More than one million people in Germany alone – incidentally more women than men – and their relatives have to live with the diagnosis of Alzheimer’s disease, and the trend is rising. Some even speak of up to 4 million. It all starts with a slight forgetfulness: For example, you forget the date you read in the newspaper 2 hours ago, or you forget where you put your wallet. These are all things that can happen to any of us. But when forgetting starts to accumulate, it is time to address it. However, most people find this difficult. Repression of the symptoms by the patients themselves, but often also by their relatives, is one of the main problems in recognising Alzheimer’s early enough.
What is Alzheimer’s?
The generic term for a failure of normal brain functions is dementia. Alzheimer’s dementia is the most common form of dementia. Forgetfulness is a first indication, but it can also have other causes than Alzheimer’s. This is precisely why it is important to diagnose the disease early enough. A second stage or symptom is that those affected develop word-finding problems, they can no longer remember the term they normally use and then use other words. A third indication is when the patient can no longer make a logically coherent argument and therefore breaks off in the middle of a sentence because he has forgotten what he wanted to say. Also, the same statements or phrases are frequently made and repeated. These are therefore the first signs that can indicate Alzheimer’s dementia if they occur in continuity.
The horror of where Alzheimer’s ultimately leads is probably in front of all of your inner eyes: abandonment of identity, loss of ego, disorientation and dozing off into apathy until unconsciousness.
The disease is psycho-social from the onset. In almost all cases, relatives are involved, and their behaviour is one of the decisive factors in how and how quickly the disease develops. Once the diagnosis has been made, there seems to be no turning back; it is then important to slow down the course of the disease as much as possible. This causes enormous stress for the patient who receives the diagnosis and also for the relatives. If you can’t find a way to relieve these two types of stress, it is difficult to fight the disease. Shame and guilt, not expressing aggression from both sides and helplessness play a big role. They are the social components of the disease. What could not be expressed before, when the disease was not yet diagnosed, can now by no means be expressed without help. This leads to the disease not being diagnosed at all or only at a late stage in about 50% of patients. This psychosocial bubble and helplessness can accelerate the course of the disease instead of slowing it down.
Early diagnosis is also important because the symptoms described could have other causes, such as vitamin deficiency or depression in old age.
What happens in the brain in Alzheimer’s disease?
In Alzheimer’s disease, the medial temporal lobe shrinks first, and later a complete shrinkage of the brain can be observed. The temporal lobe houses the hippocampus in its central part, which performs many functions, including memory, i.e. the storage of experiences. This is where the changes in the brain and shrinkage can first be noticed.
In the brain, there is often an increased amount of a protein called amyloid, which is normally broken down again. In Alzheimer’s disease, however, not enough amyloid is broken down, the nerve cells begin to stick together and work under constant high performance. Another indication of Alzheimer’s is when so-called tau fibrils can be detected, which are dead nerve cells that are no longer properly removed. The amyloid plaques and the tau fibrils together can be seen as important biological clues to the disease. In addition, the immune system signals inflammation. The sheaths of the nerve cells, the so-called cell membranes, play an important role in these processes. These consist – we have already mentioned this in several articles – to a large percentage of phosphatidylcholine or lecithin. With the help of built-in proteins, they are essentially responsible for the metabolic process and the control of the cells. So it is no wonder that phosphatidylcholine also plays a role in Alzheimer’s research. Slowly but surely, more and more nerve cells, up to and including the entire “nervous skeleton”, perish and reduce brain functions, for example, memory, speech, orientation and logical thinking.
How is Alzheimer’s diagnosed?
Diagnosing Alzheimer’s is anything but easy and impossible without medical help. MRI (magnetic resonance imaging) can detect shrinkage, but not always and certainly not in the early stages. In the advanced stages, the plaques can be detected by a certain imaging technique called PET (positron emission tomography). MRI and PET together can already give a clear indication of Alzheimer’s disease. In addition, questionnaires are used, especially the Boston Naming Test. This is carried out in a memory outpatient clinic, which now exists everywhere in Germany. An important test is the 10 after 11 test, which can even be carried out by anyone.
Here are the instructions for the 10 after 11 test: First, draw a circle. The circle should represent the face of a clock. All the hour numbers from 1-12 are then written on it without looking at your own watch. Then the position of the smaller hour hand and the longer minute hand is drawn, at the time 10 minutes past 11 o’clock (other times are also possible!). Alzheimer’s patients in a more advanced stage no longer succeed in this task.
