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Li, T., Sun, A., Dong, W., Peng, Y., Li, S., Li, Y., ... & Wang, X. (2025). Journal of Dairy Science.
Nervonic acid (NA), a monounsaturated very long-chain fatty acid (C24:1, n-9), is recognized for its role in myelin biosynthesis and neuroprotection. In a recent study, NA-containing modified milk (NA-MM) was developed and evaluated for its ability to mitigate scopolamine-induced memory deficits in mice.
NA was produced via fermentation of MOSO substrate with Rhodotorula toruloides, yielding a yeast extract with 2.39 mg/mL NA. This extract was microencapsulated using whey protein and maltodextrin through high-speed dispersion, high-pressure homogenization, and spray drying, resulting in microcapsules containing 0.513 g/g NA. The final NA-MM formulation comprised 80% milk, 10% NA microcapsules, and functional additives, prepared under controlled heating, emulsification, and sterilization conditions.
Behavioral assays, including Y-maze, novel object recognition, and open field tests, demonstrated significant improvement in cognitive performance after 30 days of NA-MM administration. Biochemical analysis revealed reduced hippocampal oxidative stress through enhanced superoxide dismutase and glutathione peroxidase activity, alongside decreased malondialdehyde levels. NA-MM also modulated the cholinergic system by increasing acetylcholine and reducing acetylcholinesterase activity.
Systemically, NA-MM improved lipid metabolism-lowering serum triglycerides, cholesterol, and LDL while raising HDL-thereby enhancing cerebral microcirculation. Additionally, gut microbiota profiling indicated increased diversity and beneficial compositional shifts.
These findings underscore NA's potential as a functional food ingredient for neuroprotection, with NA-MM offering a novel delivery system for cognitive health enhancement through dietary intervention.
Ma, Shijia, et al. Biochemical and biophysical research communications 733 (2024): 150696.
Nervonic acid (NA), a monounsaturated very long-chain fatty acid critical for myelin biosynthesis, has demonstrated neuroprotective potential in demyelination-related disorders. Recent experimental evidence reveals its promising application in major depressive disorder (MDD), a condition in which myelin integrity disruption in key brain regions contributes to pathogenesis.
In a chronic restraint stress (CRS) murine model, daily intraperitoneal administration of NA (70 mg/kg) for 14 days markedly improved depression-like behaviors, including behavioral despair and anhedonia. Black-Gold II staining indicated that CRS induced significant demyelination in the medial prefrontal cortex (mPFC) and hippocampus, but not the thalamus. Notably, NA selectively reversed demyelination in the mPFC, a region critically implicated in mood regulation, without affecting other regions.
Myelin basic protein (MBP), essential for maintaining myelin sheath integrity, was significantly reduced in the mPFC of CRS mice. Both immunofluorescence and western blot analysis confirmed that NA treatment restored MBP levels to near-control conditions. Mechanistically, NA attenuated CRS-induced neuroinflammation by downregulating pro-inflammatory cytokines and preserving brain-derived neurotrophic factor (BDNF) expression. Additionally, NA normalized aberrant axonal spine morphology in the mPFC, suggesting a structural basis for functional recovery.
These findings highlight NA's potential as a therapeutic agent targeting myelin repair in MDD. By specifically mitigating mPFC demyelination, NA offers a mechanistically distinct antidepressant strategy, bridging lipid biochemistry with psychiatric neuroprotection and opening avenues for myelin-centric interventions in mood disorders.
Zhang, Fengrong, et al. HLife 2.11 (2024): 592-606.
Nervonic acid (NA), a long-chain monounsaturated fatty acid predominantly found in mammalian nervous tissue, has emerged as a promising therapeutic candidate for neurological disorders. In a recent ischemia/reperfusion rat model, NA administration demonstrated marked neuroprotective effects, significantly reducing infarct volume, neuronal swelling, and cell death following middle cerebral artery occlusion. Cerebral blood flow improvement was evident by day five post-injury.
Molecular analysis revealed NA-induced upregulation of brain-derived neurotrophic factor (BDNF) and myelin basic protein (MBP) genes, supporting neuronal repair and remyelination. Behavioral evaluations via sucrose preference, open-field, and forced swim tests confirmed the compound's efficacy in mitigating poststroke depressive-like behaviors.
Mechanistically, NA exerted both direct neurophysiological effects and indirect modulation of gut microbiota. Treatment restored bacterial diversity and increased the relative abundance of Blautia and Sutterella-genera linked to phenylalanine metabolism. Metabolomic profiling of plasma and brain tissue indicated reduced phenylalanine-derived amino acids, alleviating their inhibitory effect on glutamine metabolism and facilitating neuronal recovery and neurotransmission.
These findings position nervonic acid as a dual-action therapeutic, promoting neuroregeneration while modulating systemic metabolic pathways. Its ability to target both central and peripheral mechanisms underscores its potential for integrated management of stroke recovery and associated mood disorders.
