TDP-43 mutation and STMN2 protein expression: a potential therapeutic target for amyotrophic lateral sclerosis

Takeaway

  • Mutations in TDP-43, linked to amyotrophic lateral sclerosis (ALS) pathology, reduce STMN2 (SCG10) at the transcriptional level, inhibiting motor neurite outgrowth and axonal regrowth.

Why this matters ?

  • This thorough analysis of how TDP-43 impacts STMN2 expression and the proof-of-principle that c-Jun N-terminal kinases (JNK) inhibition can improve stunted growth from altered STMN2 levels, makes a strong mechanistic case for STMN2 as a therapeutic target for ALS.