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Curr Opin Neurobiol. 2016 Feb;36:52-8. doi: 10.1016/j.conb.2015.09.004. Epub 2015 Sep 29.

Tau neurotoxicity and rescue in animal models of human Tauopathies.

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  • 1German Center for Neurodegenerative Diseases (DZNE), Ludwig-Erhard-Allee 2, 53175 Bonn, Germany. Electronic address:
  • 2German Center for Neurodegenerative Diseases (DZNE), Ludwig-Erhard-Allee 2, 53175 Bonn, Germany; Caesar Research Center, Ludwig-Erhard-Allee 2, 53175 Bonn, Germany; Max-Planck-Institute for Metabolism Research, Hamburg Outstation, c/o DESY, Notkestrasse 85, 22607 Hamburg, Germany. Electronic address:


Pathological Tau is a hallmark of various neuronal disorders and spreads in the brain of Alzheimer patients in a well-defined manner. Beside Tau's main function in stabilizing microtubules for axonal transport, a variety of novel functions for neurons and glia have emerged recently. Tau regulates the susceptibility to hyperexcitation and plays a role in neuron-glia contact formation. Studies implicate soluble oligomeric species of Tau, rather than insoluble aggregates, as more detrimental to proper neuronal function. Tau is not exclusively intracellular; instead Tau can be released into the extracellular space. This has led to the hypothesis of a prion-disease like mechanism to explain the stereotypical progression of Tau. Targeting pathological Tau with antibodies or aggregation inhibitors may help to prevent pathology.

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