Nervonic Acid, scientifically known as cis-15-tetracosenoic acid, is a very-long-chain monounsaturated fatty acid with unique double bond placement within its carbon chain, which gives it unique physical and chemical properties. It was first discovered in mammalian neural tissue, hence its name. Over the course of biological evolution, neuraminic acid has gradually evolved a key role within neural tissue, becoming an essential core component of sphingolipids. Sphingolipids play a crucial role in the construction of nerve cell membranes, and neuraminic acid, as a key component, is directly involved in the formation of the myelin sheath. The myelin sheath acts like insulation for electrical wiring, ensuring efficient and accurate transmission of nerve signals along the nerve fiber, avoiding interference and attenuation. Furthermore, neuraminic acid plays a key role in maintaining the stability of nerve cell membranes, ensuring that nerve cells can function normally in this complex internal environment.
One of the most remarkable properties of neuraminic acid is its ability to cross the blood-brain barrier. The blood-brain barrier (BBB) is the brain’s natural defense line, composed of tightly connected vascular endothelial cells, the basement membrane, and the end feet of astrocytes. It blocks most harmful substances and large molecules from entering the brain. Nervonic Acid, due to its unique molecular structure, can successfully cross this barrier and directly reach the central nervous system, enabling it to exert its neuroprotective and repairing effects.
When the nervous system is damaged, neuratomic acid activates pathways related to neuronal repair through a series of complex and sophisticated molecular mechanisms. Nervonic Acid plays a significant role in regulating the expression of neurotrophic factors. Neurotrophic factors are a class of proteins that play a key role in the survival, growth, differentiation, and maintenance of neurons. Nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) are the most important members. Nervonic Acid promotes the expression of these neurotrophic factors, acting as a nutrient supply to injured neurons. After neuronal damage, NGF and BDNF bind to corresponding receptors on the neuronal surface, activating a series of intracellular signaling pathways and promoting axonal regeneration. Axons are crucial structures for neuronal signal transmission, and their regeneration is crucial for restoring neurological function. These neurotrophic factors also promote synaptic remodeling, reestablishing effective connections between neurons and thus restoring nerve signal transmission.
Oligodendrocyte precursor cells play a crucial role in the repair of myelin sheaths, and neuraminic acid can induce them to differentiate into mature oligodendrocytes. Oligodendrocytes produce myelin sheaths, which wrap around nerve fibers and repair the myelin sheath. In a demyelination model, researchers found that neuraminic acid treatment significantly increased the rate of myelin repair, by 40% compared to the untreated group. This result demonstrates that neuraminic acid effectively promotes myelin repair, thereby accelerating the conduction of nerve signals and improving the recovery of neurological function.
Nervonic acid’s Multidimensional Protective Effects on the Nervous System
Nervonic acid’s Multidimensional Protective Effects on the Nervous SystemNerve Damage Repair and Degenerative Disease Intervention
1. Supporting the Regeneration of Damaged Nerve Fibers
Serious illnesses such as stroke and spinal cord injury can severely impact the human nervous system, often leading to nerve fiber rupture and, in turn, a series of severe functional impairments. Take stroke, for example, an acute cerebrovascular disease characterized by high morbidity, disability, and mortality. Once it occurs, it disrupts local brain tissue circulation, causing oxygen and blood deprivation to nerve cells, ultimately leading to nerve fiber damage and rupture. Patients may experience symptoms such as limb paralysis, speech impairment, and cognitive decline, severely impacting their quality of life. Spinal cord injury, on the other hand, typically results from trauma, disease, or other factors that damage the spinal cord structure and function, hindering the transmission of neural signals. Patients may suffer from conditions such as paraplegia and incontinence.
Neuronic acid demonstrates potent repair capabilities in addressing these nerve fiber damage issues. Its primary mechanism of action is through activation of the PI3K/Akt signaling pathway. The PI3K/Akt signaling pathway plays a key regulatory role in cell survival, proliferation, and differentiation. When neuratomic acid activates this signaling pathway, it inhibits neuronal apoptosis. Neuronal apoptosis is a common phenomenon following nerve injury, and excessive apoptosis can lead to further deterioration of neurological function. By inhibiting this process, neuratomic acid provides a stable environment for nerve fiber repair. Furthermore, neuratomic acid promotes the proliferation of Schwann cells. Schwann cells are important glial cells in the peripheral nervous system. They form myelin sheaths that surround nerve fibers and play a crucial role in nerve fiber regeneration and repair. Neuroatomic acid promotes Schwann cell proliferation, acting as a “building block” for nerve fiber regeneration and providing solid structural support for axonal regeneration.
