N-Stearidonoylethanolamine Restores CA1 Synaptic Integrity and Reduces Astrocytic Reactivity After Mild Traumatic Brain Injury.

Fuente: PubMed
Gespeichert in:
Bibliographische Detailangaben
Hauptverfasser: Egoraeva, Anastasia, Manzhulo, Igor, Ivashkevich, Darya, Tyrtyshnaia, Anna
Format: Artículo científico
Sprache:en
Veröffentlicht: International journal of molecular sciences 2026
Schlagworte:
Online-Zugang:
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
_version_ 1868266100246970369
author Egoraeva, Anastasia
Manzhulo, Igor
Ivashkevich, Darya
Tyrtyshnaia, Anna
author_facet Egoraeva, Anastasia
Manzhulo, Igor
Ivashkevich, Darya
Tyrtyshnaia, Anna
Egoraeva, Anastasia
Manzhulo, Igor
Ivashkevich, Darya
Tyrtyshnaia, Anna
collection PubMed - marine biology
contents N-Stearidonoylethanolamine Restores CA1 Synaptic Integrity and Reduces Astrocytic Reactivity After Mild Traumatic Brain Injury. Egoraeva, Anastasia Manzhulo, Igor Ivashkevich, Darya Tyrtyshnaia, Anna Animals Astrocytes Mice Male Synapses CA1 Region, Hippocampal Brain Concussion Ethanolamines Disease Models, Animal Mice, Inbred C57BL Neurogenesis Doublecortin Protein Mild traumatic brain injury (mTBI) disrupts hippocampal network function through coordinated alterations in glial reactivity, synaptic integrity, and adult neurogenesis. Effective therapeutic approaches targeting these interconnected processes remain limited. Lipid-derived molecules capable of modulating these mTBI-induced disturbances are emerging as promising neuroprotective candidates. Here, we investigated the effects of N-stearidonylethanolamine (SDEA), an ω-3 ethanolamide, in a mouse model of mTBI. SDEA treatment attenuated astrocytic reactivity, restored Arc expression, and improved dendritic spine density and morphology in the CA1 hippocampal area. In the dentate gyrus, mTBI reduced Ki-67-indexed proliferation while leaving DCX-positive immature neurons unchanged, and SDEA partially rescued proliferative activity. These effects were accompanied by improvements in anxiety-like behavior and working-memory performance. Together, these findings demonstrate that SDEA modulates several key components of the glia-synapse-neurogenesis axis and supports functional recovery of hippocampal circuits following mTBI. These results suggest that ω-3 ethanolamides may represent promising candidates for multi-target therapeutic strategies in mTBI.
format Artículo científico
id pubmed_41516344
institution PubMed
language en
publishDate 2026
publisher International journal of molecular sciences
record_format pubmed
spellingShingle N-Stearidonoylethanolamine Restores CA1 Synaptic Integrity and Reduces Astrocytic Reactivity After Mild Traumatic Brain Injury.
Egoraeva, Anastasia
Manzhulo, Igor
Ivashkevich, Darya
Tyrtyshnaia, Anna
Animals
Astrocytes
Mice
Male
Synapses
CA1 Region, Hippocampal
Brain Concussion
Ethanolamines
Disease Models, Animal
Mice, Inbred C57BL
Neurogenesis
Doublecortin Protein
N-Stearidonoylethanolamine Restores CA1 Synaptic Integrity and Reduces Astrocytic Reactivity After Mild Traumatic Brain Injury. Egoraeva, Anastasia Manzhulo, Igor Ivashkevich, Darya Tyrtyshnaia, Anna Animals Astrocytes Mice Male Synapses CA1 Region, Hippocampal Brain Concussion Ethanolamines Disease Models, Animal Mice, Inbred C57BL Neurogenesis Doublecortin Protein Mild traumatic brain injury (mTBI) disrupts hippocampal network function through coordinated alterations in glial reactivity, synaptic integrity, and adult neurogenesis. Effective therapeutic approaches targeting these interconnected processes remain limited. Lipid-derived molecules capable of modulating these mTBI-induced disturbances are emerging as promising neuroprotective candidates. Here, we investigated the effects of N-stearidonylethanolamine (SDEA), an ω-3 ethanolamide, in a mouse model of mTBI. SDEA treatment attenuated astrocytic reactivity, restored Arc expression, and improved dendritic spine density and morphology in the CA1 hippocampal area. In the dentate gyrus, mTBI reduced Ki-67-indexed proliferation while leaving DCX-positive immature neurons unchanged, and SDEA partially rescued proliferative activity. These effects were accompanied by improvements in anxiety-like behavior and working-memory performance. Together, these findings demonstrate that SDEA modulates several key components of the glia-synapse-neurogenesis axis and supports functional recovery of hippocampal circuits following mTBI. These results suggest that ω-3 ethanolamides may represent promising candidates for multi-target therapeutic strategies in mTBI.
title N-Stearidonoylethanolamine Restores CA1 Synaptic Integrity and Reduces Astrocytic Reactivity After Mild Traumatic Brain Injury.
topic Animals
Astrocytes
Mice
Male
Synapses
CA1 Region, Hippocampal
Brain Concussion
Ethanolamines
Disease Models, Animal
Mice, Inbred C57BL
Neurogenesis
Doublecortin Protein
url https://pubmed.ncbi.nlm.nih.gov/41516344/