What question did this study set out to answer?

To explore how cryptic exon burden in the hippocampus defines subtypes of TDP-43 dysfunction associated with Alzheimer's disease.

March 22, 2026Open Access

Subtyping based on hippocampal cryptic exon burden reveals proteome-wide changes associated with TDP-43 and Alzheimer’s disease pathology

Key Points

To explore how cryptic exon burden in the hippocampus defines subtypes of TDP-43 dysfunction associated with Alzheimer's disease.
Analyzed cryptic exon burden in brain samples
Identified molecular subtypes of TDP-43 dysfunction
Examined relationships between TDP-43 and proteome changes
Defined molecular subtypes independently of amyloid and tau pathology
Link between high cryptic exon levels and synaptic deficits
Connection between TDP-43 loss and endosomal proteome deficits

Abstract

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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Cite This Study

Trautwig et al. (Thu,) studied this question.

synapsesocial.com/papers/69bf86ecf665edcd009e9114 https://doi.org/https://doi.org/10.1016/j.celrep.2026.117142

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