Extensive preclinical studies have provided strong evidence for this efficacy of neuratomic acid. In one study in a nerve injury model, researchers found that treatment with neuratomic acid increased the length of regenerated axons by 35% compared to the control group. This significant difference strongly demonstrates that neuratomic acid can effectively promote the regeneration of damaged nerve fibers, offering hope for the restoration of neurological function.
2. Potential Intervention Targets for Alzheimer’s Disease
Alzheimer’s disease is the most common neurodegenerative disease, primarily affecting the elderly. Its incidence increases significantly with age. Globally, approximately 50 million people with Alzheimer’s disease are diagnosed, and this number is expected to triple by 2050. Key pathological hallmarks of the disease include the accumulation of Aβ amyloid protein and imbalanced tau protein phosphorylation. Aβ amyloid is a normal protein, but in Alzheimer’s patients, it abnormally aggregates to form amyloid plaques. These plaques accumulate in the brain, disrupting connections between neurons and impairing neural signaling. Tau, a protein that binds to microtubules, plays a crucial role in maintaining the normal structure and function of neurons. In Alzheimer’s patients, tau becomes hyperphosphorylated, reducing its ability to bind to microtubules. This leads to microtubule disassembly, ultimately forming neurofibrillary tangles, further impairing neuronal function. Nervonic acids have the potential to intervene in Alzheimer’s disease through multiple mechanisms of action. Firstly, they can reduce Aβ amyloid deposition, primarily by inhibiting β-secretase activity. β-secretase is a key enzyme in the production of Aβ amyloid. Inhibiting its activity can reduce Aβ amyloid production at its source, thereby reducing its accumulation in the brain and alleviating neuronal damage. Secondly, Nervonic acids can improve the imbalance in tau phosphorylation. They regulate the activity of related kinases and phosphatases, restoring tau phosphorylation levels to normal, preventing the formation of neurofibrillary tangles and protecting neuronal structure and function.
In a clinical study, neuratoic acid supplementation was administered to people with mild cognitive impairment. Results showed that after six months of neuratoic acid supplementation, memory scores improved by 12% compared to the control group. Memory scores are a key indicator of cognitive function, and this improvement suggests that neuratoic acid can effectively improve patients’ memory and slow cognitive decline. At the same time, cerebrospinal fluid (CSF) p-tau protein levels decreased by 18%. CSF p-tau protein levels are an important biomarker reflecting the pathological progression of Alzheimer’s disease. This decrease suggests that neuraminic acid can, to a certain extent, inhibit the hyperphosphorylation of tau protein, thereby intervening in the pathological progression of Alzheimer’s disease. These research results provide important clinical evidence for the use of neuraminic acid in the prevention and treatment of Alzheimer’s disease.
Brain Development and Cognitive Optimization
1. Essential Nutrients for Infant and Child Neurological Development
During infancy and childhood, the brain undergoes a critical period of rapid development, and the development of the nervous system plays a decisive role in a child’s future development. From birth to two years of age, the brain develops most rapidly, and during this period, the brain requires a large amount of nutrients to support its complex developmental processes. As a naturally occurring component in breast milk, neuraminic acid plays an irreplaceable role during this period.
The impact of neuraminic acid on brain development is primarily reflected in the myelination process. Myelination refers to the process by which nerve fibers are encased in myelin. The myelin sheath acts as an insulating coat, significantly increasing the speed and accuracy of nerve signal transmission. Nervonic acid accumulates most rapidly in the brain during the first two years of life, coinciding with the rapid development of myelination. A deficiency of Nervonic acid during this critical period can have serious consequences for the development of the nervous system. Studies have shown that a deficiency of Nervonic acid can lead to a 20% decrease in synaptic density. Synapses are key structures for transmitting information between neurons. A decrease in synaptic density means fewer connections between neurons and reduced efficiency of information transmission, which directly impacts a child’s cognitive development.
