Developmental deletion of amyloid precursor protein precludes transcriptional and proteomic responses to brain injury
The result's identifiers
Result code in IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F61989592%3A15110%2F25%3A73631681" target="_blank" >RIV/61989592:15110/25:73631681 - isvavai.cz</a>
Alternative codes found
RIV/00216224:14740/25:00144422 RIV/00159816:_____/25:00082308
Result on the web
<a href="https://alz-journals.onlinelibrary.wiley.com/doi/10.1002/alz.70093" target="_blank" >https://alz-journals.onlinelibrary.wiley.com/doi/10.1002/alz.70093</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1002/alz.70093" target="_blank" >10.1002/alz.70093</a>
Alternative languages
Result language
angličtina
Original language name
Developmental deletion of amyloid precursor protein precludes transcriptional and proteomic responses to brain injury
Original language description
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.METHODSWe 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.RESULTSAfter 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.DISCUSSIONThe 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.
Czech name
—
Czech description
—
Classification
Type
J<sub>imp</sub> - Article in a specialist periodical, which is included in the Web of Science database
CEP classification
—
OECD FORD branch
30103 - Neurosciences (including psychophysiology)
Result continuities
Project
Result was created during the realization of more than one project. More information in the Projects tab.
Continuities
P - Projekt vyzkumu a vyvoje financovany z verejnych zdroju (s odkazem do CEP)
Others
Publication year
2025
Confidentiality
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Data specific for result type
Name of the periodical
Alzheimers & Dementia
ISSN
1552-5260
e-ISSN
1552-5279
Volume of the periodical
21
Issue of the periodical within the volume
4
Country of publishing house
US - UNITED STATES
Number of pages
14
Pages from-to
"e70093"
UT code for WoS article
001484191800017
EID of the result in the Scopus database
2-s2.0-105003800260