Alzheimer’s disease is distinguished by two distinct brain hallmarks. They are called amyloid plaques and tau tangles. The amyloid plaques are abnormal clumps of cells that slow down and prevent transmission of information between cells. Tau tangles are fibers that become enmeshed with each other and also prevent cells from transmitting information and instructions to each other.
These changes disrupt nerve cells and eventually cause them to die. The loss of brain tissue destroys memory and thinking skills and, eventually, the ability to carry out tasks of daily living.
Studies estimate that more than 5 million people in the United States are living with Alzheimer’s disease. Ninety percent of this number are senior citizens, aged 62 and older. The National Institute on Aging (NIA) estimates that this number will double by the year 2060. This is a terminal disease, and at this time, there is no cure.
Alzheimer’s Disease: Making Patient’s Life More Comfortable
Scientists are looking for ways to better understand whether tau tangles and amyloid plaques can predict the development of Alzheimer’s. To this end, researchers need to be able to track tau and amyloid in the brain as the disease develops. Early prediction can help develop strategies to slow the progression of this disease and thereby improve the quality of life.
Recently, scientists at the University of California, San Francisco developed molecules that allow them to use PET scans to measure the levels of amyloid plaques and tau tangles in living brain tissue.
These molecules called tracers tracked amyloid plaques and tau tangles and measured their rates of increase.
Alzheimer’s Disease: Study Results:
The study included 32 people with early-stage Alzheimer’s disease. All participants underwent PET scans to assess the levels and locations of amyloid and tau. They also had MRI scans of the brain to calculate brain volume. Fifteen months later, they underwent a second MRI scan to measure loss of brain tissue.
The results were surprising. People with higher levels of tau tangles measured at the first PET scan had a greater loss of brain matter by the second MRI scan. In contrast, levels of amyloid plaques measured at the start of the study were about at the same level at the second PET scan. The researchers estimated that the tau tangles could explain about 40% of the difference in future brain degeneration, compared to only 3% for the amyloid plaques.
Of note, participants in the study were relatively young for people with Alzheimer’s disease. Sixty three percent were under the age of 65 when they enrolled. The younger patients had higher levels of tau in the brain overall and experienced more rapid loss of brain tissue.
Tau PET scan imaging predicted not only how much brain atrophy would occur, but also where it would happen. These predictions were much more powerful than other imaging tools and add to evidence that tau tangles are a major driver of this disease.
PET imaging of tau may be helpful for future clinical trials of drugs targeting the tangles. Such imaging could potentially help detect early response — or lack of response — to new treatments. More work is needed to understand other factors that can help predict loss of brain tissue in Alzheimer’s disease.