnetic field (4 times greater than that used in typical clinical MRI scanners) for a period of 20 hours. The picture they obtained showed small dots which corresponded to the amyloid plaques. In view of the extreme conditions required, it is clear that the claims in the press were misleading; we are still as far as ever from seeing plaques in the living human brain.


Anti-inflammatory drugs.

Studies on the brain of people with AD have shown signs of inflammation, especially around the amyloid plaques. There is also evidence that people who have been taking anti-inflammatory drugs might have a lower risk of developing AD. Accordingly, the National Institute on Aging in the USA sponsored a clinical trial of the most powerful anti-inflammatory drug, the steroid prednisone, in 138 patients with AD. The results reported in February are disappointing: there was no effect of a low dose of prednisone given for a year upon the progression of AD compared with patients who were not treated. Indeed, those treated with the drug actually showed a slightly more rapid decline in measures of behaviour. The results cast doubt upon the role of inflammation in the brain as part of the disease process; perhaps the inflammation is a consequence rather than a cause of the disease.

Hormone-replacement therapy.

Several studies have found that women who have taken HRT are less likely to develop AD than those who have not. This finding could be due to the hormones in the HRT treatment, but it might be simply that women who take HRT are more health conscious and that some other factor is protective. The only way to find out is to do a clinical trial in which a large number of women are given either HRT or a placebo drug. Such trials take a long time, so in the meantime a trial of oestrogen replacement therapy in patients already having AD has been carried out in the USA. The results were negative: in 40 women there was no effect of the HRT on the progression of the disease compared with 40 untreated. Some of the scores actually worsened in the treated group. The authors concluded that HRT should not be used to treat already existing AD, but the question remains: does HRT taken earlier in life prevent AD from developing? The Medical Research Council (MRC) recently announced a large clinical trial to answer this question. The MRC has already begun a trial of HRT in 22,000 women in the UK, who will be treated for 10 years and followed up for a total of 20 years to see if HRT has any effect on osteoporosis, cardiovascular disease and breast cancer. The MRC have now added to this trial an assessment of cognitive function in a subset of 12,000 of the subjects who will reach the age of 65 by the end of the period of treatment. The trial, co-ordinated from the Maudsley Hospital, London and the University of Cambridge, will be able to detect an effect of HRT not only on the development of dementia but also on the normal decline in cognitive function with ageing. The first results are expected in 2005. This trial is well designed and should give a clear answer to a very important question.


Another anticholinesterase drug.

The results of a trial of a drug called galantamine (Reminyl), derived from a substance present in Caucasian snowdrops, were announced by the manufacturer Janssen in April. This drug has the same mode of action as donepezil (Aricept) in inhibiting the enzyme acetylcholineterase which breaks down the transmitter substance acetylcholine, know to be involved in memory. Like donepezil, this drug improved the memory performance for a period of several months but it also improved the behavioural symptoms. The detailed results of this trial have not yet been published: it will be important to see how many patients responded and how effective the drug was on the behavioural symptoms before doctors can advise on its use.

A vaccine?

Last year an American company (Elan) described results of tests in mice that showed that vaccination with a protein related to the beta-amyloid protein that is deposited in the brain in AD could dramatically reduce the deposition of beta-amyloid in the mouse brain. It was announced in March that a small clinical trial of this agent has been approved by the UK authorities on 80 patients with AD. The speed of approval has surprised many, as has the name allowed by the authorities, ‘Betabloc’, which will lead to confusion since a long-established class of drugs called beta-blockers are in wide use for the treatment of high blood pressure and heart disease. It must be stressed that there is no relationship at all between the vaccine and these drugs. The purpose of this pilot trial is to test the safety of the vaccine over a 6 month period, so any changes in the disease are unlikely to show up.

Report on our first Major Grant 

which was won, after an open competition, by a combined group in Cambridge from the Laboratory of Molecular Biology, Centre for Brain Repair and The Babraham Institute. We are grateful for the support of The Freemasons’ Grand Charity with this grant.