Conversely, timely supplementation with Nervonic acid can positively promote cognitive development in infants and young children. A related study, which supplemented infants with Nervonic acid, found that these infants had increased dendritic branching. Neuronal dendrites are crucial for receiving information, and increased branching means neurons can receive more information, thereby promoting the development of the brain’s neural network. Furthermore, cognitive development scores in these infants, as assessed by the MDI scale, improved by 15%. The MDI scale is a widely used tool for assessing infants’ and young children’s cognitive development. The improvement in scores clearly demonstrates the important role of neuratomic acid in promoting brain development and enhancing cognitive function in infants and young children. Therefore, neuratomic acid is an essential nutrient for the development of infants’ and young children’s nervous systems.
2. Maintaining and Improving Adult Brain Function
Although brain development is largely complete, adults still need to maintain good brain function to cope with the challenges of work, study, and life. With aging, increased stress, and the influence of unhealthy lifestyle habits, brain function gradually shows signs of decline, such as decreased memory, difficulty concentrating, and slower reaction speed.
Neurosolic acid plays a crucial role in maintaining and improving adult brain function. Its mechanism of action is primarily through enhancing glucose metabolism in the prefrontal cortex and improving synaptic plasticity in the hippocampus. The prefrontal cortex is a brain region closely associated with higher-level cognitive functions, involved in numerous important cognitive processes such as attention, decision-making, and working memory. Neurosolic acid can enhance glucose metabolism in the prefrontal cortex, providing it with more energy and enabling it to function more efficiently. The hippocampus is a brain region closely associated with learning and memory. Synaptic plasticity, the ability of synapses to change in response to changes in environment and experience, is crucial for the formation of learning and memory. Nervonic acids can improve synaptic plasticity in the hippocampus, strengthening the connections between neurons, thereby increasing memory encoding efficiency and information processing speed.
A study of healthy adults supplemented with Nervonic acids found that these individuals significantly improved their performance on working memory tasks. Working memory, a memory system that temporarily stores and processes information, plays a crucial role in daily life and work. The results showed that after supplementing with Nervonic acids, reaction times on working memory tasks decreased by 10%, meaning participants were able to process and respond to information more quickly. Error rates also decreased by 15%, indicating increased accuracy and fewer errors. These results strongly suggest that Nervonic acids can effectively maintain and enhance brain function in adults, helping them better cope with the challenges of life and work.
Emotion Regulation and Neurotransmitter Balance
1. The Auxiliary Regulatory Role of Depression
Depression is a common mental disorder that severely impacts patients’ quality of life and physical and mental health. According to the World Health Organization, approximately 350 million people suffer from depression worldwide, and the incidence rate is increasing annually. Key symptoms of depression include low mood, loss of interest, self-blame, sleep disturbances, and loss of appetite. These symptoms can cause significant distress to patients and even lead to serious consequences such as suicide.
The pathogenesis of depression is complex, with neurotransmitter imbalance and abnormal expression of brain-derived neurotrophic factor (BDNF) as key factors. Neurotransmitters are chemical substances that transmit information between neurons. Monoamines, such as serotonin, dopamine, and norepinephrine, play a key role in mood regulation. In patients with depression, levels of these neurotransmitters are often reduced, leading to an imbalance in the concentration of monoamines in the synaptic cleft, thus triggering mood disorders. BDNF is a protein that plays a crucial role in neuronal survival, growth, and differentiation. It promotes interneuronal connectivity and synaptic plasticity, and also plays a crucial role in mood regulation. In patients with depression, BDNF expression is often decreased, further exacerbating neuronal damage and dysfunction.
Neuronic acid plays a positive role in assisting the regulation of depression. It upregulates the serotonin transporter (SERT), increasing serotonin reuptake, thereby increasing serotonin concentrations in the synaptic cleft and resolving neurotransmitter imbalances. Furthermore, neuric acid increases the expression of brain-derived neurotrophic factor (BDNF), promoting neuronal growth and repair, strengthening interneuronal connectivity, and improving brain neuroplasticity, thereby alleviating depressive-like behaviors.
In animal studies, researchers administered neuric acid to animal models exhibiting depressive-like behaviors. The results showed that neuric acid reduced forced swimming immobility time by 25%. The forced swim test is a commonly used experimental method for assessing depressive-like behaviors in animals. A reduction in immobility time indicates that the animals’ depressive-like behaviors have been alleviated, and they are more proactive in the face of stress. Furthermore, sugar water preference increased by 30%. Sugar water preference measures an animal’s interest in rewards and experience of pleasure. Increased sugar water preference indicates an improved emotional state and enhanced sensitivity to pleasurable things. These experimental results strongly demonstrate the effectiveness of neuraminic acid in assisting the regulation of depression and provide new insights and approaches for its treatment.
