Although I personally believe that Alzheimer’s disease is multi-factorial (i.e. there is not one sole cause that leads to its development or progression) below I have tried to link together the possible causes of Alzheimer’s into categories. These are listed in no particular order as, I believe, in their own small way they are all equally responsible – but if we can understand the possible causes we can then tackle them with the appropriate therapy, medication or intervention.
1. Chemical Factors of Alzheimer’s Disease.
The cells and the nerves of the brain need to be able to communicate and talk to each other in order to fully function and they do this via neurotransmitters or chemical messengers. Anything that can hinder the action of these messengers will therefore have a detrimental effect on the functioning of the brain.
Studies of Alzheimer’s sufferers have shown that they have lower levels of various neurotransmitters that are believed to influence intellectual functioning and behavior. The cause of these lower levels may be reduced production or something blocking their action – for example chemical imbalances or increased toxicity from heavy metals or homocysteine.
2. Vascular disturbances.
A poor blood supply to the brain may also be a causative factor. This may be due to a diminished supply caused by ageing or through injury such as stroke or direct head trauma. Studies have shown, for example, that there is an increased risk of dementia and other neurological conditions amongst ex boxers (who seem to be prone to having their heads hit!).
3. Pre-existing conditions.
Illnesses such as diabetes, high blood pressure and high cholesterol have all been linked as causes of Alzheimer’s. Studies show that high or uncontrolled blood pressure decreases the blood supply to the brain. Other studies have shown that almost three quarters of people who die of heart disease have amyloid plaques (which I will cover in point 9) in their brains typical of Alzheimer’s.
4. Genetic Predisposition.
There have been two genetic / hereditary factors found that predispose a person to Alzheimer’s (particularly early onset Alzheimer’s disease) and these are either suffering from Down’s Syndrome (a genetic defect) or a family history of dementia (a genetic / hereditary condition) as it seems there is a slightly higher risk of developing the condition if a first degree blood relative (parent / brother / sister) has developed it previously.
Researchers have linked at least ten percent of late onset Alzheimer’s to the inheritance of a gene mutation (on chromosome 14) that directs production of apolipoprotein (ApoE) – a cholesterol carrying protein. There have also been other genetic mutations identified that may account for a predisposition to Alzheimer’s and these occur on chromosomes 1, 12, 19 and 21.
5. Slow acting infections.
A slow-acting virus has been identified as a cause of some brain disorders that closely resemble Alzheimer’s. These infections may precede the onset of Alzheimer’s by many years and create an inflammatory process that damages the brain predisposing it to disease and deterioration.
6. Autoimmune diseases.
Autoimmune diseases may trigger a response that causes the body’s normally protective immune system to begin to attack itself by producing antibodies which destroy its own cells.
7. Inflammatory conditions.
This is similar to the infection based theory in that researchers believe that Alzheimer’s may result from an inflammatory process that creates abnormal waste products out of normal molecules and these then attack brain tissue. There seems to be some basis for this theory as researchers have found that anti-inflammatory medication (such as non-steroidal anti-inflammatories) seems to reduce the risk of developing the disease and also slow the rate of its progression.
8. The Tau Theory.
Another major theory behind the cause of Alzheimer’s lays the blame on tau. Tau is a protein whose role is to act like the skeleton of a cell and organise its shape and function. Unfortunately, during the progression of Alzheimer’s the tau protein deforms losing its ability to support the cell and it eventually aggregates and creates a tangle of nerve fibres. These aggregations are another hallmark of the progression of Alzheimer’s disease.
9. The Amyloid Hypothesis.
This theory seems to have the largest support. Amyloid precursor protein is a protein found throughout the body (although its function remains unclear) but in Alzheimer’s disease there is a malfunction in the processing of it which leads to the formation of a protein “beta-amyloid” fragment. These fragments slowly aggregate or clump together forming amyloid plaques which are characteristic of the disease. These clumps continue to build causing nerve disruption and destruction.
10. Disruption in the manufacture of nerve growth factors.
Another theory (that is gaining ground in areas of stroke, Alzheimer’s disease and spinal nerve damage) is that there may be a disruption in either the manufacture or processing of so called nerve growth factors. These “nerve growth factors” are usually proteins whose job it is to regulate and control nerve cell repair, survival and maturation.