According to the Alzheimer’s Association, Alzheimer’s disease is the most common type of dementia, accounting for 60-80% of cases that we see. This disease is not a part of normal aging, and can worsen over time. Early symptoms are of Alzheimer’s include difficulty remembering names and events, and can progress to depression, confusion, and difficulty carrying out daily activities. The progression of this disease, and the deterioration of those who suffer from it is even more worrisome as there is currently no cure for Alzheimer’s disease.
One of the trademarks of Alzheimer's disease is the formation of plaques, or abnormal collections of beta-amyloid proteins, in the brain. The second hallmark, is tangles of tau protein which is suspected to clog up dying brain cells. In the past, it has been it has been only the plaques that could be spotted. Now new imaging can spot the tau tangles in people who are still alive and not yet diagnosed with Alzheimer’s. The exact causes of Alzheimer’s are still unknown but being able to spot these two features can help identify people who might develop Alzheimer’s and hopefully target preventative treatment for them.
A new study that will test an experimental preventative Alzheimer’s drug on healthy but at-risk people, is using brain scans to identify tau and amyloid plaques in the brain. It is the combination of amyloid and tau that the researchers believe is extremely toxic. So being able to finally track both of these will be beneficial for researchers in finding new treatments.
The study is called the A4 Study, which stands for Anti-Amyloid Treatment in Asymptomatic Alzheimer's. It will aim to recruit 1000 healthy elderly people, to see if there is buildup of these proteins that may increase risk of Alzheimer’s later in life. The big thing researchers are looking for, is the point in which the tau protein begins to emerge and take effect in the decline of cognitive function in the study participants.
Normal tau acts to help nerve cells transport food and other molecules. In Alzheimer's, the tau protein strands breakdownand fold over creating the “tangles” we mentioned. This tangle eventually causes the cell to die. The sticky plaques encourage the spread of bad tau. Eventually this will spread to the memory center, impairing one’s ability function. Although most healthy people have a small amount of dysfunctional tau, too much can mean trouble.
The results of this study would help more than 35 million people worldwide, 5 million in the US alone, who suffer from Alzheimer's or other types of dementias. The current medication only mitigates the symptoms of memory loss – but none are very effective. This study has the potential to start treatment sooner rather than later, maybe even before any symptoms start to emerge. This can be likened to heart disease which cholesterol buildup starts much sooner than any adverse side effects. So too might tau and amyloid build up until a tipping point where brain function starts to deteriorate.