Editorial

The cover of this issue relates to one of five articles on tau. Using ¹⁸F-AV-1451 PET scanning, Merle Hoenig and colleagues report that tau pathology expands along independent pathways that correspond to functional networks known to be impaired in Alzheimer's disease, including the default mode network and the frontal control network. Thomas Cope and co-workers also show that highly connected networks are susceptible to tau pathology in Alzheimer's disease. Such a relationship was, however, not seen in progressive supranuclear palsy, where the burden appears to correlate instead with increased metabolic demand or lack of trophic support. The pathogenic role of tau remains at the centre of much research published in Brain. Marie d'Orange and colleagues compare the effect of viral expression of either wild-type tau or a chimeric protein designed to aggregate tau in rat brain, and conclude that potentiating tangle formation reduces acute toxicity of soluble tau species. Shelley Forrest and co-workers show that distinct mutations of the MAPT gene that encodes tau result in pathologies that strongly resemble sporatic sporadic frontotemporal tauopathies. Finally, Chad Tagge, Andrew Fisher, Olga Minaeva and colleagues report that impact head injury can result in early phosphorylated tau pathology in experimental models, and identify similar changes in a small number of young athletes who died suddenly within 4 months of a closed-head injury.

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