In general, the patient shows a deterioration of reasoning abilities, has loss of memory, exhibits mood swings, and has trouble communicating. In the later stages, physical bodily functions gradually run down, and this is what causes death.
This disease develops differently in each individual, so carers and doctors do not know what to expect as each patient inevitably deteriorates. There is no cure, and only a few medications help alleviate the symptoms; nothing slows the progress.
We know its effects, both biochemical and physical, and we have developed better methods of medical care. But, except for the few percent of cases where there is a known genetic abnormality, we still do not know the cause of AD.
Observations of the brains of Alzheimer's patients
When the brains of Alzheimer's patients are observed by non-invasive scans (Magnetic Resonance Imaging, MRI; or Positron Emission Tomography, PET), or else physically after they have died, then two types of abnormalities are found. Plaques of mis-folded proteins called 'beta-amyloid peptides' are seen around the outside of the neurons (nerve cells) and aggregates, or 'tangles' of another protein called 'tau' are found inside the cell itself. Both these things do occur in the normal brain as people age, but in Alzheimer's patients they are much more evident and in greater quantity, and also found in specific areas of the brain.
It was these that Dr Alois Alzheimer noticed in 1906, in the brain of a deceased patient who had exhibited symptoms of the disease now named after him.
The biochemistry of the way these tangles and plaques are formed has now been determined. It is also known that the symptoms of AD are caused (at least in part) by a reduction of the brain chemical acetylcholine, which is necessary for messages to get from one neuron to another around the brain. In 1991 it was postulated that the abnormal proteins somehow inhibited the nerve cells so that these nerve messages were disrupted. However, none of the medications that are known to either reduce the plaques or increase the amount of acetylcholine show improvement in the actual progress of AD.
In 2009, it was further postulated that another protein that is naturally there to 'prune' unwanted neurons is triggered to become defective as people age, and that this may be the culprit in AD. In this hypothesis, the beta-amyloid plaques are just a secondary effect. This has not yet been proven.
It is time to re-think the probably causes and effects.
Do the 'tangled proteins' and 'amyloid plaques' really cause the disease?
Just because two things occur together does not mean that one causes the other.
Researchers in USA and Australia now speculate that the plaques of 'tangled' amyloid proteins may be the RESULT of the disease and not the cause of AD. (www.abc.net.au/science/articles)
After reviewing many different trials and tests so far, the US group has come up with a new hypothesis - that the amyloid plaques are formed to protect the body from some other harmful substance.
"I like to think of them as a surgical sponge … they're very good at the site of damage to sponge up dangerous and harmful molecules that are at the site of disease," says Professor Lawrence Steinman of Stanford Univeristy.
Australian researchers have added weight to this modified hypothesis. By using mouse models of Alzheimer's disease, Dr Bryce Vissel and his team at the Garvan Institute of Medical Research have shown that both the memory problems and loss of neurons in the brain occur long before the tangled plaques of amyloid protein appear. They postulate that inflammation may be a triggering factor in the neurodegeneration seen in AD patients.
Very recent research has indicated that there may be other fatty molecules and proteins formed by the body as Alzheimer's starts to take hold, and researchers at the Georgetown University Medical Center, USA, are now working on a way to detect these in the blood of patients before symptoms appear. Even so, it will be several years of more experiments and then carefully controlled human trials before they know if this will be useful in early detection or not. (www.sciencedaily.com/releases)
Scientists need to continue the research – with open minds
Science is NOT a 'belief' system; nor does it rely on 'consensus'. Knowledge advances only when individuals have ideas based on observations, which are followed by discussions then experiments that change and improve our total understanding. It is important that scientists remain humble and realise that they need to continue observing and learning; they are 'only human' and do not know everything.
Romans 1 verses 19-20 (NIV) says: "Since what may be known about God is plain to them, because God has made it plain to them. For since the creation of the world God's invisible qualitiesâ€"his eternal power and divine natureâ€"have been clearly seen, being understood from what has been made, so that men are without excuse."
We seem to be at a crossroads now, waiting for a new technique or biochemical discovery so that we can advance our knowledge of AD. We know some of the symptoms – both social and biological – and can diagnose them earlier than in the past. We have better methods of caring for the patients. We have found that some of the medications we thought would help, do not help much.
Learning from what didn't work, scientists and doctors are now finding more about the etiology and biology of the disease in the body before symptoms occur. Hopefully this will lead to more effective medications.
Dr Mark Tronson is a Baptist minister (retired) who served as the Australian cricket team chaplain for 17 years (2000 ret) and established Life After Cricket in 2001. He was recognised by the Olympic Ministry Medal in 2009 presented by Carl Lewis Olympian of the Century. He mentors young writers and has written 24 books, and enjoys writing. He is married to Delma, with four adult children and grand-children.
Mark Tronson's archive of articles can be viewed at www.pressserviceinternational.org/mark-tronson.html