Overall, it can be stated that the diagnosis of Alzheimer’s is not easy to carry out, an MRI can be carried out but is not always informative and the PET administers a high radiation exposure to the body and is very expensive, which is why it is not currently included in the recommendations for Alzheimer’s diagnostics. A blood test for Alzheimer’s is not yet available. The lumbar puncture of the cerebrospinal fluid should also be mentioned, as it can detect excessive amyloid. However, this procedure is not without danger and is usually only carried out if absolutely necessary.
Prof. Haass, a biologist who is involved in fundamental research on Alzheimer’s, has named three genes that can trigger an amyloid excess. Genetics thus seems to play an equally important role. There is a group of Alzheimer’s patients in whom the disease is attributed to a certain state of gene activity of these three genes, who then all develop Alzheimer’s, sometimes very early.
Even more important than a genetic predisposition seems to be the influence of epigenetic factors. Epigenetics means that the environment influences the activities of the genes, and that this imprinting can even be inherited without the DNA, i.e. the genetic building blocks themselves, being directly involved.
What therapies are available for Alzheimer’s disease?
So far, there is no drug against Alzheimer’s disease. There are some promising active substances in trials that promise to be effective if used as early as possible. However, these active substances have not yet progressed beyond initial clinical trials. There are two studies that will be presented here as examples:
A team led by the Swiss researcher Prof. Roger Nitsch is working on an antibody therapy with an active substance called Aducanumab. A first small study showed that amyloid deposited in the brain was dissolved again. Now a study is being conducted with a larger group of 2,700 patients. The American company Biogen is involved. The drug could slow down Alzheimer’s, but not cure it. Another antibody approach is being pursued in Mainz with the drug Acitretin, which was originally approved for the treatment of psoriasis. Under the leadership of Prof. Fahrenholz, this approach is being pursued further.
Whether this will eventually lead to the development of drugs that at least slow down the disease remains to be seen.
The problem also seems to be that at the present time it is still not clear whether amyloid is actually causally responsible for the disease. The background for the doubts is that in a study with old nuns, the so-called Nuns’ Study, it was shown that they had a lot of amyloid plaques in their brains, but were still mentally top fit. It is clear that Alzheimer’s does not occur without an excess of amyloid.
In any case, we would like to point to studies on Alzheimer’s disease with our favourite molecule PPC/DLPC. First of all, we would like to add that Alzheimer’s disease is so complex that it is difficult to imagine that a sufficiently successful therapy can actually be achieved by chemical action via drugs alone. However, we can summarise the results on the therapy of Alzheimer’s disease with PPC in such a way that in up to 50 % of the treated patients a slowing down of the disease and in individual cases even an improvement of the current status was observed. However, the published studies were not conducted with a large number of patients. We will describe the effects of PPC in more detail in the last part of this article.
What causes Alzheimer’s?
The epigeneticist Prof. André Fischer and his team have conducted a great deal of research into the extent to which epigenetic factors play a role. This research has shed some light on the genetically determined switch-off and switch-on processes of Alzheimer’s genes. This group is also looking for suitable agents that can influence individual gene activities. Prof. Haass, who has already been mentioned, is also looking for suitable enzymes that influence the progression of Alzheimer’s. All these scientists see the causes purely physiologically, i.e. at the physical level.
But isn’t this actually only a manifestation of what the patients have experienced during their lives in interaction with their environment? Epigeneticists, at least, should actually come up with the idea that the quality of social interaction not only influences the process of darkening and forgetting to the point of ego abandonment, but possibly even helps initiate it. However, this connection would only be scientifically verifiable if interdisciplinary work were carried out.
We would like to offer our own and logical explanation here: If you want to get to the root of the real causes, you have to go beyond the way of thinking that human beings consist only of bodies. It is also about spiritual development, it is about social metabolism and how we move within it. It’s no wonder that the nuns were practically unaffected by the excess amyloid in their brains, they don’t live by the rules like most of us. We live in an economic system that has as a major interest that we consume a lot. However, a life that is too much limited to consumption can lead to a depletion of meaning and altered interpersonal relationships. This can also be seen in some medical advice on Alzheimer’s, which focuses too much on activities, satisfying desires and enjoying life. The meaningfulness of life is in danger of being neglected.
Can one prevent Alzheimer’s?