2. Anxiety and Improved Sleep Quality
Anxiety and sleep problems are common health concerns for modern people. They not only affect daily life and work but also cause long-term damage to physical health. Anxiety is a psychological state characterized by emotions such as tension, uneasiness, and fear. Chronic anxiety can lead to a range of physical symptoms, such as palpitations, sweating, hand tremors, and difficulty breathing. Poor sleep quality manifests as difficulty falling asleep, shallow sleep, frequent dreams, and frequent awakenings. Chronic sleep deprivation can affect the body’s immune system, metabolic function, and cognitive function. Nervonic acids have a unique mechanism of action in improving anxiety and sleep quality. They work by modulating the activity of GABAA receptor chloride channels. GABA, a key inhibitory neurotransmitter, binds to GABAA receptors, opening chloride channels and allowing chloride ions to flow in, thereby inhibiting neuronal excitability. In patients with anxiety and sleep disorders, GABA levels in the brain are often reduced, leading to neuronal hyperexcitability and causing anxiety and sleep problems. Nervonic acids modulate GABAA receptor chloride channel activity, enhancing GABA’s inhibitory effects and suppressing overactivation of the amygdala. The amygdala, a brain region closely involved in emotion regulation, plays a key role in the development of anxiety. By inhibiting overactivation of the amygdala, Nervonic acid can reduce abnormal firing in anxiety-related brain regions (such as the dorsolateral prefrontal cortex), thereby alleviating anxiety.
In clinical observations, Nervonic acid intervention in individuals with anxiety and sleep problems has shown a 22% improvement in the Pittsburgh Sleep Quality Index (PSQI). The PSQI is a widely used scale for assessing sleep quality. A decrease in its score indicates a significant improvement in sleep quality. These individuals experienced significant improvements in sleep onset time, sleep depth, and sleep efficiency, waking up feeling more rested and less anxious. This demonstrates the significant effectiveness of neuraminic acid in improving anxiety and sleep quality, providing a safe and effective approach to addressing these health concerns faced by modern people.
Neurovascular Unit Protection and Metabolic Regulation
1. Structural Maintenance of the Blood-Brain Barrier
The blood-brain barrier (BBB) is a critical line of defense for the brain. Composed of structures such as cerebral microvascular endothelial cells, the basement membrane, and the end feet of astrocytes, it effectively blocks harmful substances and large molecules from entering the brain, maintaining a stable internal environment and protecting neurons from external factors. However, in certain pathological conditions, such as cerebral ischemia-reperfusion injury and inflammation, the permeability of the BBB increases, allowing harmful substances to enter the brain, leading to a series of problems such as cerebral edema and neuronal cell damage.
Cerebral ischemia-reperfusion injury is a common cerebrovascular disease, commonly occurring in conditions such as stroke and cardiac arrest. When blood flow to the brain is suddenly interrupted and then restored, a complex series of pathophysiological processes are triggered, leading to damage to the blood-brain barrier. During this process, the tight junctions between brain microvascular endothelial cells are disrupted, increasing the permeability of the blood-brain barrier. Plasma proteins, water, and other substances can leak into the brain tissue, causing cerebral edema, further compressing neural tissue and exacerbating brain damage.
Neuronic acid plays a key role in maintaining the structure and function of the blood-brain barrier. It achieves this by enhancing the expression of tight junction proteins (ZO-1 and claudin-5) in brain microvascular endothelial cells. ZO-1 and claudin-5 are key proteins that form the tight junctions of the blood-brain barrier. They tightly connect adjacent brain microvascular endothelial cells, preventing the blood from leaking out.
Nervonic acids can promote the expression of these tight junction proteins, strengthening intercellular connections and thus reducing the permeability of the blood-brain barrier.
In a cerebral ischemia-reperfusion model, researchers found that treatment with Nervonic acid reduced Evans blue extravasation by 30%. Evans blue is a commonly used dye for measuring blood-brain barrier permeability. Reduced extravasation indicates reduced permeability of the blood-brain barrier, reducing the amount of large molecules in plasma entering the brain tissue, thereby alleviating brain edema damage. This experimental result fully demonstrates the protective effect of Nervonic acids on the blood-brain barrier and provides an important theoretical basis for the prevention and treatment of cerebrovascular disease.
