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Fig. 1 | Journal of Biomedical Science

Fig. 1

From: Untangling the Tauopathy for Alzheimer’s disease and parkinsonism

Fig. 1

A schematic drawing summarizes possible pathogenic mechanisms in early tauopathy and its subsequent spreading. Tau protein may encounter different post-translational modifications, and some changes could lead to the formation of Tau oligomers and subsequent development of the high-order structure such as pair-helical filament shown in the EM picture. The altered Tau function may cause aberrant mitochondria accumulation, oxidative stress, mtDNA damage, and autophagy impairment in the axon. These conditions damage axonal homeostasis and may grant a route for pathogenic Tau to propagate to the post-synaptic cell. We have incorporated the current knowledge of tau spreading and its potential links to secretory mechanisms. In physiological condition, Tau secretion is activity dependent (23). We have incorporated the current knowledge of tau spreading and its potential links of related secretory mechanisms: unguarded Tau (66); exosome (108); exophore (109)

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