VANCOUVER, British Columbia—Canadian company Aurin Biotech has announced the development of a simple saliva test that it says can diagnose Alzheimer’s disease as well as predict its future onset. The test is based on measuring the concentration of amyloid beta protein 42 (Abeta42) that is secreted in saliva. Abeta42 is a material which accumulates in the brain of Alzheimer’s disease patients and is implicated in the neuroinflammation that kills neurons.
“We believe that a teaspoon of saliva can predict an individual’s chance of getting Alzheimer’s disease, and that once you know, you can take early preventative measures,” says Dr. Patrick L. McGeer, president and CEO of Aurin Biotech. “Knowing is key, and that’s what this simple test is all about. It’s taken years of research to get to this point, but I really think we’re there.”
Historically, Alzheimer’s disease clinical trials have been long, costly and prone to failure, mainly due to the lack of a reliable biomarker available without use of invasive techniques. Several previously published studies have suggested that saliva proteins contain biomarkers for neurodegenerative diseases, most notably Felix Bermejo-Pareja’s landmark 2010 paper demonstrating a small but statistically significant increase in saliva Abeta42 levels in mild Alzheimer’s patients compared with healthy controls.
Based on this finding, Aurin Biotech undertook a more comprehensive examination of Abeta42 levels in control and Alzheimer’s patients to determine if a more accurate test might prove to be of practical value—and initial findings suggest it will. The simple saliva test indicates markers for Alzheimer’s and potentially other chronic degenerative diseases.
“The number of cases studied is small, but our results are so remarkable, we felt they should be made widely available in the medical community,” says McGeer.
Alzheimer’s disease is a relentlessly progressing neurodegenerative disease that slowly destroys brain function, memory and reasoning, eventually robbing the individual of any ability to carry out everyday activities. There are currently an estimated 35 million cases worldwide, with numbers estimated to exceed 100 million by 2050 barring an effective intervention. It represents an emerging crisis, as there are no currently approved disease-modifying therapies and it costs an estimated $500 billion a year to care for those afflicted.
Aurin Biotech’s research shows that the human body tightly regulates production of Abeta42 in all organs and, when healthy, keeps it at the same production rate throughout life, regardless of gender or age. However, previous research has shown that biomarkers for Alzheimer’s have been shown to appear sometimes decades before clinical onset. The Aurin research showed Abeta42 values nearly double the normal amount in active cases, with those at a known high risk showing demonstrably elevated levels, sometimes exceeding that of disease cases.
According to McGeer, “This [test] creates a window of opportunity between biomarker diagnosis of Alzheimer’s disease and clinical onset that can be exploited to dramatically reduce or eliminate [the disease]. Early intervention within the decade or more of preclinical development could successfully prevent Alzheimer’s onset.”
Research is underway to identify a complement inhibitor to protect against the damage that occurs when Abeta42 deposits initiates an immune response, known as complement dysregulation, that attacks crucial brain membranes. In addition, possible nonclinical prophylactic measures include a regimen of over-the-counter non-steroidal anti-inflammatory drugs such as ibuprofen, drinking coffee and sticking to a Mediterranean diet.
“It is remarkable that while Abeta42 is made at a constant rate by every organ of the body, it is the brain, and only the brain, which decompensates later in life,” comments McGeer. “Beyond the test itself, our results … should be a wake-up call for researchers and drug companies developing Abeta42-targeted therapies. Targeting the complement-mediated neuroinflammation should prove to be a much more fruitful approach than targeting Abeta42.”