2. Coordinated Regulation of Lipids and Energy Metabolism
Dyslipidemia and energy metabolism disorders are common metabolic problems that not only increase the risk of cardiovascular disease but also have adverse effects on the nervous system. High blood lipids increase blood viscosity and slow blood flow, impairing blood supply to the brain, which in turn affects the nutrient supply to nerve cells and the excretion of metabolic waste. At the same time, disrupted energy metabolism can lead to insufficient energy supply to neurons, impairing their normal function and accelerating their aging and death.
Neuronic acid exhibits unique benefits in synergistically regulating lipid and energy metabolism. It promotes fatty acid β-oxidation by activating the PPARγ receptor. The PPARγ receptor is a nuclear receptor that plays a key role in regulating lipid metabolism and energy balance. When activated by neuric acid, it promotes the entry of fatty acids into mitochondria for β-oxidation, breaking them down into carbon dioxide and water while generating energy. This process not only lowers serum low-density lipoprotein cholesterol (LDL-C) levels, reduces cholesterol deposition in blood vessels, and reduces the risk of cardiovascular disease, but also provides more energy for neurons.
Studies have shown that neuric acid can reduce serum LDL-C levels by 15%, demonstrating its significant lipid-regulating effects. Furthermore, neuric acid can increase the activity of mitochondrial complex IV in the brain. Mitochondria are the “energy factories” of cells, and mitochondrial complex IV is a key enzyme in the mitochondrial respiratory chain. It participates in the final step of cellular respiration, converting oxygen to water and generating ATP. Nervonic acid increases the activity of mitochondrial complex IV, enhancing mitochondrial energy metabolism. This provides sufficient energy for nerve cells, improves neuronal energy supply, and slows nerve cell aging. By synergistically regulating blood lipids and energy metabolism, Nervonic acid provides comprehensive protection for the health of the nervous system.
Targeted Application Scenarios for Special Populations
Scientific Additions to Infant Formula
Infancy is a golden period for brain development. As a crucial nutrient for brain development, the scientific addition of neuraminic acid to infant formula has far-reaching significance. The study “Neuraminic Acid and Brain Health” shows that many European and American countries have approved neuraminic acid as a nutritional fortifier for infant formula. This initiative is well-supported by scientific evidence. Adding neuraminic acid to premature infant formula significantly promotes their development. Research data shows that the addition of neuraminic acid can improve the developmental quotient (DQ) by 9% at 18 months of age. The DQ is a key indicator of an infant’s mental development, encompassing gross motor skills, fine motor skills, language, adaptability, and social behavior. This 9% improvement indicates improved development in all of these areas, laying a solid foundation for future growth.
In terms of specific abilities, improvements in visual tracking and language comprehension are particularly significant. Visual tracking is a crucial foundation for infants’ understanding of the world, enabling them to better observe their surroundings and acquire information. Language comprehension is a key component of language development, and good language comprehension helps infants and young children communicate effectively with others. Infants and young children supplemented with neuraminic acid were able to follow the movement of objects more accurately and quickly in visual tracking tasks, and they also understood verbal commands more acutely and responded more quickly. This suggests that neuraminic acid can effectively promote the development of the brain’s nervous system and enhance cognitive abilities.
Preventive Supplementation for the Elderly
With aging, the nervous system function of the elderly gradually declines, and the risk of cognitive impairment increases accordingly. Preventive supplementation with neuraminic acid is particularly important for those over 65. Studies have found that daily supplementation with 200-300mg of neuraminic acid can reduce the conversion rate to mild cognitive impairment by 28%. Mild cognitive impairment is a transitional state between normal aging and dementia, and without intervention, it can easily progress to dementia. Neuroaminic acid supplementation can effectively reduce this conversion rate and slow the progression of cognitive decline.
To enhance the neuroprotective effects, neuraminic acid is recommended for use in conjunction with omega-3 and B vitamins. Omega-3 fatty acids, such as DHA and EPA, also play a crucial role in brain health. They regulate cell membrane fluidity, improve the transmission of nerve signals, and possess anti-inflammatory and antioxidant properties, reducing inflammation and oxidative stress in the brain and protecting nerve cells from damage. B vitamins, including vitamins B1, B6, and B12, play a key role in the metabolism of the nervous system. They participate in the synthesis of neurotransmitters and maintain the integrity of the myelin sheath, making them crucial for normal neurological function. Nervonic acids work synergistically with omega-3 and B vitamins to protect and repair the nervous system in multiple ways, providing comprehensive support for brain health in the elderly, helping them maintain good cognitive function and improve their quality of life.
