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Understanding the Neurobiological Mechanisms of Lps-Induced Memory Impairment Publisher Pubmed



Golkar A1 ; Dalfardi M2 ; Hedayatimoghadam M2, 3 ; Askarpour H2 ; Hosseini M5, 6 ; Baghcheghi Y3, 4
Authors
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Authors Affiliations
  1. 1. Department of Immunology, School of Public Health, Tehran University of Medical Sciences, Tehran, Iran
  2. 2. Student Research Committee, Jiroft University of Medical Sciences, Jiroft, Iran
  3. 3. Department of Physiology, School of Medicine, Jiroft University of Medical Sciences, Jiroft, Iran
  4. 4. Bio Environmental Health Hazards Research Center, Jiroft University of Medical Sciences, Jiroft, Iran
  5. 5. Psychiatry and Behavioral Sciences Research Center, Mashhad University of Medical Sciences, Mashhad, Iran
  6. 6. Applied Biomedical Research Center, Mashhad University of Medical Sciences, Mashhad, Iran

Source: Acta Neurobiologiae Experimentalis Published:2024


Abstract

In recent years, growing evidence suggests that lipopolysaccharide (LPS), a bacterial endotoxin found in the outer membrane of gram-negative bacteria, can influence cognitive functions, particularly memory formation and retrieval. However, the underlying mechanisms through which LPS exerts its effects on memory remain incompletely understood. This review used various electronic databases, including PubMed, Scopus, and Web of Science, to identify relevant studies published between 2000 and 2024. Articles were selected based on their focus on LPS-induced memory impairments, including experimental models, molecular pathways, and neurochemical alterations. LPS administration has been consistently shown to disrupt memory processes in both animals and humans, although the magnitude and duration of memory impairments might vary depending on factors such as dose, timing, and context of LPS exposure. Several potential mechanisms have been proposed to explain LPS-induced memory deficits, including neuroinflammation, alterations in synaptic plasticity, disruption of neurotransmitter systems, and dysfunction of the blood-brain barrier. Moreover, LPS has been found to activate immune signaling pathways, such as toll-like receptors, interleukins, and microglia, which can further contribute to cognitive impairments. Such insights may pave the way for the development of targeted therapeutic interventions aimed at ameliorating memory deficits associated with conditions involving LPS exposure, including bacterial infections, sepsis, and neuroinflammatory disorders. © 2024 by Acta Neurobiologiae Experimentalis.