Transmission of Tau Pathology from Human to Rodent Brain: How to Humanise Animal Models for Alzheimer’s Disease Research
Received Date: Nov 10, 2017 / Accepted Date: Nov 16, 2017 / Published Date: Nov 23, 2017
Abstract
Tauopathies represent a group of neurodegenerative disorders characterised by the accumulation of conformationally altered tau protein. Alzheimer’s disease (AD) is the most prevalent primary tauopathy. In AD, tau pathology progressively spreads across a stereotypical sequence of anatomically connected brain regions. In early stages, the disease manifests in the locus coeruleus and entorhinal cortex; at later stages it spreads through the hippocampus to cortical brain areas. Recent studies suggest that spreading of pathological tau occurs predominantly through neuron-to-neuron transmission; however, glial cells can also be involved in this process. Propagation depends on the conformational state and post-translational modifications of tau protein of various tau strains. Abnormal tau can subsequently act as a seed, misfolding and aggregating normal tau proteins inside the cells. Several research groups have successfully recapitulated tau transmission in animal models. Currently, we are able to induce and drive tau neurodegeneration by using tau species isolated from diseased human brains. Such state-of-the-art “humanised” animal models represent a powerful tool for development of new drug leads and diagnostics for human tauopathies.
Keywords: Tau spreading; Tau aggregates; Tauons; Tau propagation; Tauopathies
Citation: Smolek T, Jadhav S, Valachova B, Vogels T, Legath J, et al. (2017) Transmission of Tau Pathology from Human to Rodent Brain: How to Humanise Animal Models for Alzheimer’s Disease Research. J Alzheimers Dis Parkinsonism 7: 400. Doi: 10.4172/2161-0460.1000400
Copyright: © 2017 Smolek T, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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