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Life sciences · Journal article
Nutritional Neuroscience · October 8, 2026
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OBJECTIVE: Obesity-mediated cognitive impairment is increasingly known as high levels of saturated fatty acid intake and accumulation in the body. Saturated fatty acids, mainly palmitic acid (PA) is recognized as the leading cause of oxidative stress, metabolic dysregulation, and neuronal degeneration in obesity. METHOD: The current study investigated the neuroprotective effects of syringic acid (SA) against PA-induced neuronal injury in N2a neuronal cells, as well as in a high-saturated-fat-induced obese mouse (DIO) model. RESULT: The study demonstrated that PA significantly reduced cell viability, increased lactate dehydrogenase release, nitric oxide generation, lipid peroxidation, reactive oxygen species, and intracellular lipid accumulation, following a decrease in the levels of glutathione, superoxide dismutase, catalase, and downregulation of synaptic plasticity-related molecules, including NR2a, PSD-95, and GluR1, in N2a neuronal cells. In high-saturated-fat-diet-induced mice, metabolic data showed a significant increase in body weight, basal metabolic rate, fasting blood glucose, and triglyceride levels, along with downregulation of synaptic plasticity and diminished behavioural activity. In contrast, SA treatment was able to restore cell viability and redox homeostasis by decreasing lipid peroxidation, LDH release, and NO generation, along with increasing GSH, SOD, and Catalase activity. It decreased ROS and lipid overload while maintaining neuronal morphology and synaptic molecule expression. The PPAR-α plays the main regulatory role in synaptic plasticity. DISCUSSION: study revealed that SA markedly decreased body weight, BMI, metabolic alteration, and upregulated synaptic plasticity. It improved spatial learning and memory in high-saturated-fat-induced mice. Together, these results illustrate that SA protects from neuronal dysfunction linked to obesity by means of antioxidant, anti-lipotoxic, and synaptic-plasticity-preserving mechanisms. Thus, SA might be a potential therapeutic target for cognitive impairment related to obesity and neurodegenerative disorders caused by overconsumption of saturated fats.