Understanding the neurobiological mechanisms of LPS‑induced memory impairment.

IF 1.4 4区 医学 Q4 NEUROSCIENCES
Ahmad Golkar, Mohammad Dalfardi, Mahdiyeh Hedayati-Moghadam, Hedyeh Askarpour, Mahmoud Hosseini, Yousef Baghcheghi
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引用次数: 0

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.

了解LPS诱导的记忆障碍的神经生物学机制。
近年来,越来越多的证据表明,脂多糖(LPS),一种发现于革兰氏阴性菌外膜的细菌内毒素,可以影响认知功能,特别是记忆的形成和恢复。然而,LPS对记忆影响的潜在机制仍不完全清楚。本综述使用了各种电子数据库,包括PubMed、Scopus和Web of Science,以确定2000年至2024年间发表的相关研究。文章的选择基于他们对LPS诱导的记忆损伤的关注,包括实验模型、分子途径和神经化学改变。尽管记忆损伤的程度和持续时间可能取决于LPS暴露的剂量、时间和环境等因素,但LPS的使用一直被证明会破坏动物和人类的记忆过程。已经提出了几种潜在的机制来解释LPS诱导的记忆缺陷,包括神经炎症、突触可塑性的改变、神经递质系统的破坏和血脑屏障的功能障碍。此外,已经发现LPS可以激活免疫信号通路,如toll样受体、白细胞介素和小胶质细胞,这可能进一步导致认知障碍。这些见解可能为靶向治疗干预的发展铺平道路,旨在改善与LPS暴露相关的记忆缺陷,包括细菌感染、败血症和神经炎症性疾病。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
CiteScore
2.20
自引率
7.10%
发文量
40
审稿时长
>12 weeks
期刊介绍: Acta Neurobiologiae Experimentalis (ISSN: 0065-1400 (print), eISSN: 1689-0035) covers all aspects of neuroscience, from molecular and cellular neurobiology of the nervous system, through cellular and systems electrophysiology, brain imaging, functional and comparative neuroanatomy, development and evolution of the nervous system, behavior and neuropsychology to brain aging and pathology, including neuroinformatics and modeling.
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