# Decoding ALS from the tail end of RNA

**Authors:** Yusuke Fujioka, Shinsuke Ishigaki

PMC · DOI: 10.1016/j.xgen.2025.101102 · Cell Genomics · 2025-12-10

## TL;DR

This study explores how RNA processing at the 3′ end contributes to ALS/FTLD, revealing new insights into disease mechanisms and possible treatments.

## Contribution

The paper introduces a single-nucleus transcriptomic atlas showing widespread alternative polyadenylation changes in ALS/FTLD.

## Key findings

- Alternative polyadenylation changes are widespread in ALS/FTLD brain tissue.
- 3′ end RNA processing integrates stress responses and cell-type specificity in disease.
- Findings suggest new therapeutic directions for ALS/FTLD.

## Abstract

In this issue of Cell Genomics, McKeever et al.1 generate a single-nucleus transcriptomic atlas of ALS/FTLD brain and reveal widespread alternative polyadenylation changes. Their findings highlight 3′ end RNA processing as a central integrator of stress responses, cell-type specificity, and disease susceptibility, offering new mechanistic insight and potential therapeutic directions.

In this issue of Cell Genomics, McKeever et al. generate a single-nucleus transcriptomic atlas of ALS/FTLD brain and reveal widespread alternative polyadenylation changes. Their findings highlight 3′ end RNA processing as a central integrator of stress responses, cell-type specificity, and disease susceptibility, offering new mechanistic insight and potential therapeutic directions.

## Linked entities

- **Diseases:** ALS (MONDO:0004976)

## Full-text entities

- **Genes:** SOD1 (superoxide dismutase 1) [NCBI Gene 6647] {aka ALS, ALS1, HEL-S-44, IPOA, SOD, STAHP}
- **Diseases:** FTLD (MESH:D057174)

## Full text

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## Figures

1 figure with captions in the complete paper: https://tomesphere.com/paper/PMC12802604/full.md

## References

7 references — full list in the complete paper: https://tomesphere.com/paper/PMC12802604/full.md

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Source: https://tomesphere.com/paper/PMC12802604