VPA targets Mid1 improves hippocampal neurons retrograde axonal transport function disruption in lithium manganate-induced mice learning and memory dysfunction through the ubiquitin–proteasome pathway

Key Points

• The aim is to explore how VPA treatment can improve disrupted retrograde axonal transport in a mouse model of memory dysfunction.
• Induced learning and memory deficits in mice using lithium manganate exposure.
• Administered VPA to evaluate its effects on hippocampal neurons.
• Analyzed changes in ubiquitin-proteasome pathway and axonal transport.
• VPA treatment improved retrograde axonal transport in hippocampal neurons.
• Reduced neuronal injury correlated with enhanced memory function.
• Alterations in the ubiquitin-proteasome pathway contributed to observed effects.