Tau aggregation and cytoskeletonTau aggregation and cytoskeleton

Tau aggregation and cytoskeleton

Koyo Tsujikawa^1）2）, Kentaro Sahashi^1）, Masahisa Katsuno^1）3）

^1）Department of Neurology, Nagoya University Graduate School of Medicine
^2）Institute for Advanced Research, Nagoya University
^3）Department of Clinical Research Education, Nagoya University Graduate School of Medicine

Crosstalk between microtubules and actin filaments is involved in various functions of neurons.　The crosstalk is regulated through multiple microtubule-associated proteins and actin-binding proteins.　Tauopathies are a group of neurodegenerative diseases that are histopathologically characterized by the aggregation of the microtubule-associated protein tau.　Various genetic mutations and protein modifications of tau promote the aggregation, whereas in recent years there have been a number of reports of driving factors for tau aggregation other than tau itself.　In this article, we will highlight pathological effects of filamin A and other actin-binding proteins on driving the tau aggregation.

Address correspondence to Dr. Koyo Tsujikawa, Department of Neurology, Nagoya University Graduate School of Medicine（65 Tsurumai-cho, Showa-ku, Nagoya 466-8550）