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Xinghua Ren

2 papers in the library · 11 citations · publishing 2024

Papers

Ketamine administration causes cognitive impairment by destroying the circulation function of the glymphatic system.

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie June 1, 2024 Xue Wu, Gehua Wen, Lei Yan et al. 11 citations

Ketamine, a drug originally used as an anesthetic and now commonly abused in China, can cause cognitive impairment by disrupting the brain's glymphatic system, which normally clears metabolic waste. In a mouse model of short-term ketamine administration, the drug increased expression of the 5-HT2c receptor in hippocampal astrocytes, leading to accumulation of the transcription factor ΔFosb. ΔFosb then bound to a specific DNA sequence in the regulatory region of the Aqp4 gene, suppressing Aqp4 expression and impairing glymphatic circulation, which resulted in cognitive deficits. This mechanism does not involve the Pten/Akt pathway and reveals a non-neuronal basis for ketamine-induced cognitive harm, informing clinical safety and withdrawal effectiveness.

DOI: 10.1016/j.biopha.2024.116739 (opens in new tab) Full text (opens in new tab) Ketamine 5-ht2c Aqp4 Cognitive impairment +7

Ketamine induces delirium-like behavior and interferes with endosomal tau trafficking

Xinghua Ren, Siyi Zhang, Yongyan Yang et al.

Ketamine, an anesthetic and antidepressant, can induce delirium-like behavior in mice and increase tau protein in their blood. In cultured cells, ketamine disrupts endosome function—key organelles for tau release—by increasing endosomal markers Rab5 and Rab7, inhibiting endosome maturation, and boosting tau accumulation in endosomes and the culture medium. These findings suggest ketamine may interfere with tau trafficking, potentially contributing to neurotoxicity and delirium, warranting further research into anesthetic safety.

DOI: 10.21203/rs.3.rs-1362130/v1 (opens in new tab)