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

Authors

Valentina Lacovich, Translational Aging and Neuroscience Program, Center for Translational Medicine, International Clinical Research Center, St. Anne's University Hospital, Brno, Czech Republic.
Maria Čarna, Translational Aging and Neuroscience Program, Center for Translational Medicine, International Clinical Research Center, St. Anne's University Hospital, Brno, Czech Republic.
Sebastian J. Novotný, Translational Aging and Neuroscience Program, Center for Translational Medicine, International Clinical Research Center, St. Anne's University Hospital, Brno, Czech Republic.
Shanshan Wang, Veterans Affairs San Diego Healthcare System, San Diego, California, USA.
Kateřina Texlová, Translational Aging and Neuroscience Program, Center for Translational Medicine, International Clinical Research Center, St. Anne's University Hospital, Brno, Czech Republic.
Kristina Locker Kovačovicova, PsychoGenics Inc., 215 College Road Paramus, New Jersey, New Jersey, USA.
Neda Dragišić, Translational Aging and Neuroscience Program, Center for Translational Medicine, International Clinical Research Center, St. Anne's University Hospital, Brno, Czech Republic.
Daniel Havas, PsychoGenics Inc., 215 College Road Paramus, New Jersey, New Jersey, USA.
Brian P. Head, Veterans Affairs San Diego Healthcare System, San Diego, California, USA.
Yonas E. Geda, Department of Neurology, Barrow Neurological Institute, Phoenix, Arizona, USA.
Clara Limbäck-Stokin, Neuropathology and Ocular Pathology Department, Oxford University Hospitals NHS Foundation Trust, Oxford, UK.
Gorazd Bernard Stokin, Translational Aging and Neuroscience Program, Center for Translational Medicine, International Clinical Research Center, St. Anne's University Hospital, Brno, Czech Republic.

Document Type

Article

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 following TBI. METHODS: We assessed brain morphology (n = 4-9 mice/group), transcriptome (n = 3 mice/group), proteome (n = 3 mice/group), and behavior (n = 17-27 mice/group) of wild-type (WT) and APP knock-out (KO) mice either untreated or 10-weeks following TBI. RESULTS: After TBI, WT mice displayed transcriptional programs consistent with late stages of brain repair, hub genes were predicted to impact translation and brain proteome showed subtle changes. APP KO mice largely replicated this transcriptional repertoire, but showed no transcriptional nor translational response to TBI. DISCUSSION: The similarities between WT mice following TBI and APP KO mice suggest that developmental APP deficiency induces a condition reminiscent of late stages of brain repair, hampering the control of gene expression in response to injury. HIGHLIGHTS: 10-weeks after TBI, brains exhibit transcriptional profiles consistent with late stage of brain repair. Developmental APP deficiency maintains brains perpetually in an immature state akin to late stages of brain repair. APP responds to TBI by changes in gene expression at a transcriptional and translational level. APP deficiency precludes molecular brain changes in response to TBI.

Medical Subject Headings

Animals; Amyloid beta-Protein Precursor (genetics); Mice, Knockout; Mice; Proteomics; Brain (metabolism, pathology); Proteome (metabolism); Transcriptome; Brain Injuries, Traumatic (metabolism, genetics, pathology); Mice, Inbred C57BL; Male; Brain Injuries (metabolism, genetics, pathology); Disease Models, Animal

Publication Date

4-1-2025

Publication Title

Alzheimer's & dementia : the journal of the Alzheimer's Association

E-ISSN

1552-5279

Volume

21

Issue

4

First Page

e70093

PubMed ID

40271543

Digital Object Identifier (DOI)

10.1002/alz.70093

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