Alzheimer’s Disease (AD) is the most common disease associated with dementia. It affects over five million Americans. It has been a difficult disease to diagnose, even when people have early stages of cognitive difficulty.
Recently published research in the Journal of Experimental Medicine provides insight into an early prediction of AD. Neurofibrillary tangles, tau proteins, and beta-amyloid proteins appear to be common in patients with AD.
Genetics is probably responsible for a few (very few) cases. Lifestyle choices and environmental factors are the most likely culprits in contracting AD. Why does AD affect one person and not another who has a similar lifestyle? That answer has not been found – yet!
AD, like many diseases, does not show symptoms early. You may have a disease beginning at the cellular level and not showing any symptoms until years later. When symptoms finally occur, it might be too late to effectively treat the disease. If you knew in advance what to look for, maybe something could be done to prevent, reverse, or correct the problem.
PET (positive emission tomography) scans are used to diagnose the brains of people with dementia. These scans can detect beta-amyloid plaques in the brain. PET scans rely on large plaques to make that diagnosis. Smaller clumps of plaques are not defined well enough for AD diagnosis.
PET scans are costly and not recommended for larger potential audiences – people over 50 years of age, for example. The beta-amyloid protein is one of the primary proteins associated with AD. The tau protein can be detected in blood and that is the current focus of early diagnosis and prediction.
Tau proteins are in the cerebrospinal fluid surrounding the brain and spinal cord. These proteins can be ‘tapped’ and tested. Again, this is not a good way to test a lot of people with potential AD years before symptoms begin. When large amounts of tau protein are present, some leak into the bloodstream.
A simple (maybe not so simple) blood test could be used to detect them. This is the basis of the study mentioned earlier. Two studies were done using patients’ blood to diagnose and predict the presence of future AD development.
Blood samples were taken from thirty-four people – 19 with no amyloid proteins found, five with amyloid proteins and no symptoms, and ten people with amyloid proteins and symptoms of AD. The expectations were that people with the amyloid protein also had tau proteins.
Phosphorylated tau 217 (a specific tau protein) correlates well (two to three times more) to levels of amyloid protein in the brain. Senior researchers at the Washington University School of Medicine in St. Louis determined from this study that it is possible to predict people who might likely develop AD.
The second study had forty-two people without amyloid protein, twenty with amyloid and no cognitive symptoms, and thirty with both amyloid and cognitive symptoms. The results clearly showed the same relationship of tau proteins to amyloid proteins with 90% accuracy.
The two studies demonstrated that people without mental and memory issues could be tested for the tau protein to determine potential future AD with an overall 86% accuracy rate. The difference between people with cognitive problems and those healthy (no amyloid protein or cognitive issues) was huge.
These tests lay the groundwork for future testing using phosphorylated tau protein 217 to predict AD. Earlier treatment might become successful to delay or prevent AD.
Live Longer & Enjoy Life! – Red O’Laughlin – RedOLaughlin.com