Topic: neuronal cell death

Epilepsy, a neurological disorder affecting approximately 60 million individuals globally, poses a significant medical challenge with a substantial unmet need. Temporal lobe epilepsy is the most prevalent form, often triggered by traumatic incidents or status epilepticus (SE), resulting in hippocampal damage characterized by neuronal loss, astro- and microgliosis and neuroinflammation preceding the spontaneous recurrent seizures. Recently, an AAV-PHP.B-GFAP-interleukin-2 (IL-2) gene therapy exhibited impressive neuroprotective and anti-inflammatory effects in mouse models of traumatic brain in

Status epilepticus (SE) is a prolonged, recurrent seizure leading to neuronal damage. Given the limitations of existing treatment modalities, exploring new alternatives is imperative. Emerging research suggests that inflammatory processes are implicated in epileptogenesis. Apigenin (AP), an antioxidant and anti-inflammatory flavonoid, demonstrates neuroprotective effects in brain disorders. Nevertheless, its significance in status epilepticus remains unstudied. Therefore, we investigated whether AP alleviates pilocarpine (PLO)-induced SE neuropathology. We propose that AP may reduce SE by atte

In this study, we explored the neuroprotective properties of a novel Tat-CRYM recombinant protein, designed with a Tat domain to enhance blood-brain barrier permeability, within a transient cerebral ischemia using Mongolian gerbils. Our focus was on Ketimine reductase mu-crystallin (CRYM), a protein with widespread distribution in the brain, including areas like the cerebral cortex, corticospinal tract, and basal ganglia, and its diminished expression in neurodegenerative diseases such as Huntington's and Alzheimer's.We assessed the intracellular uptake of Tat-CRYM protein by NSC34 cells, reve