The assumption of the righteous dead in the Wisdom of Solomon and the Sayings Gospel Q

From the publisher\u27s website: The Wisdom of Solomon applies language from the Genesis reference to Enoch\u27s assumption (Gen. 5:24 LXX) to the dead righteous one (Wis. 4:7-17). This unusual use of the motif of assumption, normally thought of as an escape from death, is facilitated by topoi drawn from Hellenistic consolation materials; however, the typical corollary of assumption in the Jewish tradition—heavenly or eschatological exaltation—is also applied to the righteous one in Wis. 5:1-5. This innovation is particularly instructive for Q, which may understand Jesus\u27 post-mortem vindication and exaltation in terms of assumption (Q 13:35)

TDP-43 gains function due to perturbed autoregulation in a Tardbp knock-in mouse model of ALS-FTD.

Amyotrophic lateral sclerosis-frontotemporal dementia (ALS-FTD) constitutes a devastating disease spectrum characterized by 43-kDa TAR DNA-binding protein (TDP-43) pathology. Understanding how TDP-43 contributes to neurodegeneration will help direct therapeutic efforts. Here we have created a TDP-43 knock-in mouse with a human-equivalent mutation in the endogenous mouse Tardbp gene. TDP-43Q331K mice demonstrate cognitive dysfunction and a paucity of parvalbumin interneurons. Critically, TDP-43 autoregulation is perturbed, leading to a gain of TDP-43 function and altered splicing of Mapt, another pivotal dementia-associated gene. Furthermore, a new approach to stratify transcriptomic data by phenotype in differentially affected mutant mice revealed 471 changes linked with improved behavior. These changes included downregulation of two known modifiers of neurodegeneration, Atxn2 and Arid4a, and upregulation of myelination and translation genes. With one base change in murine Tardbp, this study identifies TDP-43 misregulation as a pathogenic mechanism that may underpin ALS-FTD and exploits phenotypic heterogeneity to yield candidate suppressors of neurodegenerative disease