One of the most exciting recent findings in dementia research has been the involvement of certain key genes in the pathogenesis of dementing conditions, including Alzheimer’s disease and Lewy Body dementias. In its work funded by the Trust, the Cambridge group are exploiting molecular genetics methods, in which copies of the harmful genes such as those for abnormal human tau and amyloid precursor protein (associated particularly with Alzheimer’s) and alpha-synuclein (associated particularly with Lewy Body dementias) can be inserted into small numbers of transgenic mice – which can then be studied for signs of the human diseases. 

The programme benefits significantly from being able to assess, in detail, the effects of having these harmful genes at the molecular, neural and behavioural levels. This multi-disiciplinary approach means that they can address key issues as regards how having these genes affect the mice, particularly: i) the extent to which inheriting these genetic mutations shows up as deficits in behaviour or cognition; ii) the extent to which the progression of these deficits seem to match the pathological changes that appear in the brains of the animals as they age (because some people who have massive changes in their brains on scans only have mild symptoms of dementia, and we have no idea why); iii) whether the pathology in the brains of these mice can be consistently reproduced so that they can form a model which can then be used to design and test therapies to arrest the disease in humans. 

Work is progressing very well, and the group is about to take on a PhD student to help with the project.

The next major project we will fund will look specifically at early diagnosis and early intervention to slow the progress of the disease.


US Clinical trials of metrifonate, an acetylcholinesterase inhibitor similar to Aricept and Exelon (drugs which slow down the breakdown of the vital brain chemical acetylcholine) have been put on hold after the makers, Bayer AG, found a side effect of muscle weakness in 20 out of the 3000 patients taking it, with a few of them requiring help with breathing. Metrifonate is said to control psychiatric and behavioural disturbances as will as helping to slow loss of memory in AD, and has been in use for years as a treatment for schistosomiasis, a parasitic disorder. Bayer AG are investigating.

New types of anti-psychotic drugs such as Risperdal with far fewer side effects, are now being use to help control aggression in Alzheimer's patients. Risperdal is given in low doses and doesn't seem to sedate or cause further confusion.

Individuals suffering from Down's Syndrome are in later life at very high risk of Alzheimer's disease. Down's Syndrome is caused by a mutation leading to a duplicate copy of chromosome 21. This is the chromosome on which one of the amyloid genes is located - responsible for producing amyloid protein, part of the pathology of Alzheimer's disease. Doctors in the US are trying a small study with Aricept, one of the drugs believed to slow the cognitive decline in AD sufferers for a period of time, to see whether this can benefit the cognition of consenting Down's Syndrome individuals. So far results have been encouraging.

Nitrendipine, the anti-hypertensive drug which was shown in a European study to halve the risk of stroke, is being proposed as an anti-dementia drug. Those who took part in the study were tested for dementia after five years - 21 had developed dementia in the control group as opposed to 11 in the group of those receiving the drug.

Pfizer is working on a drug known as NGD97-1 to try to reverse memory loss, which has begun clinical trials in Europe. NGD97-1 is thought to block a chemical transmitter in the brain that reduces the ability to form a memory. Rats with induced memory deficits were able to find their way twice as quickly round a maze after having the drug as those with memory deficits who did not. It is hoped that the drug may help those with mild to moderate AD, although memory loss is only one aspect of the condition.

Phytopharm, a small botanic biotech group, hopes to start human trials this year on its drug P58, which appears to reverse age-related memory loss in aged rats, allowing them to remember a maze more easily. It hopes that eventually P58, "derived from an Asian plant", may provide a treatment for Alzheimer's disease.

The Irish American Elan Pharmaceuticals has reported in the respected Nature journal that its AN-1792 vaccine protects laboratory mice from developing the amyloid plaques in the brain that are part of the pathology of Alzheimer’s disease. In addition, Elan says that a second experiment on mice which already showed the symptoms of the disease did not continue to worsen as would normally have been expected. It is still not known whether the plaques are actually a cause or an effect of the disease , and this still leaves the question of the other major pathology, the Tau protein "tangles", which some scientists think are more important. The research, whatever the outcome, is extremely valuable as another step in understanding the biology of this highly complex disorder. Elan plans to start human testing later this year, and if this works, they will go to clinical trials. Delaying the average onset of Alzheimer’s disease by just five years would reduce the number of cases by half because people would die from other causes.

