Developmental deletion of amyloid precursor protein precludes transcriptional and proteomic responses to brain injury

Proteome
DOI: 10.1002/alz.70093 Publication Date: 2025-04-24T10:11:18Z
ABSTRACT
Abstract INTRODUCTION Amyloid precursor protein (APP) undergoes striking changes following traumatic brain injury (TBI). Considering its role in the control of gene expression, we investigated whether APP regulates transcription and translation TBI. METHODS We assessed morphology ( n = 4–9 mice/group), transcriptome 3 proteome behavior 17–27 mice/group) wild‐type (WT) knock‐out (KO) mice either untreated or 10‐weeks RESULTS After TBI, WT displayed transcriptional programs consistent with late stages repair, hub genes were predicted to impact showed subtle changes. KO largely replicated this repertoire, but no nor translational response DISCUSSION The similarities between TBI suggest that developmental deficiency induces a condition reminiscent hampering expression injury. Highlights after brains exhibit profiles stage repair. Developmental maintains perpetually an immature state akin responds by at level. precludes molecular
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