Nervonic acid is a long chain unsaturated fatty acid that is enriched in sphingomyelin. It consists of choline, sphingosine, phosphoric acid, and fatty acid. Nervonic acid may enhance the brain functions and prevent demyelination (Chemical Land21). Research shows that there is negative relationship between nervonic acid and obesity-related risk factors. Demyelination in adrenoleukodystrophy (ALD) is associated with an accumulation of very long chain saturated fatty acids stemming from a genetic defect in the peroxisomal beta oxidation system responsible for the chain shortening of these fatty acids. Sphingolipids from post mortem ALD brain have decreased levels of nervonic acid, 24:1(n-9), and increased levels of stearic acid, 18:0. Nervonic acid (C24:1), a component of membrane sphingolipids and phosphatidylethanolamines, may be a useful predictor of chronic kidney disease mortality and diabetes. Nervonic acid oils are being studied for pharmaceutical, nutraceutical and industrial applications. Nervonic acid is a major component of Lunaria oil. There is increasing evidence that dietary supplementation with nervonic acid is healthy for babies and infants during the early stage of brain development. Nervonic acid has been reported to reduce the shaking associated with Parkinson’s disease and the numbness caused by multiple sclerosis. It also has potential for treating schizophrenia and reducing early Alzheimer’s symptoms.

Domoic acid is one of the best-known marine toxins, causative of important neurotoxic alterations. In the year 1987, domoic acid was responsible for four deaths and the illness of more than 100 people after consuming blue mussels (Mytilus edulis) harvested in the Cardigan Bay of Prince Edward Island, Canada. The symptomatology comprised three kinds of signs: gastrointestinal (nausea, vomiting,), cardiovascular (unstable blood pressure and arrhythmias), and neurological signs (disorientation, confusion, hallucinations, coma, and memory impairment). After this event was discovered the domoic acid epileptic. Nearly a year after the amnesic shellfish poisoning event, an 84 years old male survivor re-experienced severe seizures and was diagnosed with temporal lobe epilepsy caused by domoic acid intoxication. This toxin has a high affinity for the glutamate receptors (GluRs) subtypes: alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) and KA receptors. The binding of domoic acid to receptors provokes an increase of calcium (Ca2+) levels, causing the release of Glu to the extracellular space, and the activation of N-methyl-d-aspartate (NMDA) receptors. The histological consequences of these cellular alterations comprise astrocytosis, cytoskeletal disarrangement and, finally, cell death.

N,N-dimethylglycine or dimethylglycine (DMG) is an amino acid derivative found in the cells of all plants and animals and can be obtained in the diet in small amounts from grains and meat. The human body produces DMG when metabolizing choline into glycine. DMG has been found acting at glycine binding site of the N-methyl-d-aspartate receptor (NMDAR). DMG has had wide acceptance as a nonfuel nutrient; presumably it enhances oxygen utilization by tissue and complexes free radicals. There were published studies, which have shown little to no difference between DMG treatment and placebo in autism spectrum disorders and the same no effect was observed in case of investigated DMG for epilepsy. This compound was also suggested to use to improve the athletic performance enhancer, but this usage was ineffective as well.