Now what was I going to write about in this column? I can’t remember – perhaps I have incipient Alzheimer’s. That’s the clue. Alzheimer’s was just what I planned to write about. (Forgive the gallows humour but people of my age are all too familiar with the condition – too many of our friends have been affected. And its possibility looms ahead of us: will it be me? Will it be her? And when? So we make the occasional wry joke as if it were a charm to ward off the phantom.)
Dementia of different types affects well over half a million people in England. Sixty per cent of these have Alzheimer’s. It is estimated that one in 14 people over the age of 65, and one in six over 80, have the condition. The incidence of Alzheimer’s worldwide is expected to quadruple by 2050.
The disease was first demonstrated in 1906 by Alois Alzheimer who described the brain changes, discovered post mortem, in a 55-year-old patient. Since then an enormous amount of work has been devoted to studying the disease, although at present we can do no more than delay its onset to a degree. Our strides in knowledge of genetics and methods of surveying the action of the brain put us in a better position nowadays to discover effective therapies to alleviate or cure the problem. But don’t hold your breath.
At a macro level, Alzheimer’s causes growing atrophy of the brain, and the hallmarks are described as amyloid proteins plaques and tau proteins causing tangles (together with a number of other “biomarkers”). The technical details are perhaps of less importance than our current recognition that the processes leading to severe symptoms may start 10 or more years beforehand. New clinical guidelines for the disease itself have recently been published by The Journal of the Alzheimer’s Association. Three approximate stages are described: preclinical, mild cognitive impairment and Alzheimer’s dementia (more details here, if you can bear them).
At the pre-clinical stage the brain changes may already have started although significant symptoms are not apparent. In some instances special tests can demonstrate changes but, as yet, the likelihood of progression to full Alzheimer’s for such people is not yet known. A great deal more work must be done to establish and standardise such markers, and the studies can only be for research for the time being. There are, of course, ethical problems in diagnosing a future condition where no reliable way of averting it has been established.
Mild cognitive impairment means roughly what it describes. The changes in performance and biomarkers can more easily be identified although they do not tell clinicians for certain whether Alzheimer’s will result. Again, the studies here are mainly to be used as a framework for research.
Alzheimer’s dementia is the final stage. Investigations go beyond memory loss, and look at other forms of cognitive impairment. Alzheimer’s must, as accurately as possible, be distinguished from other forms of dementia. The disease follows a typical course of gradual impairment which may start at a level which is only externally obvious to close relatives and progresses until the sufferer is totally dependent on nursing care. The whole dementia phase lasts from seven to 10 years, and results in death.
The bad news is that the long build up to the beginning of dementia proper means that many of us reading this are, unbeknown to us, already on the path. That certainly includes me in my eighth decade. The good news is that our techniques for brain diagnosis and our understanding of genes have made great advances, and it is a reasonable hope that we will eventually develop cures and alleviations which can be employed while, or before, the disease is in its preparatory phase. You may get an idea of the activity on the Alzheimer front from the fact that in 2011 my files show that I have noted one new study of significance published for every week of the year.
Almost at random I give you some examples. Clinical trials of a vaccine which may halt or even reverse amyloid plaque build-up (Southampton University). A new approach to analysing brain signals which may give early warning of the approach of the disease (University of Strathclyde). New refinements in MRI scanning may enable early detection (Radiology). Discovery of several new genes which may help to establish Alzheimer risk, and provide the basis of a cure (Cardiff University and Mount Sinai School of Medicine). Progress made in attempts to recover damaged neurons through use of Stem Cells (Stem Cells). Value of increased social activity in warding off cognitive decline (Rush University). A “state-of-the-art” review, invaluable for this column, (Hozman, Morris, and Goate, April 2011). Even as I write I see another Alzheimer story looming on my electronic horizon – but I have to stop somewhere.
We have to approach philosophically the likelihood that, while the scientists are hacking their way through the undergrowth, few of us reading this will benefit ourselves. After all, I avoided my grandfather’s death through a heart attack by having bypass surgery not available in his time. She who would have been my mother-in-law died from TB during World War II; a few years later and she would have survived. Cancer is far from beaten but there are many cures developed recently. So the work that is done today – either by scientists or by those who support them – is our way of repaying the extra years which previous generations have gained for us.