Amgen Inc and Guildford Pharmaceuticals Inc have started human testing of a drug which aims to regenerate damaged nerve cells in the brain in Parkinson’s disease. This is only the second human study of a new class of drugs called neuroimmunophilins, which may have implications for Alzheimer’s disease. Years of testing lie ahead.


American researchers have isolated stem (non-specific) cells in the brain which can grow into nerve cells while continuing to reproduce, something until recently thought to be impossible. This would mean that scientists could grow nerve cells for transplantation. In addition, work on mice revealed that neurones themselves can divide (though very slowly), contrary to accepted wisdom, and that "a challenging environment [learning new things] for elderly mice promoted brain cell growth (neurogenesis)". This occurs in the hippocampus, as well as other areas, which is responsible for memory and learning, and the research could be of benefit in AD.

Additional research is looking at using nose drops to deliver Nerve Growth Factor (NGF) directly to the brain to see if it will allow brain cells to regenerate.

The discovery by London-based molecular biologists, Gillian Bates and Stephen Davies, of a key event in Huntington's disease (HD) has intensified research with the hope of finding a cure or therapy in the next ten years. Huntington's disease, like Alzheimer's disease, is a neurodegenarative disorder, and the research being done may have implications for AD. In HD, symptoms appear in middle age, with jerky movements, loss of memory and concentration, depression and mood swings. The gene for HD was discovered in 1993, and work with transgenic mice showed that it produced an abnormal protein which them "clumped" in brain cells. Work is being done in a number of scientific disciplines - chemicals to stop the "clumping", gene therapy, and looking for a way to delay the onset of the disease.

Watching AD patients make tea has allowed Sussex researchers to conclude that patients in familiar surroundings retain their ability to do tasks much longer as they can still pick up cues from where things are. As they often lose the ability to describe how to do the task, verbal tests to determine competence can sometimes lead to the assumption that they can no longer be independent.

American researchers have discovered an enzyme called Pin 1 in the brains of Alzheimer’s patients. This is a crucial component of other cells to allow them to divide, but it was an unexpected finding in brain cells. Pin 1 latches onto Tau protein which forms "tangles" – because the enzyme is responsible for getting cells back to normal after they divide – or it could be that Pin 1 is triggering them to form – because the enzyme readies cells for division by changing their shape. Whatever the outcome, the research will be valuable at looking at possible treatments. This work follows from research at the Oxford Network centre two years ago that identified abnormal expression of proteins involved in cell division in nerve cells in Alzheimer’s Disease.

A study in the Proceeding of the National Academy of Sciences suggests that the ability of stem cells (non-specific cells) to transform themselves might be useful in Alzheimer’s disease. Stem cells transplanted into the brains of mice spread and changed into the type of cell they needed by the brain.

Researchers in Nottingham have discovered how presenilin, a protein associated with familial early onset AD, is processed in the brain and how its levels are controlled, leading to hope of a better understanding of the mechanism of the disease.

Edinburgh scientists are doing a long-term study into the effect of stress – and the hormones this produces – on the part of the brain responsible for memory, the hippocampus. They will ask volunteers in their sixties to undertake intellectual tasks and give them MRI scans every 18 months to see if there is a link between stress and an increase in shrinkage in the hippocampus.


A recent report to the government on closing the gap between rich and poor on health recommends adding folate to flour as folic acid helps to prevent spina bifida and may be beneficial in preventing heart disease. Work by the Oxford team headed by the Chairman of ART's Scientific Advisory Board, Professor David Smith, leads them to believe that the risks for Alzheimer's disease may be the same as those for heart disease and other vascular disorders, so regular exercise and a good diet might be important.

Increased accuracy of diagnosis and an ageing population means that deaths recorded as being from Alzheimer's disease have increased twenty-fold in the last 15 years, the Office of National Statistics says, and it believes that death rates "greatly underestimate the burden of the diseases", as some studies indicate that possibly only a quarter of patients diagnosed with dementia have that recorded as the underlying cause of death. This means that it is still difficult to calculate the full cost to society.