Of course, a balanced diet as well as physical and mental activity are essential elements to prevent a disease like Alzheimer’s as well. It is not said for nothing: Mens sana in corpore sano est (A healthy mind is in a healthy body). In addition, the continued search for meaning and the striving to always develop oneself further are essential building blocks against forgetting.
Oral intake of memphosan (PPC) to protect cell membranes can also be considered useful, but the importance of social metabolism is too often underestimated. We can quietly take an example from the nuns: Meditation (prayer), seeking connection to something higher, hard physical work, mental engagement with the important things in life, even living together in a larger community – all of these can delay, perhaps even prevent, the onset and progression of dementia, including Alzheimer’s. While there are still not enough people who see it this way, if one looks into people’s current lives, such a conclusion suggests itself.
What can relatives do when confronted with a diagnosis of Alzheimer’s disease?
Those who have a lot to do with Alzheimer’s patients also have the above thoughts to some extent and direct their recommendations accordingly. In principle, it is a matter of first relieving the patients and also their relatives of the stress that the horror vision of the last stage of the disease causes them.
Alzheimer’s patients need a mentally active environment, they need social contacts, they certainly do not need isolation and the removal of all challenges. The less the patients have to do, the faster the disease worsens. Smaller, manageable groups seem to be best suited for these tasks, such as dementia living communities or small, unsegregated groups within homes. Giving one person all the care is inhumane and neither good for the carer nor for the person being cared for.
PPC – is there a link to Alzheimer’s?
In reviewing the studies, we need to distinguish between three directions that are, however, interrelated: What evidence is there to show that the phosphatidylcholine (PC) in the membranes of nerve cells is damaged? Can observed membrane changes be used diagnostically? And are there studies that administration of PPC, i.e. polyenylphosphatidylcholine from soybean, can improve the status of patients? These three questions will be briefly examined.
As already communicated, one of the greatest diagnostic difficulties in Alzheimer’s is the earliest possible detection of the disease. If one could easily obtain the respective status of the disease from the composition of the PCs in the membrane, as early as possible in its development, this would be an important step towards improving diagnostics.
There are several studies on the therapeutic effects of PPC. A recent Japanese study from 2013, in which the memory performance of 310 patients was measured before and after taking PPC, evaluated the memory performance of the patients with the help of a measurement method called MMSE score. The study showed that many patients not only had a slower progression of the disease, but even an improvement. The best results were found when two specific PCs were administered, the DLPC and the POPC. Both molecules are included in the formulations used by the Network Extended Medicine. It should be added that the dose recommended by the network is about 8 times higher than that given in the study. We do not want to raise too much hope at this point. Therefore, we want to emphasise here that a few small studies do not yet allow a general statement on the effect of PPC. However, we can certainly speak of hopeful indications.
The study of cell membranes and their importance for the activities of their cells and also the mitochondria within the cells is already quite advanced. When we talk in this blog about phosphatidylcholine, which forms a large percentage of the membranes, this is more rough information, which is therefore no less correct. However, scientific studies are more concerned with the very precise composition of the membranes. A distinction is made between many different phosphatidylcholines, all of which together give the membrane stability and at the same time flexibility and functionality. These different phosphatidylcholine components have been and are also being studied in detail in connection with Alzheimer’s disease. Some studies have already shown that at least three different phosphatidylcholines are proportionally broken down in Alzheimer’s disease.
Perhaps a very general comment on this: the aim of these thoughts is to take away guilt, not to build up guilt. This means that the economic and, partly affected by this, the social conditions of our living together are causally responsible for the fact that all kinds of chronic diseases of civilisation arise from them. We ourselves are not responsible for this. But we can and may take responsibility for not completely submitting to these conditions, because we have this choice.
We would also like to point out another connection. A substance called acetylcholine (ACh) is needed for the brain to function properly. ACh is one of the most important neurotransmitters that transmit information in the network of nerve cells. Without acetylcholine, there is no nerve activity. Choline is absorbed through food. PPC contains choline in every molecule, which after its release is able to be used for the synthesis of ACh.
Further information on Alzheimer’s disease
You can get extensive information about Alzheimer’s at the Alzheimer’s Association website https://www.alz.org/
The Japanese study
Tomoyuki Nishizakia, Takeshi Kannoa, Akinobu Gotohb: DL-/PO-phosphatidylcholine may shed light on the treatment of Alzheimer dementia. http://dx.doi.org/10.1016/j.pmu.2013.04.001