Tau neurotoxicity and rescue in animal models of human Tauopathies. (February 2016)

• Record Type: Journal Article
• Authors: Krüger, Lars; Mandelkow, Eva Maria
• Is Part Of: Current opinion in neurobiology. Volume 36(2016)
• Page Start: 52
• Page End: 58
• Publication Date: 2016-02
• Subjects: Neurobiology -- Periodicals; 573.8
• DOI: 10.1016/j.conb.2015.09.004
• Languages: English
• ISSNs: 0959-4388

Abstract

Highlights: Soluble species of Tau, rather than aggregates, are more detrimental to proper neuronal function. Tau is released from synaptic terminals into the extracellular space. Tau plays a role in controlling susceptibility to hyperexcitation. Tau based antibody or aggregation inhibitor treatment is beneficial in murine Tauopathy models. Abstract : 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.