9,000 preserved brains of those who were diagnosed at death as suffering from Alzheimer's disease are being examined to see that none of them died from Creutzfeldt-Jakob disease (CJD), a new variant of which, it is believed, may be caused by eating meat infected with BSE, and which has many similar symptoms.

Hormones, Memory decline and Alzheimer’s disease
Dr. Eva Hogervorst, Oxford Project To Investigate Memory and Ageing,
Radcliffe Infirmary, Woodstock Road OX2 6HE, United Kingdom 

Alzheimer’s disease is characterised by memory loss and other cognitive deficits and affects about 1 in 5 people aged over 80. The risk of developing Alzheimer’s disease is twice as low in men compared with women. It is possible that there are protective mechanisms in men. For instance, elderly men have higher levels of sex hormones, such as estrogens, than elderly women. After the menopause, levels of estrogens are very low in women. Animal studies have shown that estrogens can possibly have protective effects in the brain.

The abrupt decline in estrogens after the menopause is not necessarily accompanied by an abrupt decline in memory. However, it is possible that increasing estrogen levels with hormone replacement therapy could protect the ageing brain. Previous short experiments have shown that in healthy ageing women, hormone replacement therapy has small positive effects that include better memory functions. It is difficult to investigate long term effects in the population as women who choose to start using hormone replacement therapy are often healthier than women who do not; which could also protect them against memory decline. It is therefore currently unclear whether hormone replacement therapy can protect against the development of Alzheimer’s disease. Two large studies in the U.K. and the U.S.A. each including over 22.000 elderly women are currently underway to investigate this and should present their results in 2010 and 2006. Three large studies this year showed that in women already affected by Alzheimer’s disease, hormone replacement therapy does not slow down progression of the disease. 

Further reading
E. Hogervorst, J. Williams, M. Budge, W. Riedel & J. Jolles (In press) The nature of the effect of female gonadal hormone replacement therapy on cognitive function in post-menopausal women: A meta-analysis. Neuroscience (published by Elsevier)
This is a review of the studies done of the effect of hormone replacement therapy on cognitive function in healthy and demented women

Motion Blindness

A study published in the journal Neurology suggests that AD patients wander off not because they forget where they are going - a result of damage to the part of the brain responsible for memory - but because they are unable to sense direction and motion properly, due to damage in a different part of the brain. 6 out of 11 patients could not identify the direction of movement of a "snowflake" pattern on a screen, though all of the control volunteers could do so. These six also found it more difficult to perform a navigational test along a simple path, giving rise to the hope that there might be a way in the future to do a simple test to identify those with AD who are more likely to wander off.


This is the beginning of a report on Centres participating in the Alzheimer's Research Trust Research Centre Network. Click here for more information. Network funding for each of the eleven Members is £12,000 per year to facilitate the exchange of information about research between scientists around the country via Network Co-ordinators and Network Administrators.

A is for Aberdeen

Professor Claude Wischik, the Network Centre Director at Aberdeen, is the recently appointed Professor of Psychiatric Geratology at the University and was formerly a Senior Research Fellow in Cambridge. He states, "The newly-established Network is an important step towards developing an effective new Alzheimer's disease research force in Aberdeen which will hopefully have the capacity to impact internationally in the field.

There are tremendous possibilities in Aberdeen to combine a powerful molecular research environment at the institute of Medical Sciences with sophisticated brain imaging technologies and also with clinical and health economic studies at the Aberdeen Royal Infirmary and Royal Cornhill Hospital. This is a winning combination."

Prof Wischik and his team have leading-edge technology which they hope to develop over a 5-year time scale into a preventative treatment for AD. A full development programme will require an investment of £2 million. Prof Wischik believes that dementia care in the Grampian region alone costs the health service £84 million per annum.

C is for Cambridge
(a Member of The Alzheimer's Research Trust Network). Click here for more.

