Axonal transport rates in vivo are unaffected by tau deletion or overexpression in mice.
Elevated tau expression has been proposed as a possible basis for impaired axonal transport in Alzheimer's disease. To address this hypothesis, we analyzed the movement of pulse radiolabeled proteins in vivo along retinal ganglion cell (RGC) axons of mice that lack tau or overexpress human tau isoforms. Here, we show that the global axonal transport rates of slow and fast transport cargoes in axons are not significantly impaired when tau expression is eliminated or increased. In addition, markers of slow transport (neurofilament light subunit) and fast transport (snap25) do not accumulate in retinas and are distributed normally along optic axons in mice that lack or overexpress tau. Finally, ultrastructural analyses revealed no abnormal accumulations of vesicular organelles or neurofilaments in RGC perikarya or axons in mice overexpressing or lacking tau. These results suggest that tau is not essential for axonal transport and that transport rates in vivo are not significantly affected by substantial fluctuations in tau expression.
Yuan
Aidong
A
Center for Dementia Research, Nathan Kline Institute, Orangeburg, New York 10962, USA. yuan@nki.rfmh.org
Kumar
Asok
A
Peterhoff
Corrinne
C
Duff
Karen
K
Nixon
Ralph A
RA
D000818:Animals; D001370:Axonal Transport / Q000235:genetics*; D051379:Mice; D018345:Mice, Knockout; D008822:Mice, Transgenic; D009900:Optic Nerve / Q000378:metabolism / Q000648:ultrastructure; D012165:Retinal Ganglion Cells / Q000378:metabolism / Q000648:ultrastructure; D050825:Synaptosomal-Associated Protein 25 / Q000378:metabolism; D016875:tau Proteins / Q000378:metabolism*
D050825:Synaptosomal-Associated Protein 25; D016875:tau Proteins