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A single measurement taken from an X-ray image of the brain can distinguish
between people with Alzheimer’s disease and those with no evidence of dementia.
The technique’s developers say it is a ‘first step’ towards a future screening
test and could be used immediately to improve the accuracy of population
studies of the disease, and in identifying patients for trials of new anti-Alzheimer’s
drugs.

Alzheimer’s disease affects an estimated 500 000 people in Britain causing
progressive dementia for which there is no cure. Nor is there a definitive
diagnostic test, short of dissecting the brain after the patient has died.
Doctors rely on the descriptions of symptoms given by patients and their
carers to identify the disease – a method that is far from conclusive.

The new test is based on the observation that, in Alzheimer’s patients,
certain structures within the brain shrink. David Smith and colleagues at
Radcliffe Infirmary in Oxford and Nicholas Wald of St Bartholomew’s Hospital
Medical College in London, have focused on the medial temporal lobe, an
area involved in memory.

The researchers used a computerised tomography (CT) scanner, which generates
X-ray images of the brain’s geography as if a series of horizontal slices
had been made through the head. Patients are normally scanned horizontally,
but the researchers adopted a different angle – 20 degrees from the horizontal
– so they were able to see the temporal medial lobe as a ‘horseshoe’ of
tissue around the brain stem.

In a long-term study, they found that measurements of the thinnest point
of the lobe in 44 Alzheimer’s patients were lower than for 75 controls,
and that there was little overlap between readings from the two groups.
‘It’s a big effect,’ says Wald.

The researchers were able to identify 92 per cent of the patients, but
at the cost of falsely identifying 5 per cent of controls as sufferers.
By choosing a lower value for the cut-off measurement between patients and
controls, Smith and colleagues could detect 79 per cent of sufferers and
reduce the ‘false positive’ rate to 1 per cent.

Because some patients and controls slip through the net, the practical
value of the test is limited. But Smith says combining the X-ray measurement
with another ‘marker’ for the disease could overcome this problem. For example,
he has found that Alzheimer’s sufferers often produce a variant of the enzyme
acetylcholinesterase. Using the two tests in parallel could reduce the number
of false positive identifications.

Other types of scanners can identify Alzheimer’s disease in living people,
but suffer several disadvantages. Positron emission tomography scanners,
for example, are very expensive and are few and far between. Magnetic resonance
imagers can measure the volume of structures within the brain but, according
to Smith, being scanned is ‘noisy and claustrophobic’, and very unpleasant
for demented people. By contrast, CT scanners are readily available and
someone can hold the patient’s hand for the 10 minutes it takes to survey
the brain.

One promising property of the test is that in 10 people who did not
have Alzheimer’s disease but were demented, measurement of the medial temporal
lobe gave readings partway between those of controls and Alzheimer’s sufferers.
This suggests that the test would distinguish between Alzheimer’s and other
forms of dementia, but more work is needed, Smith says.

What is needed most says Martin Rossor, a neurologist at St Mary’s Hospital
in London, is a test that identifies patients with Alzheimer’s early in
the disease, preferably before signs of dementia appear. ‘The patients in
this study were very demented,’ he says. Smith agrees, but points out that
one patient tested positive five years before he died. Further trials may
show that the test picks up disease very early.