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• The future of preventing Alzheimer's moves closer to reality

Just a Thought

While researchers continue to scramble for new treatments that can help Australians with Alzheimer's disease, we learn that this talk about dementia existed centuries ago. It was regarded as a normal feature of ageing to the extent that even Shakespeare in his work, As You Like It, traced the life of a man from mewling infant, to whining schoolboy, to sighing lover, to cursing soldier, to pompous middle age and piping old age; and then:

Last scene of all
That ends this strange eventful history
Is second childishness and mere oblivion
Sans teeth, sans eyes, sans taste, sans everything.

— Act II, Scene vii

Despite Shakespeare’s verse, until the public health advances of the late 19th century, most of the dying in societies was done by children overwhelmed by infectious diseases. Age-related conditions of dementia, blindness, muscular weakness and loss of teeth were mixed up in people’s understanding as old age. Therefore, the first step of medical science was to separate the several aspects of ageing (including dementia) so that each could be understood separately in devising treatments for the problems of ageing.

A recent study from Sweden reported that some subtle features of cognitive decline can become evident ten or more years before someone is diagnosed with full-blown Alzheimer's disease, thus offering the chance for early intervention. Also, neurologists identified dementia as a condition separate from just “getting old”; and categorised the different types of dementia as discussed in the previous issue of 9 September 05 in this series.

Early in the 20th century German neurologists, Alois Alzheimer and Emil Kraepelin, proposed recognition of another form of dementia characterised by three features. First, it appears in people who are not old (age group 40s or 50s); second, it occurs insidiously, without any other known cause of dementia; and third, it provides evidence in a pathology of the brain. Scattered throughout such brains are seen abnormal blobs of protein called plaques (sometimes called “senile plaques” or “amyloid plaques”). The plaques have become very important, and eventually confusing, to the understanding of dementia. They are abnormal regions where the complex circuitry of the brain has broken down and a range of abnormal proteins has been deposited, and they are used by pathologists throughout the world to diagnose a dementia as Alzheimer’s disease. Many scientists believe that the cause of dementia lies in one of the many proteins found in the plaques. The protein is called amyloid. It is believed to deposit in brain tissue as nerve cells die forming a toxic breakdown product called beta-amyloid. This then poisons more nerve cells, which die and release their amyloid; and a destructive cycle follows.

Study after study through the middle of the 20th century has shown that the early-onset cases were just early instances of age-related dementia. Alzheimer’s idea of a discrete early-onset condition has been quietly abandoned and the term Alzheimer’s disease is currently applied to age-related dementia, provided the brain shows plaques in sufficient number. A few genetically driven forms of early-onset dementia have been identified, but we now know, thanks to some clever DNA detective work done in the 1990s, that Alzheimer’s patients did not carry these genes.

On 18 September 2005, as I listened to Robyn Williams’ science show program “Ockham’s Razor” on Radio National (AM 576), I heard an interview of Professor Jonathan Stone, Director of the Research School of Biological Sciences at the Institute of Advanced Studies, Australian National University (ANU), Canberra. Professor Stone was talking about some new research findings suggesting that Alzheimer's is actually a vascular disease. This finding has important implications in treatment and prevention of Alzheimer's condition. Extracts of what Professor Stone said are reproduced below:

'I became involved in trying to understand the causes of dementia a decade or so ago, when a private Sydney-based charitable trust, the Sir Zelman Cowen Universities Fund, asked me to help manage its research grants program, in which work on dementia had high priority. Through that program I became aware of the work of a young neuropathologist at the University of Sydney, Karen Cullen, who showed me some of her material from the brains of patients diagnosed with Alzheimer’s disease. In a critical step she had deliberately searched for signs of bleeding in these brains, using a range of techniques to detect blood residue and to relate it to plaque. Her material showed that every plaque in every brain she studied — in young brains where the plaques were uncommon, in older brains, in demented brains where the plaques are numerous — is the site of a small bleed, a tiny stroke. Her finding confirms the growing evidence that the Alzheimer-like dementias involve vascular disease, and show precisely what is happening: blood vessels break down in the ageing brain, as they do in ageing skin for example, creating first one, then a few, then many dead patches of brain, which we see after death as plaques.

'A finding as striking as this is rarely accepted without argument, and Karen’s work has struck its share of dismissal and delay. But the papers describing her findings will shortly appear in international journals and, we hope, a door to prevention and delay of dementia, half open for over a decade, will be opened more widely.

'Karen’s observations suggest that Alzheimer-like dementias occur because of the breakdown of cerebral capillaries, the smallest blood vessels of the brain. Each breakdown is a micro-stroke, too small to cause symptoms, which is why the sufferers often have no clinical history of stroke. But as these micro-strokes accumulate, their effects accumulate, and the familiar, sad pattern of cognitive loss, loss of memory, then personality, follows. Her results suggest that age-related dementia is a vascular disease. That is why anti-inflammatory and statin drugs are protective. That is why the risk factors for cardiovascular disease and dementia overlap so extensively. That is where prevention and delay are already available. That is where advances in the design and deployment of drugs which preserve blood vessels should give the long-awaited tools to delay and prevent this slow, troubling, destruction of personality known to family and carers as the long goodbye.'

References

• Eric Sabo http://www.healthology.com/focus_article.asp
• Jonathan Stone, Director, Research School of Biological Sciences, Institute of Advanced Studies, Australian National University, Canberra jonathan .stone@anu.edu.au
• Robyn Williams, Ockham’s Razor, ABC Radio National Science Show, http://www.abc.net.au/rn/science/ockham/stories/s1460970.ht

Follow the Mind your Mind signposts adapted from Alzheimer's Australia

Click here to enlarge above brochure http://www.alzheimers.org.au/upload/Brochure.pdf

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Senior Moments - Memory Loss: Real or Imagined? 09 09 05

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Monika Bhatia
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30 September 2005

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