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Front cover: Mutation of profilin 1 (PFN1) can cause amyotrophic lateral sclerosis (ALS). To assess how PFN1 mutation causes the disease, we created transgenic rats with human genomic DNA that harbors both the coding and the regulatory sequences of the human PFN1 gene. Selected transgenic lines expressed human PFN1 with or without the pathogenic mutation C71G at a moderate and a comparable level and in the similar pattern of spatial and temporal expression to rat endogenous PFN1. Detergent‐insoluble PFN1 inclusions were detected as the first pathology in otherwise asymptomatic transgenic rats expressing mutant human PFN1. The findings suggest that protein aggregation is involved in the neurodegeneration of ALS associated with PFN1 mutation. Image Content: Toluidine blue staining revealed degeneration of motor axons in the L3 ventral root dissected from a mutant PFN1 transgenic rat at paralysis stage.Read the full article   ‘Detergent‐insoluble inclusion constitutes the first pathology in PFN1 transgenic rats’ by G. Yuan, S. Cui, X. Chen, H. Song, C. Huang, J. Tong, Z. Yuan, L. Yu, X. Xiong, J. Zhao, B. Huang, Q. Wu, Y. Zhou, G. Chen, H. Zhou and X.‐G. Xia ( J. Neurochem. 2021, vol. 157 (4), pp. 1244–1252) on doi: 10.1111/jnc.15139