Journal
JOURNAL OF NEUROSCIENCE
Volume 27, Issue 37, Pages 9916-9927Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.0927-07.2007
Keywords
Alzheimer's disease; axonal transport; microtubules; tau; mitochondria; synapse
Categories
Ask authors/readers for more resources
Long-haul transport along microtubules is crucial for neuronal polarity, and transport defects cause neurodegeneration. Tau protein stabilizes microtubule tracks, but in Alzheimer's disease it aggregates and becomes missorted into the somatodendritic compartment. Tau can inhibit axonal transport by obstructing motors on microtubules, yet tau itself can still move into axons. We therefore investigated tau movement by live-cell fluorescence microscopy, FRAP (fluorescence recovery after photobleaching), and FSM (fluorescence speckle microscopy). Tau is highly dynamic, with diffusion coefficients of similar to 3 mu m(2)/s and microtubule dwell times of similar to 4 s. This facilitates the entry of tau into axons over distances of millimeters and periods of days. For longer distances and times, two mechanisms of tau transport are observed. At low near-physiological levels, tau is cotransported with microtubule fragments from cell bodies into axons, moving at instantaneous velocities similar to 1 mu m/s. At high concentrations, tau forms local accumulations moving bidirectionally at similar to 0.3 mu m/s. These clusters first appear at distal endings of axons and may indicate an early stage of neurite degeneration.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available