This means that, although it is possible to eliminate pathological proteins from the brain, dementia can not be stopped. This is the result of recent clinical studies, which is why more attention is being paid to prevention.
Professor Peters, after many years of research, medicine knows a lot about Alzheimer's disease. How far is today's treatment approaches?
We know that Alzheimer's disease is accompanied by protein deposits in the brain. These so-called amyloid plaques are thought to be involved in the death of nerve cells in the brain. Amyloid plaques can be detected by positron emission tomography, a nuclear medicine procedure. A possible therapeutic approach is to remove the diseased protein deposits. However, it has been shown that in the symptomatic phases of Alzheimer's disease, if there already existed dementia, had little benefit – the progression of the disease could not be stopped.
How does the research deal with this discovery?
The logical consequence of this awareness is prevention. So, if possible, it should under no circumstances result in excessive death of nerve cells in the brain. For functions that are once lost can not be found. I like to make parallels with hypercholesterolemia, the disorder of fat metabolism prevalent in industrialized countries, for the sake of comparison. Even fats in the blood are not noticed by patients, they can only be measured by laboratory tests. However, as a result of hypercholesterolemia, serious cardiovascular disease can occur. Here again, we are trying to eliminate risk factors, that is to say, to reduce cholesterol levels again by early intervention – such as drug treatment or a change in lifestyle – and thus reduce the risk of heart attack or stroke.
With Alzheimer's, should prevention be the same as high blood lipid levels in protein metabolism?
Exactly – and as soon as possible. More specifically, in the prevention of Alzheimer's disease, the precursor protein is said to be blocked, so that the amyloid can be produced in a reduced amount. To this end, what are known as secretase inhibitors, which deactivate an enzyme involved in the formation of amyloid. The hope is that it will not only cause fewer plaques, but also that secretase inhibitors will have a lasting effect on the pathway. Because at the moment, it must be assumed that precursors of amyloid plaques have negative effects on the brain.
To what extent is this preventive approach promising?
This is currently demonstrated by two very similar clinical studies that have been starting and continuing for five years. Both aim to show if the development of Alzheimer's disease can be prevented in people who are not yet sick, but who are at increased risk because of their genes. The difference between the two studies is based on the genetic requirements of the participants.
What is the genetic risk?
We now know that people with the APOE4 gene are at a much higher risk of developing Alzheimer's disease. As a result, clinical research is currently focused primarily on people with this biological trait. It is precisely these carriers of the APOE4 gene that are currently selected mainly for this study.
In other words, if more cases of dementia have occurred in my family, am I a good candidate for the clinical prevention study?
The genetic examination and the determination of the risk gene indicate in the first place whether you are eligible to become a candidate. In addition, there is an age limit to participate in the study. We are specifically looking for patients aged 60 to 75 years old.
Why exactly this age bracket?
This is due to the design of the study, the assumptions about the risk of developing Alzheimer's disease and the number of case studies based on it. This does not mean, however, that the prevention of Alzheimer's disease makes no sense in any other phase of life. On the contrary, the sooner you can intervene in this previously incurable disease and prevent it, the better. We must not forget that Alzheimer's disease is characterized by a slow and slow evolution. It is not a sudden deterioration. So, as long as possible to preserve as many brain functions as possible, early prevention is a valid and meaningful approach.
Because you have drawn a parallel with blood lipids: can I fight Alzheimer's disease through a healthier lifestyle?
Here are some interesting long-term studies that show that co-factors of Alzheimer's disease can be optimized, but that a healthier lifestyle can not reduce your risk to zero.