Fuyuki Kametani

Correction to: Nature https://doi.org/10.1038/s41586-020-2317-6 Published online 27 May 2020 In the version of the article initially published, the “DLB Case 1” image in Extended Data Fig. 7 was a duplicate of the “MSA case 1, Cerebellum” image in Extended Data Fig. 1. Extended Data Fig. 7 has now been amended to include the correct “DLB Case 1” image in the HTML and PDF versions of the article. About this article Schweighauser, M., Shi, Y., Tarutani, A. et al.

Abstract Dominantly inherited mutation D395G in the gene encoding valosin-containing protein causes vacuolar tauopathy, a type of behavioural-variant frontotemporal dementia, with marked vacuolation and abundant filamentous tau inclusions made of all six brain isoforms. Here we report that tau inclusions were concentrated in layers II/III of the frontotemporal cortex in a case of vacuolar tauopathy. By electron cryo-microscopy, tau filaments had the chronic traumatic encephalopathy (CTE) fold.

Abstract The abnormal assembly of TAR DNA-binding protein 43 (TDP-43) in neuronal and glial cells characterizes nearly all cases of amyotrophic lateral sclerosis (ALS) and around half of cases of frontotemporal lobar degeneration (FTLD)1,2. A causal role for TDP-43 assembly in neurodegeneration is evidenced by dominantly inherited missense mutations in TARDBP, the gene encoding TDP-43, that promote assembly and give rise to ALS and FTLD3,4,5,6,7.