Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Traumatic Brain Injury Increases the Expression of Nos1, Aβ Clearance, and Epileptogenesis in APP/PS1 Mouse Model of Alzheimer's Disease.

Molecular neurobiology - 1 Dec 2016

Miszczuk Diana, Dębski Konrad J, Tanila Heikki, Lukasiuk Katarzyna, Pitkänen Asla

Abstract excerpt

To test the hypothesis that an amyloidogenic genetic background predisposes to worsening of post-TBI outcome, we investigated whether traumatic brain injury (TBI) in amyloid precursor protein (APP)/PS1 mice aggravates epileptogenesis and/or enhances somatomotor and cognitive impairment. To elaborate the mechanisms of worsening outcomes, we studied changes in the expression of genes involved in APP processing and...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Amyloid beta-Peptides
Share to Astrocytes

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Brain Injuries, Traumatic

Share to Cerebral Cortex

Share to Memory

Share to Nitric Oxide Synthase Type I

Share to Presenilin-1

Share to tau Proteins

Source

Identifiers

PMID: 26671618
DOI: 10.1007/s12035-015-9578-3

Genes

APP
NOS1

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Traumatic Brain Injury Increases the Expression of Nos1, Aβ Clearance, and Epileptogenesis in APP/PS1 Mouse Model of Alzheimer's Disease.PMID 26671618Read ↗

Traumatic Brain Injury Accelerates the Onset of Cognitive Dysfunction and Aggravates Alzheimer’s-like Pathology in the Hippocampus by Altering the Phenotype of Microglia in APP/PS1 Mouse ModelSemantic proximity Read ↗

Genetic predisposition to Alzheimer's disease alters inflammasome activity after traumatic brain injury.Semantic proximity Read ↗

Age at injury and genotype modify acute inflammatory and neurofilament-light responses to mild CHIMERA traumatic brain injury in wild-type and APP/PS1 mice.Semantic proximity Read ↗

Chronic evoked seizures in young pre-symptomatic APP/PS1 mice induce serotonin changes and accelerate onset of Alzheimer’s disease-related neuropathologySemantic proximity Read ↗

Traumatic brain injury exacerbates mitochondrial dysfunction in APP/PS1 knock-in mice through time-dependent pathwaysSemantic proximity Read ↗

Gene-environment interaction promotes Alzheimer's risk as revealed by synergy of repeated mild traumatic brain injury and mouse App knock-inSemantic proximity Read ↗

Traumatic brain injury in mice generates early-stage Alzheimer’s disease related protein pathology that correlates with neurobehavioral deficitsSemantic proximity Read ↗

Distinct temporal and anatomical distributions of amyloid-β and tau abnormalities following controlled cortical impact in transgenic mice.Semantic proximity Read ↗

Brain trauma in aged transgenic mice induces regression of established abeta deposits.Semantic proximity Read ↗

Traumatic Brain Injury Induces Tau Aggregation and SpreadingSemantic proximity Read ↗

Overexpression of Metallothionein-1 Modulates the Phenotype of the Tg2576 Mouse Model of Alzheimer's Disease.Semantic proximity Read ↗

Traumatic Brain Injury Exacerbates Alzheimer’s Disease Pathology in the Retinas of TgF344-AD RatsSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.