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• W4386135813 abstract "Abstract Epilepsy is a neurological disorder characterized by recurrent seizures resulting from abnormal electrical activity in the brain. During acute neurological diseases, defective lysosomal functioning can lead to the accumulation of toxic substrates in cellular organelles, causing impaired autophagy. Phosphodiesterase-4 (PDE4) is an enzyme that regulates cyclic adenosine monophosphate (cAMP) levels by breaking it down into adenosine monophosphate (AMP). PDE4 also influences lysosomal function and the release of pro-inflammatory cytokines. In pathological conditions, increased PDE4 activity leads to reduced cAMP levels. In a recent study, researchers investigated the potential of Amlexanox, an anti-inflammatory drug and non-selective PDE4 inhibitor, as a protective agent against lysosomal dysfunction and neuroinflammation, with the goal of preventing neuronal death. The study utilized a pilocarpine-induced epilepsy animal model, where Amlexanox was administered at a dosage of 100 mg/kg intraperitoneally daily following seizures. Brain tissue samples were collected at various time points for analysis. The results of the study were significant, revealing that Amlexanox effectively improved lysosomal function, reduced inflammation, attenuated hippocampal neuronal death, and ameliorated cognitive impairment in the animal model. These promising findings suggest that Amlexanox holds potential as a therapeutic agent for the treatment of epileptic brain disorders, particularly due to its neuroprotective effects related to lysosomal dysfunction and neuroinflammation. Further research and clinical trials are warranted to fully explore the therapeutic benefits of Amlexanox in managing epilepsy and related neurological conditions." @default.
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• W4386135813 date "2023-08-24" @default.
• W4386135813 modified "2023-10-17" @default.
• W4386135813 title "A phosphodiesterase 4 (PDE4) inhibitor, amlexanox, reduces neuroinflammation and neuronal death after pilocarpine-induced seizure" @default.
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• W4386135813 doi "https://doi.org/10.21203/rs.3.rs-3268191/v1" @default.
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