Subtyping based on cryptic exon burden reveals proteome changes linked to TDP-43 in Alzheimer's disease, suggesting new molecular insights.
Highlights Cryptic exon (CE) burden defines molecular subtypes of TDP-43 dysfunction in the brain CE subtypes stratify LATE and AD independently of amyloid and tau pathology High CE levels link TDP-43 loss to synaptic and endosomal proteome deficits
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Trautwig et al. (2026) studied this question.
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