To date, the physiological function of dendritic tau has not been well characterized. It may be involved in the regulation of synaptic plasticity, as pharmacological synaptic activation induces translocation of endogenous tau from the dendritic shaft to excitatory postsynaptic compartments in cultured mouse neurons and in acute hippocampal slices
Hyperphosphorylation, mutations and overexpression of tau can drive the mislocalization of tau into postsynaptic spines, resulting in synaptic dysfunction
Tau oligomers from TauRDΔK and TauFLΔK mice reduced the density of the synapses by w50%, whereas tau from wild-type mice had no effect on the density (Fig. 7G).
p(HGNC:MAPT) causesNoChange a(GO:synapse)
First, hyperphosphorylation of tau might induce tau missorting from axons to the somatodendritic compartment, which can cause synaptic dysfunction
BEL Commons is developed and maintained in an academic capacity by Charles Tapley Hoyt and Daniel Domingo-Fernández at the Fraunhofer SCAI Department of Bioinformatics with support from the IMI project, AETIONOMY. It is built on top of PyBEL, an open source project. Please feel free to contact us here to give us feedback or report any issues. Also, see our Publishing Notes and Data Protection information.
If you find BEL Commons useful in your work, please consider citing: Hoyt, C. T., Domingo-Fernández, D., & Hofmann-Apitius, M. (2018). BEL Commons: an environment for exploration and analysis of networks encoded in Biological Expression Language. Database, 2018(3), 1–11.