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.
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http://dx.doi.org/10.55782/ane-2024-2629 | DOI Listing |
JAMA Netw Open
January 2025
Laboratory of NeuroImaging, National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland.
Importance: Cannabis use has increased globally, but its effects on brain function are not fully known, highlighting the need to better determine recent and long-term brain activation outcomes of cannabis use.
Objective: To examine the association of lifetime history of heavy cannabis use and recent cannabis use with brain activation across a range of brain functions in a large sample of young adults in the US.
Design, Setting, And Participants: This cross-sectional study used data (2017 release) from the Human Connectome Project (collected between August 2012 and 2015).
Naunyn Schmiedebergs Arch Pharmacol
January 2025
Department of Pharmacology, ISF College of Pharmacy, Ghal Kalan, GT Road, Moga, 142001, Punjab, India.
In examining the enduring consequences of diabetes, recent research has focused on the anticipated outcomes of the condition. Specifically, cognitive impairment has been linked to diabetes mellitus dating back to the discovery of insulin. This study delves into the neuroprotective effects of TZP, i.
View Article and Find Full Text PDFNaunyn Schmiedebergs Arch Pharmacol
January 2025
Department of Pharmacology, College of Medicine and Health Sciences, Afe Babalola University, Ado-Ekiti, Ekiti State, Nigeria.
Stress is linked to oxidative imbalance, neuroendocrine system malfunction, and cognitive dysfunction. It is a recognized cause of neuropsychiatric diseases. Natural flavonoid apigenin (API) has neuroprotective and antidepressant properties, but little is known about its potential in restoring memory function under stress-related circumstances.
View Article and Find Full Text PDFJ Vis
January 2025
Department of Psychology, Humboldt-Universität zu Berlin, Berlin, Germany.
Previous research has shown that, when multiple similar items are maintained in working memory, recall precision declines. Less is known about how heterogeneous sets of items across different features within and between modalities impact recall precision. In two experiments, we investigated modality (Experiment 1, n = 79) and feature-specific (Experiment 2, n = 154) load effects on working memory performance.
View Article and Find Full Text PDFJ Neurophysiol
January 2025
Department of Psychology, University of Wisconsin-Milwaukee, Milwaukee WI, USA.
The hippocampus has a known role in learning and memory, with the ventral subregion supporting many learning tasks involving affective responding, including fear conditioning. Altered neuronal intrinsic excitability reflects experience-dependent plasticity that supports learning-related behavioral changes. Such changes have previously been observed in the dorsal hippocampus following fear conditioning, but little work has examined the effect of fear conditioning on ventral hippocampal intrinsic plasticity.
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