Alzheimer’s disease is associated with neurofibrillary tangles within the nerve cell body and abnormal (senile) plaque deposits containing the protein beta amyloid (Aβ) which disrupt normal electrical conduction of messages within the brain.
Alois Alzheimer, a German psychiatrist and pathologist, first published his findings on these “tangles and plaques” in 1907. They occur consistently in people with Alzheimer’s disease but interestingly, have also been observed in older people free from dementia.
As with so many major diseases, the causes of Alzheimer’s are complex and research is only gradually identifying all the potential contributing factors.
Alzheimer’s disease (AD) primarily affects the cerebral cortex, basal forebrain and hippocampus areas of the brain. The classic features of Alzheimer’s disease are amyloid plaques, neurofibrillary tangles and inflammation.
A scientific consensus has recently emerged that Alzheimer’s disease originates with Amyloid beta peptide accumulation caused by genetic and environmental factors. A vicious cycle then begins, and when one part of the pathology is in place it then acts as a trigger for the other parts. A progression of nerve cell death, followed by inflammation and then more nerve cell death follows.
All of this means that the brain cells can’t survive the presence of the tangles and proteins, and the brain’s functions are compromised.
The Build-up of Beta Amyloid
The reason why these tangles and proteins form remain uncertain and the beta amyloid story is complex.
Research has discovered there are different forms of this protein with some forms being far more toxic than others. There is also uncertainty as to why this protein builds up and becomes toxic in some people while not in others.
Vascular (blood vessel) issues are highly associated with Alzheimer’s disease. There is a high correlation between issues associated with vascular problems such as cholesterol levels, blood pressure, obesity and the level of beta amyloid in the blood.
A genetic link
There is considerable evidence of a genetic link in the onset of Alzheimer’s disease. It has been found that populations with certain genes are at a far higher risk than the normal population.
Genes identified to date as being significantly associated with Alzheimer’s disease include APOE 4 and presenillin. Other genes are currently being studied.
As with beta amyloid, the action of genes is not straight forward. Most of the genes most highly associated with Alzheimer’s are mutations and the presence of a gene in one generation does not automatically mean it will be passed on to the next generation.
There is also some research evidence that genetic risk may be able to be modified through lifestyle interventions.
It is hypothesized that the increase in Alzheimer’s disease with age is associated with the hormonal changes also associated with age.
There is an increasing body of research implicating hormones in the increased production and accumulation of beta amyloid and therefore, potentially linked to the onset of Alzheimer’s disease.