John Hodges, the Network Co-ordinator at Cambridge, is Professor of Behavioural Neurology at the MRC Cognition and Brain Sciences Unit and the University of Cambridge. He is Chairman of the British Neuropsychiatric Association and the World Federation of Neurology: Research Group on Aphasia and Cognitive Disorders. The Cambridge Network draws together researchers at Addenbrooke's Hospital, the MRC Cognition and Brain Sciences Unit, the MRC Laboratory for Molecular Biology, The Institute of Public Health, The Babraham Institute, The Brain Repair Centre and renowned departments of the University of Cambridge.

The groups comprising the Cambridge part of the Network have interests in the characterisation of Alzheimer's disease (AD) in its early stages, imaging techniques, neuropsychiatry, neuropsychology, clinical genetics, epidemiological studies of AD and basic biology. Frontotemporal dementia (Pick's Disease) is also a topic of major interest. Those from Cambridge who are participating in the Network have a phenomenal combined publishing record of more than 250 papers per year, greatly contributing to new information on the disease. Major discoveries made in recent years at Cambridge include:

C is for Cardiff

(a Member of the Alzheimer’s Research Trust Network). Click here for more.

Prof. Mike Owen, Head of Department of Psychological Medicine at the University of Wales College of Medicine and Art Network Co-ordinator in Cardiff, leads a team involved in searching for genes associated with late onset of Alzheimer’s disease (AD). The search for genes associated with early onset AD has been successful in isolating a number of genes which have helped in understanding the disease process, but early onset disease has a clear inheritance pattern which makes the associated genes relatively easy to find. Late onset AD is much more complicated and likely to be caused by both inherited and non-inherited factors, which makes studying its genetics more difficult. Prof. Owen and his team have a wealth of expertise in mapping disease genes in such complex disorders, and are applying their expertise to late onset AD with funding from ART and the Medical Research Council.

The Cardiff Group in collaboration with John Hardy (Mayo Clinic, Jacksonville, USA) and Alison Goate (Washington University, St Louis, USA) is currently completing a study of 600 pairs of siblings where both have late-onset AD, in order to locate the genes responsible for conferring susceptibility to the disorder. They have been studying the particular genes which could possibly be involved in the disorder and have identified a variation, or polymorphism, in a gene called DCPI, whose product is the angiontensin-converting enzyme (ACE), which seems to predispose people to develop AD. This enzyme is known for be important in body water balance, but was examined as a candidate gene for AD because of its know association with longevity.

Further studies are now essential to define the relationship of this gene to AD and to examine its possible role in the course of the disease. The ART network has funded a PhD studentship to carry out this work. Berwyn Lloyd will start work in Cardiff in Sept1999, with Dr Lesley Jones, Dr Julie Williams and Prof. Owen initially refining the genetic association with AD by looking at other variants in the gene and subsequently carrying out functional studies of the enzyme cells to examine the effect of genetic variations on activity on the enzyme. Berwyn graduated from the School of Biosciences at the University of Cardiff this summer, and has already had a year’s laboratory experience in many of the techniques required in the project as he undertook a 12 month practical placement during his four year undergraduate training.

As well as providing information about the association of AD and ACE, this project provides a good opportunity for a student to gain a wide variety of technical skills. Importantly, it also provides a blueprint for the analysis of other genes which prove to be associated with AD.

D is for Dundee

The Dundee Network centre is co-ordinated by Dr. Kieran Breen, Senior Lecturer from the Department of Pharmacology and Neuroscience at the University of Dundee, Ninewells Hospital and Medical School. Dr. Breen’s current research interests include the biochemical analysis of AD pathology - particularly the function and processing of the amyloid ß precursor protein. In collaboration with Dr. David Balfour, Reader in the Department of Pharmacology & Neuroscience, Dr. Breen has recruited a PhD student from Malta who will investigate both the behavioural and biochemical effects of nicotine on memory and behaviour.

The Dundee Network centre comprises 20 researchers and clinicians whose interests include the biomedical, behavioural and clinical aspects of Alzheimer’s disease. 

Other research interests of those affiliated with the Dundee Network centre include: 

The role of anti-oxidants in nerve cell survival

The relationship between lipid metabolism, inflammation and AD

Involvement in clinical research projects such as antipsychotic drug trials in AD.

