Read with caution!

This post was written during early stages of trying to understand a complex scientific problem, and we didn't get everything right. The original author no longer endorses the content of this post. It is being left online for historical reasons, but read at your own risk.

From yesterday’s New York Times:


And the study they cite:


The upshot of this article appears to be strong evidence that Alzheimer’s spreads through the brain by means of misfolded, infectious tau proteins – so, not unlike the mechanism underlying prion diseases or, probably, other neurodegenerative diseases like Parkinson’s and Huntington’s.  These researchers developed genetically engineered mice that express abnormal human tau proteins only in their entorhinal cortexes.  Tauopathy then appeared in cells outside of the entorhinal cortex, even though those cells were not capable of themselves producing human tau.  The authors conclude:


We have demonstrated that tau pathology initiating in the EC can spread to other synaptically connected brain areas as the mice age, supporting the idea that AD progresses via an anatomical cascade as opposed to individual events occurring in differentially vulnerable regions. Thus, our NT transgenic mouse provides a model in which the spatial and temporal propagation of the disease can be predicted, and correlative functional outcomes can now be tested.


Sounds like good news for Alzheimer’s research, and also for all neurodegenerative disease research.  From what I understand lack of reliable animal models has been a big obstacle and frustration for this field, and a sticking point in wooing investment, so maybe this will help!  Also it’s encouraging to see different neurodegenerative diseases coalescing around common identified mechanisms.  Although obviously they each have their own idiosyncrasies, maybe a common effort can at least move us forward on the basics of conformational disease.