GSDMD knockdown attenuates phagocytic activity of microglia and exacerbates seizure susceptibility in TLE mice.

Background: Temporal lobe epilepsy (TLE) is often characterized pathologically by severe neuronal loss in the hippocampus. Phagocytic activity of microglia is essential for clearing apoptotic neuronal debris, allowing for repair and regeneration. Our previous research has shown that gasdermin D (GSDMD)-mediated pyroptosis is involved in the pathogenesis of TLE.

GSDMD knockdown exacerbates hippocampal damage and seizure susceptibility by crosstalk between pyroptosis and apoptosis in kainic acid-induced temporal lobe epilepsy.

Background: Neuronal loss is a vital pathological feature of temporal lobe epilepsy (TLE). However, the exact mechanism of neuronal loss in TLE is not fully understood. Pyroptosis, a novel form of programmed cell death (PCD), has been considered a contributor to the pathogenesis of TLE.

Dl-3-n-butylphthalide promotes synaptic plasticity by activating the Akt/ERK signaling pathway and reduces the blood-brain barrier leakage by inhibiting the HIF-1α/MMP signaling pathway in vascular dementia model mice.

Aims: DL-3-n-butylphthalide (NBP) exerts beneficial effects on global cognitive functions, but the underlying molecular mechanisms are still poorly understood. The present study aimed to investigate whether NBP mediates synaptic plasticity and blood-brain barrier (BBB) function, which play a pivotal role in the pathogenesis of vascular dementia (VaD), in a mouse model of bilateral common carotid artery stenosis (BCAS).

Methods: NBP was administered to model mice at a dose of 80 mg/kg by gavage for 28 days after surgery.

Transient neuroinflammation following surgery contributes to long-lasting cognitive decline in elderly rats via dysfunction of synaptic NMDA receptor.

Background: Perioperative neurocognitive disorders (PNDs) are considered the most common postoperative complication in geriatric patients. However, its pathogenesis is not fully understood. Surgery-triggered neuroinflammation is a major contributor to the development of PNDs.

GPR120 modulates epileptic seizure and neuroinflammation mediated by NLRP3 inflammasome.

Background: The complex pathophysiology of epilepsy hampers the development of effective treatments. Although more than ten kinds of anti-seizures drugs (ASDs) have good effects on seizure control worldwide, about 30% of patients still display pharmacoresistance against ASDs. Neuroinflammation seems to play a crucial role in disease progression.

Intestinal Klebsiella pneumoniae infection enhances susceptibility to epileptic seizure which can be reduced by microglia activation.

Epilepsy is a common nervous system disease, and the existing theory does not fully clarify its pathogenesis. Recent research suggests that intestinal microbes may be involved in the development of epilepsy, but which microbe is involved remains unclear. We used 16s rRNA sequencing to identify the most relevant gut microbe.

Seizures in steroid-responsive encephalopathy.

Steroid-responsive encephalopathy is a general term for diseases that are characterized by diffuse brain injury and respond well to corticosteroids or immunosuppressive agents, including Hashimoto's encephalopathy (HE), limbic encephalitis (LE), systemic lupus erythematosus encephalopathy (SLEE), antineutrophil cytoplasmic antibodies (ANCA)-associated systemic vasculitis encephalopathy (AASV), viral encephalitis (VE), and primary central nervous system lymphoma (PCNSL). Epilepsy and status epilepticus are the main manifestations of steroid-responsive encephalopathy. The spectrum of "autoimmune epilepsy" diseases, which has been approved by the epilepsy diagnostic recommendations of the International Antiepileptic League, is characterized by a high prevalence of epilepsy in central nervous system (CNS) autoimmune diseases and a variety of neuron-specific autoantibodies.

Stability of hydrogen-bonded supramolecular architecture under high pressure conditions: pressure-induced amorphization in melamine-boric acid adduct.

The effects of high pressure on the structural stability of the melamine-boric acid adduct (C3N6H(6).2H3BO3, M.2B), a three-dimensional hydrogen-bonded supramolecular architecture, were studied by in situ synchrotron X-ray diffraction (XRD) and Raman spectroscopy.