Multi-omics analysis reveals alcohol exposure affects ferroptosis pathway in brain.

Behavioral and emotional abnormalities in mice with orthotopic colitis-associated colorectal cancer.

Carrier-free nanoassembly with dual antioxidant and anti-inflammatory activities camouflaged by melanoma cell membrane for tau-targeted therapy of Alzheimer's disease.

Bmal1 regulates hippocampal oxidative damage in cognitive memory impairment induced by artificial light at night in mice.

Targeting astrocytic Nrf2 by Trilobatin alleviates lipopolysaccharide-induced depressive-like behaviors and cognitive impairment in mice: Mechanistic insights into gut microbiota and metabolites modulation.

Oxidative stress alleviated DL-3-n-Butylphthalide against chronic intermittent hypoxia-induced cognitive deficit by regulating Nrf-2/HO-1 Pathway.

Probiotics reverse prenatal stress-induced anxiety and memory impairment in rats through gut-hippocampus axis regulation.

Comparative effects of voluntary and forced exercise on cognitive performance, thyroid function, and hippocampal integrity in a rat model of post-traumatic stress disorder.

NOTCH3 R545C mutation drives vascular-neuronal dysfunction and cognitive impairment in CADASIL pathogenesis.

Non-canonical K27 polyubiquitination is a sex-specific regulator of contextual fear memory in the hippocampus but not the amygdala.

MiR-372-3p alleviates isoflurane-induced cognitive dysfunction by targeting STAT3 to mitigate neuroinflammation and oxidative stress.

Optimization and validation of an animal model for perioperative neurocognitive disorders based on SAMP8 mice.

Agmatine diminishes pro-inflammatory response by modulating IL-1β and NF-κB expression in the prefrontal cortex and reverses behavioral impairments following chronic social isolation in rats.

Aphantasia and visual working memory: No direct evidence of impaired visual working memory in aphantasics, either in behavioral performance or the accuracy of a multivoxel pattern classifier.

Repeated opioid exposure, including therapeutic or illicit fentanyl (Fnt) use, disrupts the hippocampal network activity that supports learning and memory. However, the cellular mechanisms underlying these effects remain elusive. To elucidate how Fnt alters hippocampal-dependent behavior, synaptic physiology, and neuroinflammation in the dorsal hippocampus, we conducted behavioral testing, electrophysiological recordings, and immunofluorescence analyses for GFAP, CD11b, and the inflammasome NLPR3 in rats repeatedly administered with Fnt (0.1mg/kg, three times daily for 7 days; 19 injections). At the end of the administration protocol, Fnt reduced the exploration of relocated objects in the object location task, indicating impaired spatial memory. Extracellular recordings in acute brain slices of the dorsal hippocampus revealed that Fnt decreased the population spike amplitude of CA1 pyramidal cells, the fiber volley-fEPSP synchronization ratio, and altered the paired-pulse facilitation of glutamatergic transmission. Consistent with these findings, the magnitude of long-term potentiation (LTP) induced by theta-burst stimulation was reduced, mirroring decreased synaptic plasticity. Immunoreactivity analyses revealed increased GFAP and CD11b expression, accompanied by microglial hypertrophy and elevated NLRP3 expression in neurons and interneurons in area CA1, indicating astrogliosis and inflammasome priming. These findings indicate that repeated Fnt administration disrupts neuronal and glial homeostasis in the hippocampus.

Enhanced brain delivery of oleanolic acid by GSH-PEGylated liposomes and its amelioration of scopolamine-induced cognitive dysfunction via multi-target regulation.

Role of NMDAR-NMNAT in sevoflurane exposure-induced learning memory deficits.

Pre-treatment with royal jelly, environmental enrichment, and their combination role in stress induced neurobehavioral deficits in male rats.

Resting-state functional magnetic resonance imaging study of voxel-mirrored homotopy connections in patients with schizophrenia.

Sabinene's neuroprotective effect reverses ketamine-induced experimental schizophrenia in mice through enhancement of cholinergic, antioxidant, and anti-inflammatory mechanisms.