Kazuo Fushimi

TL;DR: Results indicate that TNF-alpha and Ang II cause hypertrophy in part via the generation of ROIs in cardiac myocytes.

TL;DR: Comparing wild-type and an ALS-associated mutant TDP-43 in vitro and in vivo provides evidence for biochemical similarities between TPD-43 and prion proteins, raising the possibility that T DP-43 derivatives may cause spreading of the disease phenotype among neighboring neurons.

TL;DR: Transgenic flies expressing hTDP-43 recapitulate important neuropathological and clinical features of human TDP- 43 proteinopathy, providing a powerful animal model for this group of devastating diseases.

TL;DR: It is suggested that blocking or reversing mitochondrial damage may provide a potential therapeutic approach to these devastating diseases and uncovered a previously unknown role of LonP1 in regulating mitochondrial TDP-43 levels, but also advanced the understanding of the pathogenic mechanisms for T DP-43 proteinopathy.

TL;DR: Evidence for mitochondrial localization of FUS and its induction of mitochondrial damage is provided and mitochondrial damage may be a target in future development of diagnostic and therapeutic tools for FUS-proteinopathies, a group of devastating neurodegenerative diseases.