Summary of Study ST003165
This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR001969. The data can be accessed directly via it's Project DOI: 10.21228/M86Q81 This work is supported by NIH grant, U2C- DK119886.
See: https://www.metabolomicsworkbench.org/about/howtocite.php
This study contains a large results data set and is not available in the mwTab file. It is only available for download via FTP as data file(s) here.
| Study ID | ST003165 |
| Study Title | Spatial Lipidomics Maps Brain Alterations Associated with Mild Traumatic Brain Injury. |
| Study Summary | Traumatic brain injury (TBI) is a global public health problem with 50-60 million incidents per year, most of which are considered mild (mTBI) and many of these repetitive (rmTBI). Despite their massive implications, the pathologies of mTBI and rmTBI are not fully understood, with a paucity of information on brain lipid dysregulation following mild injury event(s). To gain more insight on mTBI and rmTBI pathology, a non-targeted spatial lipidomics workflow utilizing ultrahigh resolution mass spectrometry imaging was developed to map brain region-specific lipid alterations in rats following injury. Discriminant multivariate models were created for regions of interest including the hippocampus, cortex, and corpus callosum to pinpoint lipid species that differentiated between injured and sham animals. A multivariate model focused on the hippocampus region differentiated injured brain tissues with an area under the curve of 0.994 using only four lipid species. Lipid classes that were consistently discriminant included polyunsaturated fatty acid-containing phosphatidylcholines (PC), lysophosphatidylcholines (LPC), LPC-plasmalogens (LPC-P) and PC potassium adducts. Many of the polyunsaturated fatty acid-containing PC and LPC-P selected have never been previously reported as altered in mTBI. The observed lipid alterations indicate that neuroinflammation and , oxidative stress and disrupted sodium-potassium pumps are important pathologies that could serve to explain cognitive deficits associated with rmTBI. Therapeutics which target or attenuate these pathologies may be beneficial to limit persistent damage following a mild brain injury event. |
| Institute | Georgia Institute of Technology |
| Last Name | Leontyev |
| First Name | Dmitry |
| Address | 311 Ferst Dr NW Atlanta GA 30332 |
| dleontyev3@gatech.edu | |
| Phone | 301 538 2301 |
| Submit Date | 2024-04-08 |
| Raw Data Available | Yes |
| Raw Data File Type(s) | imzML |
| Analysis Type Detail | MALDI |
| Release Date | 2024-04-30 |
| Release Version | 1 |
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Treatment:
| Treatment ID: | TR003293 |
| Treatment Summary: | Prior to injury, rats were anesthetized and maintained with 2-3% isoflurane. Rats were then placed on 1-inch-thick ethylene-vinyl acetate foam (McMaster-Carr, Elmhurst, IL, USA). rmTBI was induced by subjecting rats to three closed head impacts (2 min interval, 5 m s-1 velocity, 5 mm, 2 mm, and 2 mm head displacement) to the dorsal head surface using a CCI pneumatic injury device (Pittsburgh Precision Instruments, Pittsburgh, PA, USA). This device was equipped with a 1-cm diameter silicone stopper (Renovators Supply Manufacturing, Erving, MA, USA) attached to the piston tip. The sham group underwent identical procedures as the injured group, except for the impacts. |
