Tau Protein, Not Amyloid, Now Thought To Be Responsible For Alzheimer's
Researchers are continuously discovering new information about what causes Alzheimer's disease, the most common form of dementia--a neurodegenerative brain disorder that will affect an estimated 53 million Americans in the United States in 2015.
New findings published in the journal Brain now show that the progression of the dysfunctional tau protein is believed to be responsible for the health problem, not the amyloid protein.
"The majority of the Alzheimer's research field has really focused on amyloid over the last 25 years," said Melissa Murray, a neuroscientist at Mayo Clinic. "Initially, patients who were discovered to have mutations or changes in the amyloid gene were found to have severe Alzheimer's pathology -- particularly in increased levels of amyloid. Brain scans performed over the last decade revealed that amyloid accumulated as people progressed, so most Alzheimer's models were based on amyloid toxicity. In this way, the Alzheimer's field became myopic."
For the study, researchers looked at 3,618 brains from Mayo Clinic's postmortem brain bank. From the sample, 1,375 were confirmed to have had Alzheimer's disease and the patients died at different ages and different stages of the Alzheimer's progression.
Throughout the first part of the study, researchers used a scoring system to evaluate the evolution of the amyloid and tau in the brain samples. Severity of tau predicted the onset of age and the duration of the disease. Yet this was not quite the case for amyloid.
"Tau can be compared to railroad ties that stabilize a train track that brain cells use to transport food, messages and other vital cargo throughout neurons," Murray added. "In Alzheimer's, changes in the tau protein cause the tracks to become unstable in neurons of the hippocampus, the center of memory. The abnormal tau builds up in neurons, which eventually leads to the death of these neurons. Evidence suggests that abnormal tau then spreads from cell to cell, disseminating pathological tau in the brain's cortex."
During the second half of the study, researchers examined amyloid brain scans that were taken from patients before they died. Then, they compard the results to scans that measured tau and amylouid brain pathologies and found that signals from the amyloid brains scans also matched up with amyloid pathologies that were observed in the vessel but not the tau pathology. Furthermore, amyloid was even found in the brains of some that had not reached cognitive decline, nor exhibited Alzheimer's disease.
What can be concluded of the observations is that as amyloid begins to accumulate in parts of the brain, whether cognitive decline is involved, Tau entering the picture signals the initial entry into Alzheimer's--contrary to what was once believed.
"Our findings highlight the need to focus on tau for therapeutics, but it also still indicates that the current method of amyloid brain scanning offers valid insights into tracking Alzheimer's," Murray concluded. "Although tau wins the 'bad guy' award from our study's findings, it is also true that amyloid brain scanning can be used to ensure patients enrolling for clinical trials meet an amyloid threshold consistent with Alzheimer's -- in lieu of a marker for tau."
The initial onset of dementia can be slow or quite progressive, with symptoms relanging from memory loss, to behavioral changes and chronic confusion, as well as a host of other issues. If you or a loved one is noticing issues, contact your primary care physician for guidance.