12 September 2010. For years, the two classic proteins of
Alzheimer disease—Aβ and tau—seemed to move in separate orbits.
Gradually, researchers are finding these proteins revolve more
closely around each other than they had thought, as two new
papers highlight. In a September 8 paper in the Journal of
Neuroscience, researchers led by Eva-Maria and Eckhard Mandelkow
at the Max-Planck Unit for Structural Molecular Biology,
Hamburg, Germany, showed that when they added Aβ to healthy
neuronal cultures, one of its earliest effects was to
mislocalize tau into neuronal dendrites. In areas where tau was
missorted, the authors also saw a dramatic loss of microtubules
and synaptic spines, two effects believed to occur in early AD.
Meanwhile, in the September 9 Science, researchers led by
Lennart Mucke at the University of California, San Francisco,
report that the loss of tau protects against axonal transport
defects brought on by Aβ treatment. Both findings add intriguing
new data to the nebulous picture of tau and A