Objectives Neuroinflammation is closely associated with the poor prognosis of patients with subarachnoid hemorrhage (SAH). Lycopene (Lyc), a naturally occurring carotenoid, possesses multiple pharmacological effects, especially its neuroprotective function. However, the role of Lyc in SAH has never been evaluated. Methods In this study, the C57BL/6 mouse SAH model was induced by the endovascular perforation method. Lyc was administered to the mice intragastrically, and tunicamycin, an endoplasmic reticulum stress (ERS) agonist, was injected intravenously. The effects of Lyc on early brain injury (EBI) were assessed using neurological scoring, hematoxylin and eosin staining, and Nissl staining. Western blotting was used to analyze ERS-related proteins. Immunofluorescence staining was used to analyze microglial cell activation. Results Lyc significantly improved the neurobehavioral scores and alleviated neuronal degeneration at 24 h after SAH. Moreover, Lyc significantly reduced the expression levels of proteins p-eIF2a/eIF2a, ATF4, and CHOP and decreased the activation of microglial cells. Furthermore, tunicamycin reversed the inhibitory effect of Lyc on ERS and microglial cell activation, accompanied by improvement in neurological function. Conclusion Lyc relieved SAH-induced EBI partly through the p-eIF2a/ATF4/CHOP pathway.
Objective Paratonia is defined as an inability to relax the muscles during tone assessment, resulting in participants either opposing or facilitating the examiner’s movement involuntarily. This phenomenon is frequently found in patients with cognitive impairment and has been attributed to frontal lobe dysfunction, although a direct correlation has not been established. This study aimed to explore the correlation between frontal lobe function, as assessed by functional brain imaging, and paratonia, as assessed by electromyography. Methods Memory clinic outpatients with suspected Alzheimer’s disease who were prescribed an amyloid PET scan underwent a thorough neuropsychological examination and a paratonia assessment involving surface electromyography recording of the elbow flexors and extensors. PET image acquisition started immediately after tracer injection, and the early phase perfusion amyloid PET was used as a surrogate biomarker of neuronal injury. Multiple regression analysis was performed on amyloid-positive patients to identify the correlation between paratonia and brain perfusion. Results Twenty-one amyloid PET-positive participants with a median age of 72 years were diagnosed with Alzheimer’s disease and included in the analysis. All participants were right-handed, and paratonia was assessed in the left arm. Whole-brain voxel-wise analysis revealed a significant inverse correlation between the total paratonia score and cortical perfusion in a cluster encompassing the superior frontal gyrus in the left hemisphere (Brodmann areas 6, 8, and 9; P < 0.006). Conclusion This study demonstrates for the first time an inverse correlation between prefrontal perfusion and paratonia. Participants with better-preserved premotor function also show less paratonia, as reflected by reduced electromyographic activation of the muscles undergoing passive mobilization.
Objective Long‑term engagement in professional behavioral training and the resulting behavioral changes are known to influence human cognition. The present study investigates whether and how photography training is associated with individuals’ inhibitory control. Methods Fifteen photographers, 15 athletes, and 15 controls were recruited to complete a Go/Nogo task with concurrent electroencephalogram recording. Results Behavioral results showed slower response times and fewer commission errors for both photographers and athletes compared with controls, with no significant difference between the two training groups. Event‑related potential analyses revealed more negative Bereitschaftspotential amplitudes and more positive N2 amplitudes for photographers and athletes than for controls, again with no significant difference between photographers and athletes. Furthermore, a more negative prefrontal negativity amplitude was observed for athletes than for both photographers and controls, whereas no significant difference was found between photographers and controls. Conclusion Photography training was associated with a shift in the speed–accuracy trade‑off toward a greater emphasis on accuracy, as well as motor preparation and conflict monitoring—two core subprocesses of inhibitory control. Moreover, photographers and athletes showed improvements in inhibitory control through different neurocognitive pathways: while both groups showed enhanced motor preparation and conflict monitoring, athletes additionally exhibited enhanced cognitive preparation compared with photographers. This differential pattern may reflect athletes’ need to respond to unpredictable, real‑time emergencies during competition.
Background Neuroinflammation contributes to cerebral ischemia-reperfusion injury, and microglial inflammatory responses are regulated in part by Notch signaling. This study investigated whether laminarin, a brown algae-derived β-glucan polysaccharide, protects against cerebral ischemia-reperfusion injury by modulating Notch1-dependent microglial responses. Methods A rat middle cerebral artery occlusion/reperfusion model was established, and laminarin was administered intraperitoneally at 10 mg/kg for seven consecutive days. Neurological deficits and infarct volume were assessed by modified neurological severity score and 2,3,5-triphenyltetrazolium chloride staining. Transcriptomic and bioinformatic analyses were used to identify laminarin-associated pathways. BV2 microglial cells were stimulated with lipopolysaccharide, and Jagged1 was used to reactivate Notch signaling. Inducible nitric oxide synthase (iNOS), Arginase 1 (Arg1), Notch pathway proteins, and inflammatory cytokines were examined by immunofluorescence, western blotting, and enzyme-linked immunosorbent assay. Results Laminarin reduced infarct volume and improved neurological recovery in rats. Bioinformatic analysis and immunofluorescence indicated involvement of the Notch pathway. In vivo and in vitro , laminarin decreased iNOS-associated pro-inflammatory activation and increased Arg1-associated reparative responses, accompanied by reduced Notch1/Hes1/Hes5 activation. Jagged1 attenuated these effects and partially reversed laminarin-mediated changes in inflammatory markers and cytokine production. Conclusion Laminarin attenuates cerebral ischemia-reperfusion injury by reprogramming microglial inflammatory responses, at least partly through inhibition of the Notch1/Hes1/Hes5 signaling pathway. These findings support laminarin as a potential marine-derived immunomodulatory candidate for ischemic stroke research.
Objective In the present study, we investigated whether deep brain stimulation (DBS) of the nucleus basalis magnocellularis (NBM) improves autism spectrum disorder (ASD)-related behavioral abnormalities in a valproic acid (VPA)-induced rat model of autism, consistent with changes in cholinergic markers in the medial prefrontal cortex (mPFC). Methods On the 12.5th day of gestation, pregnant rats ( n = 16) received a single intraperitoneal injection of 500 mg/kg sodium valproate dissolved in 0.9% saline, while others ( n = 5) received saline alone. Male offspring were allowed to reach 3 months of age and then were randomly assigned to one of four experimental groups: Contr – prenatally saline injected, VPA – prenatally VPA-injected, VPA/I – VPA-injected with electrode implantation in the NBM, and VPA/S – VPA-injected with electrical stimulation. DBS was initiated in rats of the VPA/S group 10 days after surgery (two consecutive hours per day, every day for 2 weeks; DBS parameters: 60 Hz, 120 µs, and 50 µA). Results The prenatally VPA-exposed rats demonstrate deficits in social behavior, increased locomotor activity, and reduced anxiety levels. Immunohistochemical evaluation shows a decrease in the number of acetylcholinesterase-immunoreactive neurons in the mPFC and choline acetyltransferase-immunoreactive neurons in the NBM. NBM-DBS improves VPA-induced autistic behavior and increases the number of acetylcholinesterase-immunoreactive neurons in the PFC. Conclusion The correlation between ASD-like behavior and cholinergic markers in the mPFC supports our hypothesis that NBM-DBS improves behavioral deficits by modulating cholinergic neurotransmission in the PFC in a rat model of autism.