The subjective experience of dementia and the implications for care and treatment.

Language and memory in Alzheimer’s disease.

A feasibility study into the possible applications of communication and information technology to assist people with  dementia, such as memory aids, multi-media reminiscence experiences, information organisers for carers, and further ideas suggested by experts and carers.

Since Dundee became part of Alzheimer’s Research Trust Network, other activities have included:

Two public lectures at which five Alzheimer’s researchers and clinicians combined efforts to educate the lay public about current developments in Alzheimer’s research in Dundee and internationally and also about how these research efforts are currently incorporated into clinical practice. A similar lecture is planned as part of Brain Awareness Week (13 – 19 March 2000). 
Co-hosting a workshop on ‘The Social and Medical Aspects of Dementia – Bridging the Gap’ with funds from the Scottish Hospital Endowments Research Trust (SHERT) in collaboration with the Centre for Social Research on Dementia, University of Stirling. The workshop brought together a diverse group of professionals including carers, old age psychiatrists, social workers, policy makers, GPs, and biomedical and social researchers from the Tayside area. Recommendations from the meeting will serve as a basis for future AD research. 

A web site for the Dundee Network that includes information about the research conducted in Dundee, the Alzheimer’s Research Trust, and Alzheimer’s disease in general. 

A monthly newsletter to the members of the Centre that contains information about research grants and events that relate to Alzheimer’s disease.

L is for London 

The London Network centre is led by Professor Martin Rossor and focuses on the younger onset dementias. The group of more than 30 researchers provides a multidisciplinary approach ranging from collaborative work on the genetics of young onset dementia through to the emotional impact on carers of the frontotemporal dementias. A Cognitive Disorders Clinic provides a tertiary referral service for unusual and early onset dementias. A telephone advisory service was set up to provide information to patients, families, carers and all professionals involved in the management of this complex group of disorders. The CANDID (Counselling ANd Diagnosis In Dementia) Service was awarded the BUPA and Patient Association Award for Patient Communication in 1999.

A long-standing interest has been the study of familial dementias. Many of the degenerative dementias can occur as an early onset autosomal dominant disorder with clinical features that are similar to those without a prominent family history. These families provide the opportunity to locate the genes responsible for the disease and this has had a major impact on our understanding of the pathophysiology of familial Alzheimer's disease. The group in collaboration with John Hardy were the first to identify a disease mutation in the amyloid precursor protein gene that can cause Alzheimer's disease. Similar genetic studies in the familial non-Alzheimer dementias causing frontotemporal degeneration have identified mutations in the tau gene. However, it is clear that the genetic factors that influence the apparent sporadic cases are much more complex, as discussed by Professor Owen (C is for Cardiff).

The familial cases also offer an ideal opportunity for solving a number of clinical problems of early diagnosis. Since the disorders are autosomal dominant, 50% of children of an affected parent are likely to develop the disease which often starts at a relatively constant age within a family. Thus one can enter individuals into a study at a presymptomatic stage and follow them through the development of the very earliest abnormalities to established disease. Such research can be very demanding upon individuals who are already aware of their potential risk.

The group uses neuropsychological measures of language, perception and memory; biochemical measures and neuroimaging. It has focused on magnetic resonance imaging which can give very detailed structural information. Dr Nicholas Fox, MRC Clinician Scientist, has developed a technique for positionally matching volume images which are then directly superimposed or registered. This can provide a very precise measure of the amount of tissue lost. Using this the group has been able to demonstrate a clinical phase of tissue loss in Alzheimer's disease which recedes symptoms by a number of years. It has also explored environmental and genetic factors which may influence the rate of progression as measured by tissue loss.

To take some of the imaging research forward the ART have funded a PhD studentship for Rachael Scahill. Rachael obtained her Zoology degree from Oxford University and then did her MSc in Scientific Computing before joining the group in 1998.

