Nuclear Science: Mapping Out Alzheimer’s
Canadian women over 65 are at the greatest risk for developing dementia and that number is drastically rising. It is predicted that the number of Canadians living with dementia will almost double, affecting one million people by 2030. In the United States, a person is diagnosed with dementia every 66 seconds.
A large aging population and rising dementia rates are placing tremendous strains on an already stressed health care system, particularly long-term care facilities. Across the country, wait lists for long-term care varies from province to province but wait times in excess of a year are not unheard of. An overwhelming care demand coupled with a shortage of beds has meant many seniors are forced to stay at home longer.
Early diagnosis of Alzheimer’s is an important step in planning for both patients and their families. A step that is closer to reality thanks to nuclear science and the stable isotope labeling kinetics (SILK) technique.
Inside your brain’s nerve cells are tau proteins. These proteins work to stabilize other proteins in the brain known as microtubules. These microtubules are responsible for cell structure and movement. New findings from the Washington University’s School of Medicine in St. Louis this past spring reveal the importance of tau proteins in early Alzheimer’s progression.
“Tau is abundant in the brain’s nerve cells, where it stabilizes the scaffold-like microtubules that play a critical role in transporting cargo within cells. But in Alzheimer’s disease as well as other “tauopathies,” such as progressive supranuclear palsy and frontotemporal dementia, clumps of tau protein are abnormally deposited in nerve cells in tangles.”
In order to assess the health and levels of tau protein a patient is given a stable isotope of amino acids and then through a positron emission tomography (PET) scan, the amount of labeled tau produced in the brain is measured. Knowing how much tau is produced, researchers can then calculate how fast the protein is produced and cleared away by the brain.
Research has shown brains that are prone to dementia tend to have a buildup of dysfunctional proteins and have a harder time clearing the excess proteins away compared to brains of healthy patients. While it’s not a cure, this discovery could lead to new hope for patients and their families.
“Usually we can only diagnose patients later in the disease process, when brain function already is diminished,” according to senior author Beau M. Ances, MD, PhD, an associate professor of neurology. “We want to develop ways to make an earlier diagnosis and then design trials to test drugs against amyloid buildup and against tau buildup. While we currently cannot prevent or cure Alzheimer’s disease, delaying the onset of symptoms by 10-15 years would make a huge difference to our patients, to their families and caregivers, and to the global economy.”
In addition to their work on tau proteins, the school was recently awarded $4.3 million dollars from the Alzheimer’s Association to expand an international clinical trial which will attempt to identify drugs that can slow down or prevent Alzheimer’s in patients who are genetically predisposed but are symptom free. Working towards a cure and improving the lives of patients around the world, thanks in part to nuclear science.