Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Beyond component optimization: systems-level biodesign for lanthanide recovery.

Current opinion in biotechnology·2026
Same author

Visual exoproteomics of <i>Clostridium thermocellum</i> during anaerobic biomass-degradation identifies functional spirosomes.

bioRxiv : the preprint server for biology·2026
Same author

Time to normalise protected characteristics in written assessments: A pilot study.

MedEdPublish (2016)·2026
Same author

The influence of electrical charge on plasmodesma conductivity.

Proceedings of the National Academy of Sciences of the United States of America·2026
Same author

Systematic scale-up and enhanced purification of marine cyanophage P-SSP7.

Frontiers in microbiology·2026
Same author

Membrane-associated Rhes-Slc4a7 complex orchestrates tunneling nanotube formation and mutant Huntingtin spread.

Science advances·2026
Same journal

Near‑Infrared Photobiomodulation in White‑Matter Disease: From Microglial States to Measurable Endpoints.

Neuromolecular medicine·2026
Same journal

<sup>64</sup>Cu Hypoxia Imaging Radiotracer Targeting the Human Copper Transporter.

Neuromolecular medicine·2026
Same journal

Curculigoside Alleviates CSDS-induced Depressive-like Behavior by Modulating Pyramidal Neuron Excitability and Synaptic Transmission.

Neuromolecular medicine·2026
Same journal

Association of Cathepsin Proteins with Alzheimer's Disease Risk: An Integrated Observational and Genetic Analysis.

Neuromolecular medicine·2026
Same journal

Single-cell Transcriptomics Reveals that the SORBS1/FBXO22/BAG3 Axis Drives Astrocyte Senescence via Calcium Signaling and Affects Alzheimer's Disease-Related Neuronal Damage.

Neuromolecular medicine·2026
Same journal

Subgroup-Specific Associations of GRIA Genes Encoding AMPA Glutamate Receptor Subunits with Patient Survival in Medulloblastoma.

Neuromolecular medicine·2026
See all related articles

Related Experiment Video

Updated: Mar 16, 2026

Modified Mouse Model of Repetitive Mild Traumatic Brain Injury Incorporating Thinned-Skull Window and Fluid Percussion
04:54

Modified Mouse Model of Repetitive Mild Traumatic Brain Injury Incorporating Thinned-Skull Window and Fluid Percussion

Published on: April 19, 2024

1.4K

Mild TBI Results in a Long-Term Decrease in Circulating Phospholipids in a Mouse Model of Injury.

Tanja Emmerich1,2,3, Laila Abdullah4,5,6, Joseph Ojo4,5

  • 1The Roskamp Institute, 2040 Whitfield Avenue, Sarasota, FL, 34243, USA. temmerich@roskampinstitute.net.

Neuromolecular Medicine
|August 20, 2016
PubMed
Summary
This summary is machine-generated.

Mild traumatic brain injury (mTBI) can cause long-term phospholipid changes in mice, mirroring human patient data. These chronic alterations may serve as diagnostic biomarkers for persistent TBI pathology.

Keywords:
LipidomicsMild traumatic brain injury (mTBI)Mouse modelPhospholipids (PL)Plasma biomarkers

More Related Videos

Electromagnetic Controlled Closed-Head Model of Mild Traumatic Brain Injury in Mice
09:07

Electromagnetic Controlled Closed-Head Model of Mild Traumatic Brain Injury in Mice

Published on: September 28, 2022

2.9K
A Mouse Model of Single and Repetitive Mild Traumatic Brain Injury
04:19

A Mouse Model of Single and Repetitive Mild Traumatic Brain Injury

Published on: June 20, 2017

11.8K

Related Experiment Videos

Last Updated: Mar 16, 2026

Modified Mouse Model of Repetitive Mild Traumatic Brain Injury Incorporating Thinned-Skull Window and Fluid Percussion
04:54

Modified Mouse Model of Repetitive Mild Traumatic Brain Injury Incorporating Thinned-Skull Window and Fluid Percussion

Published on: April 19, 2024

1.4K
Electromagnetic Controlled Closed-Head Model of Mild Traumatic Brain Injury in Mice
09:07

Electromagnetic Controlled Closed-Head Model of Mild Traumatic Brain Injury in Mice

Published on: September 28, 2022

2.9K
A Mouse Model of Single and Repetitive Mild Traumatic Brain Injury
04:19

A Mouse Model of Single and Repetitive Mild Traumatic Brain Injury

Published on: June 20, 2017

11.8K

Area of Science:

  • Neuroscience
  • Biochemistry
  • Pathology

Background:

  • Mild traumatic brain injury (mTBI) often leads to short-term dysfunction, but ~15% of patients experience chronic symptoms.
  • Phospholipid (PL) alterations in plasma suggest a role in chronic TBI pathology.
  • Understanding long-term biochemical changes is crucial for diagnosing and managing persistent TBI disabilities.

Purpose of the Study:

  • To investigate long-term plasma phospholipid profiles in a mouse model of mTBI.
  • To assess the translational value of mouse mTBI models for human PL changes.
  • To identify potential chronic TBI biomarkers.

Main Methods:

  • Mice were subjected to mTBI or sham procedures, with plasma collected at acute (24h) and chronic (3, 6, 12, 24 months) timepoints.
  • Liquid chromatography/mass spectrometry was used to identify and quantify phospholipids.
  • Malondialdehyde levels were measured to assess lipid peroxidation.

Main Results:

  • Chronic mTBI mice showed significantly lower levels of major PL classes compared to controls.
  • Polyunsaturated fatty acid (PUFA) levels decreased at 3 months, coinciding with elevated lipid peroxidation.
  • Ether-containing phosphatidylethanolamine (PE) species were elevated acutely but decreased chronically; arachidonic and docosahexaenoic acid species were reduced long-term.

Conclusions:

  • Plasma PL profiles in chronic mTBI mice resemble those observed in human patients.
  • Persistent biochemical abnormalities after TBI may offer insights into ongoing pathogenesis.
  • Identified long-term PL changes could serve as diagnostic biomarkers for chronic TBI.