DLG4 (Discs Large MAGUK Scaffold Protein 4)

Mice were assigned into 6 groups(n=10): blank, model, positive drug(donepezil hydrochloride, 0.65 mg·kg~(-1)), and low-, medium-, and high-dose(0.3, 1.5, and 7.5 g·kg~(-1), respectively) Shenzao Jiannao Oral Liquid, and administrated with corresponding agents by gavage for 28 days...Furthermore, Shenzao Jiannao Oral Liquid groups showed significantly down-regulated expression levels of TNF-α, IL-1β, and NF-κB signaling pathway proteins and up-regulated expression levels of SYN and PSD95. The results verify that Shenzao Jiannao Oral Liquid can alleviate the cognitive impairment and pathological changes in the brain tissue of AD mice by inhibiting the activation of the NF-κB signaling pathway, reducing inflammation, and enhancing synaptic plasticity.

In vivo experiments demonstrated that AIGG significantly reversed depression-like behaviors in both forced swim and tail suspension tests, suppressed Interleukin-6 (IL-6), tumor necrosis factor α (TNF-α), and elevated β-nerve growth factor (β-NGF) levels, attenuated neuroinflammatory infiltration and neuronal apoptosis in brain tissue, and upregulated protein expression of protein kinase cAMP-activated catalytic subunit alpha (PRKACA), brain-derived neurotrophic factor (BDNF), and postsynaptic density protein 95 (PSD95). The study confirmed that AIGG alleviates depression by activating the cAMP-PRKACA-BDNF axis to restore synaptic plasticity, providing a novel natural product-based strategy for treatment of the resistant depression.

Rat pups received lipopolysaccharide (LPS) on postnatal Day 1 (P1), followed by tapering doses of dexamethasone (Dex) or hydrocortisone (HC) from P2 to P4. GR mRNA was significantly reduced in cortex, striatum, hippocampus, and cerebellum in LPS-HC group, with MR mRNA reduction limited primarily to the striatum. LPS sensitized the immature brain to Dex or HC-related cell death to possible apoptosis and augmented the LPS-induced disruption of synaptic integrity in certain brain regions, potentially via altered GR and MR expression that may modulate corticosteroid receptor signaling.

This study provides a peri-infarct human cortical snRNA-seq atlas after IS, revealing coordinated glial transcriptional responses that promote cellular adaptation and repair. The upregulation of NMNAT2, HIF3A, NRP1, SEZ6L, and GPM6A highlights potential therapeutic targets for enhancing neuroprotection and remyelination after stroke.

No hippocampal pathological change and abnormal dendritic length or spine density were observed. Furthermore, no significant alterations in the expression levels of CREB, BDNF, or PSD95 were detected.ConclusionsNeonatal single exposure to propofol anesthesia does not impair recognition function in either the short- or long-term.

Importantly, the CRISPR-Cas9 mediated deletion of dlg4a in oligodendroglia impairs myelin sheath growth in vivo. Overall, our data indicate that PSD-95 is a key component of axons to oligodendrocytes neurotransmission that regulates myelin sheath growth.

N-acetylcysteine (NAC), a well-known antioxidant, could attenuate cognitive behavioral impairments and neuroinflammatory damage by restoring inflammatory and neurodevelopmental mediators. In general, our study uncovered that chronic ethanol exposure may exacerbate AD progress at the pathological and molecular levels and NAC may act as a potential drug for the treatment of AD patients with chronic ethanol exposure.

Altogether, our findings support the potential role of CACNG8 as a genetic modifier in IRDs, pending further validation in larger cohorts. The study illustrates how combining genomic and structural approaches can uncover hidden contributors to complex retinal disorders.

LPS-induced NF-κB pathway activation partially averted melatonin's beneficial effects on ASD mice. Melatonin ameliorated ASD-induced CD in mice by modulating the NF-κB pathway and oxidative stress.

In summary, our findings highlighted the essential role of Ca2+ signaling in oligodendrocyte biology and its therapeutic potential for demyelinating diseases. Targeting VGCCs and chemogenetic pathways may accelerate myelin repair and improve functional recovery in CNS disorders.

DHYZ could improve mitochondrial dynamics and synaptic plasticity in APP/PS1 mice, inhibit oxidative stress, and thereby enhancing learning and memory abilities in APP/PS1 mice. Its mechanism might be related to activation of the cAMP/PKA/CREB-BDNF signaling pathway.

Histological assessments showed significantly reduced neuronal degeneration in BDL rats supplemented with fisetin, suggesting its ability to ameliorate HE-associated neurodegeneration. These findings collectively underscore fisetin's neuroprotective potential in BDL rats by mitigating neurodegeneration, preserving synaptic integrity, and enhancing cognitive function.