AI Article Synopsis
- * Exposure to ACR leads to the upregulation of eEF2K, which is linked to learning and memory deficits, and manipulating eEF2K levels improved these cognitive issues in experiments.
- * The findings suggest that eEF2K could be a promising target for clinical interventions aimed at countering ACR-related cognitive impairments by influencing lipid metabolism in the brain.
Article Abstract
Background: The impact of acrylamide (ACR) on learning and memory has garnered considerable attention. However, the targets and mechanisms are still unclear.
Results: Elongation factor 2 (eEF2) was significantly upregulated in the results of serum proteomics. Results from in vitro and in vivo experiments indicated a notable upregulation of Eukaryotic elongation factor 2 kinase (eEF2K), the sole kinase responsible for eEF2 phosphorylation, following exposure to ACR (P < 0.05). Subsequent in vitro experiments using eEF2K siRNA and in vivo experiments with eEF2K-knockout mice demonstrated significant improvements in abnormal indicators related to ACR-induced learning and memory deficits (P < 0.05). Proteomic analysis of the hippocampus revealed Lpcat1 as a crucial downstream protein regulated by eEF2K. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses indicated that eEF2K may play a role in the process of ACR-induced learning and memory impairment by affecting ether lipid metabolism.
Conclusions: In summary, eEF2K as a pivotal treatment target in the mechanisms underlying ACR-induced learning and memory impairment, and studies have shown that it provides robust evidence for potential clinical interventions targeting ACR-induced impairments.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11344312 | PMC |
| http://dx.doi.org/10.1186/s13578-024-01285-7 | DOI Listing |
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