Caprylic acid promotes synaptic plasticity potentially through enhancing Leptin/NM2B signaling

Abstract

Synaptic plasticity is crucial for memory formation and can be impaired in metabolic diseases. Insulin and insulin-like growth factors play important roles in synaptic plasticity, while leptin protects neurons and stimulates growth. Diets can affect synaptic plasticity through macronutrients and appetite signals, highlighting the need for deeper research and interventions for synaptic dysfunction in metabolic diseases. Recent research suggests that while saturated fatty acids (SFA) have been viewed as unhealthy for cognition, they may benefit memory and learning in certain conditions. High levels of SFA were found to improve recollection in young people. In specific, low-level intake of caprylic acid may reduce neuroinflammation and protect against neural degeneration. This anti-neuroinflammatory effect of caprylic acid may be mediated through the JAK2/STAT3 signaling pathway, which is a crucial part in the modulation of synaptic plasticity by leptin/NM2B signaling. Therefore, this work hypothesized that caprylic acid can enhance leptin/NM2B signaling pathway by increasing the expression of JAK2/STAT3 signaling pathway. In this proposal, a 12-week mice experiment is proposed with fEPSP measurements, immunoblotting, and immunoprecipitation to test the long-term potentiation (LTP) and the expression level as well as regions of the signaling molecules. This work may offer another perspective on the complex role of SFA in brain health.