Elovanoid neuroprotection targets cell transcriptomics and proteomics to sustain synaptic integrity after brain injury
Document Type
Article
Publication Date
4-10-2026
Publication Title
Communications Biology
Abstract
Traumatic brain injury (TBI), a leading cause of death and disability, is the largest non-genetic, non-aging-related contributor to cognitive impairments. Currently, there are limited effective therapies to protect neurons after acute brain injury. Our results suggest that intranasal-delivered (IN) elovanoid (ELV) shortly after TBI elicits neuroprotection that involves synaptic and mitochondrial pathways that mediate neuroprotection. Using a single-cell multiome approach, we found an upregulation of genes involved in synaptic integrity. Furthermore, we discovered that ELVs improve synaptosomal mitochondrial function, reduce lipid peroxidation, and increase the activity of antioxidant transcriptional programs, including the NRF2 pathway, in neurons. We suggest that these changes, together with the induction of cell-type-specific gene regulation in glutamatergic neurons and other cells, underlie ELV-elicited neuroprotection.
PubMed ID
41963623
Creative Commons License
This work is licensed under a Creative Commons Attribution-NonCommercial-No Derivative Works 4.0 International License.
Recommended Citation
Giles, Brian L.; Bhattacharjee, Surjyadipta; Ji, Jeff X.; Mukherjee, Pranab K.; Belayev, Ludmila; Vieira, Carlos M.; and Bazan, Nicolas G., "Elovanoid neuroprotection targets cell transcriptomics and proteomics to sustain synaptic integrity after brain injury" (2026). School of Medicine Faculty Publications. 4746.
https://digitalscholar.lsuhsc.edu/som_facpubs/4746
10.1038/s42003-026-09931-1