What causes Alzheimer’s disease? What do we know and not know about it?
What makes Alzheimer’s more likely? What can keep our brains healthier for longer? How can we minimise our chances of developing Alzheimer’s disease?
Almost everyone has heard of Alzheimer’s disease since Alois Alzheimer analysed and classified the cluster of symptoms in 1901 in Frankfurt, Germany. It is a degenerative neurological disorder characterised by the death of brain cells and atrophy or shrinking of the brain, resulting in progressive loss of cognitive functions.
Depending on the calculation method, Alzheimer’s disease is the 6th or 7th most common cause of death in developed countries. It is the most common of all the possible causes of dementia.
Many people ask, what are the symptoms of Alzheimer’s disease? As with all progressive diseases, the cluster of symptoms depends on the severity and progression of the disorder. At its most severe, just before death, the person has lost all higher cognitive function, including speech, and appears to have no awareness of their surroundings, loss of bowel and bladder control, and all but autonomic bodily control has gone.
In the final stages, it is common for aspiration pneumonia to develop because the person no longer has the ability to swallow properly or to clear their lungs by coughing.
Early symptoms at the mild to moderate stages
- Difficulty coping with novel contexts and situations.
- Increasing problems with learning anything new.
- Decreased ability to think logically and structure thoughts effectively.
- Reduced capability and duration of concentration.
- Impairments of memory, especially of new events or ideas.
- Becoming confused.
- Decreasing ability to process words and numbers (in both written and verbal forms).
- Reduced levels of initiative.
- Decreased spontaneity.
- Requiring more time to conduct everyday activities.
- Repeating questions (due to not recalling the answers previously given).
- Increased frequency of misplacing items and missing agreed meetings.
- More likely to become lost in unfamiliar places.
- Apparent aimless wandering or becoming lost in familiar places.
Alzheimer’s disease typically goes through seven stages
- Pre-symptomatic.
- Minor forgetfulness (usually brushed off as normal for some time).
- Marked memory difficulties.
- More widespread cognitive dysfunction.
- Diminishing ability to function independently.
- Severe symptoms and multiple impairments.
- Loss of physical control.
Over the years, I have repeatedly heard various forms of this question: ‘When people know what lies ahead of them when they have reasonable grounds to suspect that they have or have been diagnosed as having Alzheimer’s disease, why do more not choose to end their lives in a way, and at a time and place, of their choosing?’
There seem to be many answers
Many people would not choose to end their lives; however, well they know what awaits them on religious grounds. Others are hopeful that a cure, or at least a means to stop the progression of the disease, is just around the corner.
Some are not aware of what Alzheimer’s disease will do to them
An unknown number of people with Alzheimer’s disease have lost the ability to choose the means of their end because one of the features of Alzheimer’s disease is the loss of initiative. For a person to choose to end their lives, they must have the ability to initiate such a plan, recall methods of self-termination, and remember the plan long enough to carry it out.
We know the progression of Alzheimer’s disease but very, very little about its causes. As is usually the case with apparently inexplicable diseases, there has been much speculation over the decades.
Serious and credible scientists have believed that many factors cause Alzheimer’s disease. Alas, so far, none have proven to be accurate. Most have proven to be coincidences that were misread as causal. For instance, as the use of aluminium pots and pans increased, so did the number of cases of Alzheimer’s disease. Ergo, ‘aluminium causes Alzheimer’s disease.’ Not so.
The use of pesticides, plastics, zinc, mercury, toothpaste, tuna (and many other suspects) was increasing, as was the number of cases of Alzheimer’s disease. Again, all such alleged ‘causes’ have proven to be coincidences.
Correlation does not prove causation. Neither does ‘linked with’. Among the latest theories to be covered in the media is that Alzheimer’s disease is caused by or ‘linked with’ the consumption of highly processed and pro-inflammatory foods.
Alzheimer’s disease is ‘linked with’ many factors: drinking pure, clean water, having a heartbeat, breathing oxygen, the sun rising in the east, and living on a planet in a Milky Way. Alas, ‘linked with’ is often used to imply a causal link covertly without saying so openly.
‘Linked with’ also masks the possibility of mediating variables. For instance, a hammer does not cause a nail to go into a piece of wood. The hammer is inert; it will remain where it has been placed until and unless acted on by an outside force.
Neither is the force the cause of the nail going into the wood. A human has to use the hammer to apply sufficient force in a controlled and precise direction while guiding the nail. The hammer is a mechanism through which the force is applied; it is just one variable in a complex causal chain of events. Did the hammer cause the nail to enter the wood? No. The human intention and actions did; the hammer was just one of several involved variables.
As with most complex diseases and problems, looking for a single cause can prevent progress. The wisest scientists look for causal sequences, not causes; causal chains, not single links.
Entirely reasonable and plausible theories of the causal chains for Alzheimer’s disease have been researched for decades.
The ‘cholinergic hypothesis’ is that AD is caused by a neurotransmitter shortage of acetylcholine. Even if that were true, it would not be ‘the cause’ of AD; it would a mediating variable. The bigger question would be: what causes the shortage of acetylcholine?
