News on the Amyloid-Tau Dynamic

When Alois Alzheimer used a microscope to examine the brain of the deceased Auguste Deter in 1902 he observed what we now call "plaques and tangles."  These were a consequence of the two unusual proteins and fragments that characterize AD: amyloid plaques and collapsed microtubules.  We have discussed these plenty of times before.  The amyloids form when the "amyloid precursor protein" is cut by some enzymes (for unknown reasons).  The microtubules collapse because of the presence of an aberrant form of tau protein that's supposed to be holding the microtubules together.  So doctors and researchers may look for these substances in cerebrospinal fluid as evidence of the progression of AD.

This week's issue of ALZForum carried an interesting article about research on the progression of AD.  This progression is described in this year's Alzheimer's Association Facts and Figures report, which we discussed earlier.  What the recent article discusses is research using serial PET scans to further refine the dynamic of how the disease progresses, at least from the standpoint of the accumulation of beta-amyloid and abnormal tau and how that relates to cognition.

The short version is that amyloid begins to accumulate for a long time before there is any outward evidence of trouble.  Eventually the abnormal tau begins to appear at about the same time as there is evidence of cognitive decline.  The tau spreads throughout the brain, possibly propagating the disease. 

By taking a series of PET scans over a period of time, the rate of change of amyloid and tau accumulation can be measured and correlated.  Increasing accumulation of amyloid appears to signal advent of the tau pathology, suggesting that the amyloid is somehow influencing it.  One thing interesting to researchers is how tau pathology accelerates.  They are also curious about what level of amyloid correlates with initiation and acceleration of tau pathology.