Cytoplasmic aggregates of the protein TDP43 are a feature of neurodegenerative diseases including amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD) and Alzheimer disease, but the mechanisms linking TDP43 with neuropathology are not fully understood. A study in Science now shows that aberrant processing of stathmin 2 (STMN2) pre-mRNA, encoding a protein that promotes neuronal health and survival, is a key pathophysiological step downstream of aberrant TDP43 biology. Moreover, antisense oligonucleotides (ASOs) can be used to restore stathmin 2 expression in mouse models.

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doi: https://doi.org/10.1038/d41573-023-00056-2

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Tackling TDP43 proteinopathies - Nature.com