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

J 2025

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

LACOVICH STRAŠIL, Valentina; Maria CARNA; Sebastian J. NOVOTNY; Shanshan WANG; Katerina TEXLOVA et al.

Základní údaje

Originální název

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

Autoři

Vydání

ALZHEIMERS & DEMENTIA, HOBOKEN, WILEY, 2025, 1552-5260

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

30500 3.5 Other medical sciences

Stát vydavatele

Spojené státy

Utajení

není předmětem státního či obchodního tajemství

Odkazy

URL

Impakt faktor

Impact factor: 11.100 v roce 2024

Označené pro přenos do RIV

Ano

Organizační jednotka

Středoevropský technologický institut

Klíčová slova anglicky

amyloid precursor protein; behavior; brain morphology; brain repair; gene expression; transcription; translation; traumatic brain injury

Štítky

rivok

Příznaky

Mezinárodní význam, Recenzováno

Změněno: 2. 2. 2026 14:23, Mgr. Eva Dubská

Anotace

V originále

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 or 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.

Návaznosti

GX21-27329X, projekt VaV

Název: ADAR-dependentní RNA editace; Jak imunitní systém a mozek porušují Centrální Dogma.

Investor: Grantová agentura ČR, ADAR RNA editing, how immune systems and brains breach The Central Dogma

Citovat

LACOVICH STRAŠIL, Valentina; Maria CARNA; Sebastian J. NOVOTNY; Shanshan WANG; Katerina TEXLOVA; Kristina Locker KOVACOVICOVA; Neda DRAGISIC; Daniel HAVAS; Brian P. HEAD; Yonas E. GEDA; Clara LIMBACK-STOKIN a Gorazd Bernard STOKIN. Developmental deletion of amyloid precursor protein precludes transcriptional and proteomic responses to brain injury. ALZHEIMERS & DEMENTIA. HOBOKEN: WILEY, 2025, roč. 21, č. 4, s. 1-14. ISSN 1552-5260. Dostupné z: https://doi.org/10.1002/alz.70093.

@article{2515368,
   author = {Lacovich Strašil, Valentina and Carna, Maria and Novotny, Sebastian J. and Wang, Shanshan and Texlova, Katerina and Kovacovicova, Kristina Locker and Dragisic, Neda and Havas, Daniel and Head, Brian P. and Geda, Yonas E. and LimbackandStokin, Clara and Stokin, Gorazd Bernard},
   article_location = {HOBOKEN},
   article_number = {4},
   doi = {https://doi.org/10.1002/alz.70093},
   keywords = {amyloid precursor protein; behavior; brain morphology; brain repair; gene expression; transcription; translation; traumatic brain injury},
   language = {eng},
   issn = {1552-5260},
   journal = {ALZHEIMERS & DEMENTIA},
   title = {Developmental deletion of amyloid precursor protein precludes transcriptional and proteomic responses to brain injury},
   url = {https://alz-journals.onlinelibrary.wiley.com/doi/10.1002/alz.70093},
   volume = {21},
   year = {2025}
}

TY  - JOUR
ID  - 2515368
AU  - Lacovich Strašil, Valentina - Carna, Maria - Novotny, Sebastian J. - Wang, Shanshan - Texlova, Katerina - Kovacovicova, Kristina Locker - Dragisic, Neda - Havas, Daniel - Head, Brian P. - Geda, Yonas E. - Limback-Stokin, Clara - Stokin, Gorazd Bernard
PY  - 2025
TI  - Developmental deletion of amyloid precursor protein precludes transcriptional and proteomic responses to brain injury
JF  - ALZHEIMERS & DEMENTIA
VL  - 21
IS  - 4
SP  - 1-14
EP  - 1-14
PB  - WILEY
SN  - 15525260
KW  - amyloid precursor protein
KW  - behavior
KW  - brain morphology
KW  - brain repair
KW  - gene expression
KW  - transcription
KW  - translation
KW  - traumatic brain injury
UR  - https://alz-journals.onlinelibrary.wiley.com/doi/10.1002/alz.70093
N2  - 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 or 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.
ER  -

LACOVICH STRAŠIL, Valentina; Maria CARNA; Sebastian J. NOVOTNY; Shanshan WANG; Katerina TEXLOVA; Kristina Locker KOVACOVICOVA; Neda DRAGISIC; Daniel HAVAS; Brian P. HEAD; Yonas E. GEDA; Clara LIMBACK-STOKIN a Gorazd Bernard STOKIN. Developmental deletion of amyloid precursor protein precludes transcriptional and proteomic responses to brain injury. \textit{ALZHEIMERS \&{} DEMENTIA}. HOBOKEN: WILEY, 2025, roč.~21, č.~4, s.~1-14. ISSN~1552-5260. Dostupné z: https://doi.org/10.1002/alz.70093.

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