Elovanoids and Precursor Free Fatty Acid 34:6 Confer Robust Neuroprotection after Experimental Traumatic Brain Injury

Elovanoids and Precursor Free Fatty Acid 34:6 Confer Robust Neuroprotection after Experimental Traumatic Brain Injury

One-third of the close to 70 million people suffering from traumatic brain injury (TBI) have an increased risk for developing chronic cognitive impairments, including Alzheimer’s-like Dementia (AD). We studied neuroprotection by Elovanoid-34:6 (ELV-N34) and its precursor free-fatty- acid-34:6 (FFA34...

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Veröffentlicht in:International journal of biomedical science 2023-12, Vol.19 (4)
Hauptverfasser: Baum, Samuel E., Obenaus, Andre, Belayev, Ludmila, Bhattacharjee, Surjyadipta, Ji, Jeff, Giles, Brian, Mohiuddin, Alina, Bazan, Nicolas G.
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container_title International journal of biomedical science
container_volume 19
creator Baum, Samuel E.
Obenaus, Andre
Belayev, Ludmila
Bhattacharjee, Surjyadipta
Ji, Jeff
Giles, Brian
Mohiuddin, Alina
Bazan, Nicolas G.
description One-third of the close to 70 million people suffering from traumatic brain injury (TBI) have an increased risk for developing chronic cognitive impairments, including Alzheimer’s-like Dementia (AD). We studied neuroprotection by Elovanoid-34:6 (ELV-N34) and its precursor free-fatty- acid-34:6 (FFA34:6) following TBI in male Sprague-Dawley rats using fluid percussion injury (FPI) or controlled cortical impact (CCI) models. At 1 and 24 hours post-surgery, rats were intranasally administered saline, ELV-N34, or FFA34:6 (only in the CCI model). Rats underwent composite neurological testing to assess sensorimotor integration. On day 14, FPI animals were sacrificed, and MRI and diffuse tensor imaging (DTI) were performed to assess lesion size and white matter connectivity. On day 3, CCI animals were used for multi-omic analysis using 10x Chromium, Illumina Sequencing, and Seurat v4.0.1. Total neurological scores for animals administered ELV-N34 and FFA34:6 were lower than controls, and scores for FFA34:6 treated rats were lower than those of ELV34:6 treated rats (p
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We studied neuroprotection by Elovanoid-34:6 (ELV-N34) and its precursor free-fatty- acid-34:6 (FFA34:6) following TBI in male Sprague-Dawley rats using fluid percussion injury (FPI) or controlled cortical impact (CCI) models. At 1 and 24 hours post-surgery, rats were intranasally administered saline, ELV-N34, or FFA34:6 (only in the CCI model). Rats underwent composite neurological testing to assess sensorimotor integration. On day 14, FPI animals were sacrificed, and MRI and diffuse tensor imaging (DTI) were performed to assess lesion size and white matter connectivity. On day 3, CCI animals were used for multi-omic analysis using 10x Chromium, Illumina Sequencing, and Seurat v4.0.1. Total neurological scores for animals administered ELV-N34 and FFA34:6 were lower than controls, and scores for FFA34:6 treated rats were lower than those of ELV34:6 treated rats (p&lt;0.05). MRI and DTI showed smaller lesions and preserved white matter connectivity in the ELV34:6 group. Single cell analysis with ELV-N34 treatment revealed downregulation of Spp1, Fos, and Gfap genes and upregulation of Trem2 and Pld5 genes. FFA34:6 treatment revealed downregulation of inflammatory genes Spp1, Ccl2, and Vim. These changing gene cluster patterns are implicated in neurodegenerative diseases. We demonstrated that ELV-N34 and FFA34:6 convey behavioral, structural, and genetic neuroprotective bioactivity in experimental TBI.</description><identifier>ISSN: 1550-9702</identifier><identifier>EISSN: 1555-2810</identifier><identifier>DOI: 10.59566/iabs.2023.p053</identifier><language>eng</language><ispartof>International journal of biomedical science, 2023-12, Vol.19 (4)</ispartof><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27922,27923</link.rule.ids></links><search><creatorcontrib>Baum, Samuel E.</creatorcontrib><creatorcontrib>Obenaus, Andre</creatorcontrib><creatorcontrib>Belayev, Ludmila</creatorcontrib><creatorcontrib>Bhattacharjee, Surjyadipta</creatorcontrib><creatorcontrib>Ji, Jeff</creatorcontrib><creatorcontrib>Giles, Brian</creatorcontrib><creatorcontrib>Mohiuddin, Alina</creatorcontrib><creatorcontrib>Bazan, Nicolas G.</creatorcontrib><creatorcontrib>Department of Pediatrics, University of California, Irvine, Irvine, CA, 92697</creatorcontrib><creatorcontrib>Neuroscience Center of Excellence, School of Medicine, LSU Health New Orleans, New Orleans, New Orleans, LA 70112</creatorcontrib><title>Elovanoids and Precursor Free Fatty Acid 34:6 Confer Robust Neuroprotection after Experimental Traumatic Brain Injury</title><title>International journal of biomedical science</title><description>One-third of the close to 70 million people suffering from traumatic brain injury (TBI) have an increased risk for developing chronic cognitive impairments, including Alzheimer’s-like Dementia (AD). 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Single cell analysis with ELV-N34 treatment revealed downregulation of Spp1, Fos, and Gfap genes and upregulation of Trem2 and Pld5 genes. FFA34:6 treatment revealed downregulation of inflammatory genes Spp1, Ccl2, and Vim. These changing gene cluster patterns are implicated in neurodegenerative diseases. We demonstrated that ELV-N34 and FFA34:6 convey behavioral, structural, and genetic neuroprotective bioactivity in experimental TBI.</abstract><doi>10.59566/iabs.2023.p053</doi></addata></record>
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