Alzheimer's disease is one of the most mysterious diseases of the nervous system. There are many hypotheses about its causes. Recently, the world of science has been touched by the information that the initiation of the degradation of the functions of the cerebral cortex may occur as a result of … infection. We discuss this hypothesis, as well as other problems related to Alzheimer's disease with prof. Michael Davidson, a world-renowned expert in Alzheimer's research.
Alzheimer's diseaseis of interest to many researchers. Some factors in the development of the disease are known, i.e. features the presence of which increases the statistical risk of developing the disease. These include older age, female gender, low level of education, diabetes, and a close relationship with people who have been previously diagnosed with the disease. However, there is no certainty as to its causes. A new direction of research is set by the publication of researchers from University College London in the pages of the journal "Nature" (the full text of the article in question can be read in Nature, Volume 525 Number 7568 pp157-284, September 10, 2015, http://www.nature.com/news/ autopsies-reveal-signs-of-alzheimer-s-in-growth-hormone-patients-1.18331).
We are talking about it with prof. Michael Davidson, a world-renowned expert in Alzheimer's research.
- Could the research published in Nature magazine be a breakthrough in the fight against this disease?
Prof. Michael Davidson: This publication is well documented and the first to suggest that Alzheimer's disease may be contagious. While we knew that a particular type of dementia - Creutzfeldt-Jakob disease - was contagious, this is only a fraction of a percent of dementia. I hope that scientists from University College London are right, because it is much easier to treat an infectious disease than the multifactorial disease, which Alzheimer's disease is considered to be. However, we must remember that the results of research published even in such prestigious periodicals as "Nature", "The Lancet" or "New England", in half of the cases it is impossible to repeat. I am not saying that it will be like that this time, but statistics prove that it concerns almost 2/3 of articles presenting scientific research.
- What does it mean that this disease can develop as a result of infection?
M.D .: It is about the presence of amyloid protein in the brain whichforms plaques that destroy the cerebral cortex. Researchers from University College London detected this protein in people who had been injected with growth hormone. Of course, that doesn't mean that all the people with dementia who have amyloid plaques in their brains were infected this way - they could have developed the disease in a completely different way. I assume that the amyloid protein may be transmitted by surgical instruments. To confirm this, we would need research on a very large sample of at least 1,000 people who underwent neurosurgical operations in their youth. We could trace their lives to an older age and compare them with the fate of people after abdominal surgery. Then we would find out if patients after neurosurgical operations suffer from Alzheimer's disease more often.
M.D .: We inherit pretty much everything we are. Alzheimer's disease, like heart attack, is hereditary in some way, but not one gene, but a combination of them. One gene can only cause rare diseases, and Alzheimer's disease is common. Epidemiological data show that if we have a first-degree relative, the risk will be increased in our case - not much, but still. One gene may be responsible for much less than 1% of dementia. If we are talking about many genes or their combinations, the situation changes. Scientists are developing a mathematical model of the genome to find out what gene combinations can cause Alzheimer's disease. But environmental factors also need to be considered - each set of genes interacts differently with a specific set of environmental factors, and this obscures the picture. Age is the biggest risk factor for Alzheimer's disease. Usually people between the ages of 78 and 82 suffer from it.
M.D .: It used to be thought that it was due to the lack of a single neurotransmitter, later - that it developed due to the lack of many neurotransmitters, then - that a specific protein was to blame. Whoever made the brain didn't simplify our tasks - it's a very complicated organ.
I would compare Alzheimer's disease to cancer or cardiovascular diseases - just as they are a disease caused by many factors. When we get to know them thoroughly, we will be able to lower the risk, heal the symptoms, and delay the progression.
I would compare Alzheimer's disease to cancer or cardiovascular disease - just as it is a diseasecaused by many factors. When we get to know them thoroughly, we will be able to lower the risk, treat symptoms, and delay progression.
- Are there currently any experimental therapies that give hope for successful treatment?
M.D .: Of course. For the last 20 years, we have been testing substances that induce the body to produce antibodies to fight amyloid protein. These antibodies do work, but they do not improve cognition. The body does not regain its former efficiency, at most the patient's condition does not deteriorate. Hence the conclusion that these types of medications should be given to elderly people who have not yet experienced symptoms of the disease to prevent amyloid protein build-up.
- This means that pharmacological prevention can save us from Alzheimer's disease?
M.D .: This is the optimistic version. Pessimistic: that amyloid protein is not the real cause of the disease. Comparing this with diabetes, for example, there is a high sugar level, but it does not cause blindness. And in Alzheimer's disease: amyloid protein is present, but it does not cause dementia. Research is ongoing. Medicines are given to he althy people or people in the early stages of the disease to check the effects of their action.
- Do you think that a drug will be found that will eliminate this disease?
M.D .: I don't believe in one drug. Here it is like with hypertension that can be treated with many preparations. But I believe that by using different methods we will achieve improvement.
According to an expertprof. Michael DavidsonExpert in Alzheimer's disease research and drug development for dementia. He has published over 250 works in international scientific literature. He has a professorship at Tel Aviv University. Co-founder of the comprehensive Angel Care Center for Senior Citizens in Wrocław.
Worth knowingThree Degrees of Alzheimer's Disease
- Mild dementia
Attention disorders and problems with remembering new information appear. Working memory, i.e. memory concerning currently performed activities, is failing. Difficulties with concentration impair the persistence of the memory trace in the brain - the patient does not know where to put the keys, he asks the same questions because he does not remember that the answer has already been given. Depression, mood swings, personality disorders appear, isolation from the environment, etc.
- Intermediate dementia
Apart from memory disorders, there are also disorientation (first in foreign places, and then also in familiar places, e.g. the patient confuses floors, apartments) and speech (difficulty in finding the right word or namingdifferent things). The patient does not recognize family members, is aggressive, irritable or apathetic, has hallucinations and delusions, most often of persecutory content or marital infidelity. Must be under constant care.
- Very advanced dementia
The sick person loses the ability to perform everyday activities. He cannot dress, prepare a meal, cannot use cutlery, etc. He cannot distinguish between the people around him, the time of day and night. Its silhouette is tilted forward. He has a hard time walking around and he reluctantly gets
out of bed. There are problems with keeping urine and stool, as well as swallowing disorders, which lead to the exhaustion of the body.
Brain scan
Thanks to a PET (positron emission tomography) scanner, we can view the brain and see what the amyloid protein that destroys the cerebral cortex looks like. The results of the research are surprising: some people do not have dementia despite the fairly large accumulation of amyloid protein. In others, dementia develops despite having little protein accumulation. Moreover, it appears that among people already suffering from dementia, the amount of amyloid protein in the brain does not increase as the disease progresses. It is likely that the build-up of this protein in the brain begins much earlier than the first symptoms of Alzheimer's disease appear.
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