N is for Newcastle

The Newcastle Alzheimer’s Research Trust Network centre is located in the Institute of Health for the Elderly where the University of Newcastle, the Medical Research Council and NHS colleagues have formed a partnership on clinical brain ageing. The centre benefits hugely from the diversity of its members’research expertise which includes old age psychiatry, neuropathology, neurochemistry, genetics, nursing, psychology, and brain imaging as well as technical, administrative and IT support. The Newcastle dementia research group played a lead role in identifying the characteristics of dementia with Lewy Bodies (DLB) and in giving its first recognised diagnosis guidelines. It is now thought to be the commonest form of dementia after Alzheimer’s disease (AD). Ongoing research is developing ways to clarify the clinical diagnosis of DLB, and identify what causes particular symptoms so that they can be treated using drug therapy. Newcastle also played a role in the discovery of the loss of the brain transmitter, acetylcholine, as a central mechanism in dementia, prompting the development of the first drug treatments for Alzheimer’s disease (Aricept, Exelon and Reminyl), which prevent the breakdown of this transmitter. Newcastle is investigating whether these drugs may be more effective in those with DLB than with AD, and that DLB patients do not respond well to the usual drugs used in Alzheimer’s to control behaviour problems (neuroleptics) in order to target present and future therapies more effectively, helping patients and carers. Vascular dementia (VaD) is a complex and little understood condition and it is not clear how the different elements of the disease contribute to damage the patient’s cognition. The aims of the Newcastle VaD dementia research programme are to look at vascular pathology in both AD and DLB and also to investigate why there is such a high risk of cognitive decline in elderly patients who have had strokes or have neurocardiovascular instability (NCVI).

ART is funding two research projects which will complement Newcastle’s MRC- funded work. The first is a PhD studentship examining the impact of cerebrovascular disease on Alzheimer’s pathology in the elderly. The second is a programme grant in collaboration with Professor Jacoby of the Oxford ART Network Group to look into the effects of neuroleptics and examine whether they accelerate cognitive decline in dementia patients, as has been independently suggested by earlier Newcastle and Oxford research. Newcastle has also been awarded £50,000 by ART for an imaging suite in honour of former MP Roland Boyes. The money was raised by Roland and his wife Pat with the help of their many friends and supporters, and through the “Run for Roland” campaign.

The Irish-American Elan Pharmaceuticals has reported in Nautre that its AN-1792 vaccine protects laboratory mice from developing the amyloid plaques in the brain that are part of the pathology of Alzheimer’s disease. It is still not known whether the plaques are a cause or an effect of the disease, and there is still t other major pathology – “tangles” Elan plans to start human testing later this year, and if this works, they will go to clinical trials.

Amgen Inc and Guildford Pharmaceuticals Inc have started human testing of a drug which aims to regenerate damaged nerve cells in the brain in Parkinson’s disease. This is only the second human study of a new class of drugs called neuroimmunophilins, which may have implications for Alzheimer’s disease. Years of testing lie ahead.

Scientists at Washington University have found a protein called “slit” which is produced in the brain during childhood development to guide nerve cells to their final destination by repelling them into place. This might allow in the future a technique to be developed to deliver therapeutic cells to specific areas of the brain.

A recent report in the journal Nature describes an experiment that demonstrates a link between caspase-12, an enzyme that plays a key role in cell death, and the neurotoxic substance, b-amyloid, which many scientists believe is central to the ways in which the brain becomes damaged in AD. Brain tissue in which caspase-12 activity was prevented showed reduced neurotoxic effects of b-amyloid. Therefore, the scientists from Harvard Medical School have suggested that blockade of caspase-12 activity may be a potential therapy in Alzheimer’s disease. 

A team at New York University has reported in The Lancet that they have a discovered a chemical that in mice will make the prion which is thought to be responsible for Creuztfeld-Jacob Disease harmless. The so-called beta sheet breaker peptides cause the proteins to refold from the faulty shape associated with CJD back to their normal configuration. They hope that it will be possible to extrapolate some of their findings from CJD to Alzheimer’s disease, which is their main target, by looking at whether it is possible to do something similar with the beta-amyloid protein. However, it is still not definitely known whether beta-amyloid is a cause of Alzheimer’s disease or just a symptom, and therefore whether this would have any effect.

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