Alas, even when ‘medicines’ were developed to increase or prevent the reduction of acetylcholine, they had no effect on the progression of the disease. Thus, indicating that acetylcholine is, at best, one of many mediating variables and that its deficit is not causal.
The ‘amyloid cascade’ hypothesis holds that the build-up of amyloid plaques in the brain triggers an inflammatory response which destroys brain cells. Amyloids are proteins that the body produces normally. In a healthy brain, fragments of amyloids (known as beta amyloids) are broken down and eliminated. In the AD brain, beta-amyloid plaques build up.
In this hypothesised causal chain, we can see that even if true, the build-up of beta-amyloid is not the cause of AD. It is a mediating variable. The bigger question is: What prevents the beta amyloids from being broken down normally?
Sadly, even when methods have been developed to reduce the build-up of plaques, that does not stop the progression of the disease. It seems then that the plaques are a consequence and not a cause.
‘Neurofibrillary tangles’ are found in the brain cells of AD patients. Another hypothesis is that a protein named Tau, which seems to play a part in creating microtubules (which enable substances to be transported inside a cell), is involved in AD.
In AD cases, the Tau protein is abnormal, and the microtubules collapse, creating tangled fibres. Again, the question emerges: what causes the Tau protein to be abnormal? Is that abnormality causal, consequential, or merely mediatory?
In the last 10 or so years, thinking in the field of AD has developed. It is now more thought of, at least in the scientific community, as a pathological process that eventually leads to a fatal disease.
Scientists are a cautious bunch, generally, and are prone to understate their findings. Alas, even with that rational and well-balanced approach, some scientists have misled the scientific community, and the public, by exaggerating their findings or even falsifying their data.
Indeed, if we were to catalogue the entirety of such cases, you would still be reading this time next year.
Recently, it was discovered that the research that had led to vast resources being allocated to Alzheimer’s disease research (specifically beta amyloid research) appears to have been, let’s give the benefit of the doubt, less than properly presented. Some have said, ‘fraudulent’.
Images, it is alleged, appear to have been altered ‘to fit the hypothesis’. That is, vast resources that could have led to progress in understanding the causal factors, chains and variables in AD have been allocated and spent (wasted?), based on what appears to be ‘fraudulent’ research.
Despite the many reasons for our inability to understand the causal chain and processes that lead to AD, the good news is that, worldwide, vast numbers of brilliant and honest researchers are diligently trying to comprehend AD.
Until they do, and until society can develop treatments, the best action that we, as individuals, can take is to be aware of the preventative factors; the methods we can adopt to reduce the risks.
People who stay physically fit and healthy and engage in the ‘big five’ health protection factors are much less likely to develop AD.
The big five are: not smoking, not drinking alcohol, keeping body weight within healthy limits, eating five or more items of fruit and veg per day, and regular exercise.
We can also reduce our risk by remaining brain active. Brain-active adults are 2.7 times less likely to develop Alzheimer’s disease.
Here is my hypothesis on the causal chain of Alzheimer’s disease. We still don’t have the data to prove this, but it can be verified or falsified by scientific testing. What would happen to your muscles if you lay in bed, immobile for six weeks? They would atrophy.
What happens to the performance of a concert pianist if they do not practice on their piano for a year? They would quickly drop below the minimum standard. What happens to any skill or knowledge if neglected? It deteriorates.
As we go through life, we have less and less need to learn. In their 50s and 60s, people know almost everything they need to know to survive and function in society. In the first ten years of life, we learn at an amazing rate; our brains grow at incredible speeds.
Putting those factors together, what will happen to a person’s brain if they have not needed or chosen to learn a new skill for years? Their ability to learn will be reduced. The longer the period of non-learning, the greater the atrophy of their learning skill.
What if the brain is our learning organ, and we don’t use that organ? What is likely to happen to it? The same as happens for any other organ; if it is not used, it will atrophy.
Will we find in years to come that the as yet unknown processes that lead to the deterioration of the brain in AD are an inevitable consequence of not using the learning organ as a learning organ?
Does the brain that is used for constant learning produce chemicals that are protective? Does the absence of those chemicals allow entropy to do its work? Entropy is the natural process where all systems degenerate into dysfunction unless acted on in such a way to maintain effective function.
Could it be that the biggest risk factor for the development of AD is the lack of use of the learning organ? Can AD be explained, at least in part, by the ‘use it or lose it’ hypothesis?
In most healthcare fields, there is a ‘prime directive’: first, do no harm. If you engage in health-preserving and enhancing activities and keep your learning organ in good working order, you will do no harm by frequently learning. Even if the hypothesis is wrong (as all the others have been to date), by acting as though it is true, you will keep yourself healthier for longer and acquire lots of interesting knowledge and enjoyable new skills.
Let’s nail our colours to a mast. In years to come, I believe that the biggest protective factor against AD will be found to be: a lifetime of learning and healthy living. What do you think?
Professor Nigel MacLennan runs the performance coaching practice PsyPerform.