Safe Use and Scientific Supplementation Strategies
Natural Sources and Formulation Development
Natural sources of neuraminic acid primarily include Acer truncatum seed oil and shark brain extract. Acer truncatum seed oil, a unique plant oil with a neuraminic acid content of 6% to 8%, is currently a key botanical resource for neuraminic acid. Acer truncatum is a tree species endemic to China, and its kernels are rich in oil. Advanced pressing and extraction techniques allow the extraction of neuraminic acid-rich Acer truncatum seed oil from Acer truncatum seeds. This source is not only sustainable but also boasts a relatively high neuraminic acid content compared to other plant oils, providing strong support for the industrial production and application of neuraminic acid. Shark brain extract is also an important source of neuraminic acid, as it is rich in neuraminic acid. However, due to the need to protect shark resources and the high cost of extraction, shark brain extract currently accounts for a relatively small proportion of neuraminic acid supply.
In formulation development, the application of modern technologies has enabled the efficient utilization of neuraminic acid. Nanoliposome delivery technology is a leading approach, encapsulating neuraminic acid within nano-sized liposomes. Liposomes are tiny vesicles composed of a phospholipid bilayer, offering excellent biocompatibility and targeting. Encapsulating neuraminic acid within liposomes effectively increases its intestinal absorption rate, reaching three times that of traditional formulations. The small particle size of nanoliposomes allows them to more easily penetrate the intestinal mucosa and enter the bloodstream, thereby enhancing the bioavailability of neuraminic acid. Furthermore, nanoliposomes protect neuraminic acid from degradation by gastrointestinal enzymes, ensuring its maximum efficacy within the body. Studies have shown that neuraminic acid bioavailability is optimal when taken on an empty stomach, providing scientific guidance for the clinical use and daily supplementation of neuraminic acid.
Dosage and Contraindications
1. Recommended Supplementation Dosage
For adults, the dosage of neuraminic acid supplementation should be adjusted appropriately based on the intended use. For the prevention of neurological diseases, the recommended dosage is 100-200 mg/day. This dosage range effectively maintains normal nervous system function, enhances nerve cell vitality, and prevents the onset of neurodegenerative diseases. For example, for those experiencing high work pressure and chronic mental stress, supplementing with 100-200mg of neuraminic acid daily can help alleviate neural fatigue, improve memory and concentration, and maintain a positive mental state.
When adjunctive intervention is needed for neurological disorders, the dosage should be appropriately increased, generally to 300-600mg/day, and it is recommended to be taken in two divided doses. This dosage and administration method ensures that neuraminic acid continues to work in the body, promoting the repair of nerve damage and the recovery of neural function. In clinical studies, patients with mild cognitive impairment who received 300-600mg/day of neuraminic acid supplementation showed significant improvements in cognitive function, including significant increases in memory and executive function, after a period of intervention.
Neuraminic acid supplementation should also be scheduled scientifically and rationally. It is generally recommended to continue supplementing for 3-6 months. This is because the repair and improvement of nervous system function is a relatively slow process, requiring time for the effects to accumulate. During this process, neuraminic acid continuously provides nutrients to nerve cells, promoting their regeneration and repair, and gradually improving nervous system function. For example, in the treatment of some Alzheimer’s patients, after six months of neuraminic acid supplementation, their condition was effectively controlled, and their cognitive abilities and ability to care for themselves improved to a certain extent.
2. Contraindications and Precautions
Pregnant and breastfeeding women should exercise extreme caution when using neuraminic acid and must use it under the strict guidance of a physician. This is because pregnant and breastfeeding women are in a unique physiological state, and the nutrient requirements and metabolism of the developing fetus or infant are unique. While neuraminic acid plays an important role in the development and repair of the nervous system, its metabolism in pregnant and breastfeeding women and its effects on the fetus or infant are not fully understood. Indiscriminate supplementation of neuraminic acid may pose potential risks to the development of the fetus or infant. Therefore, during this period, the decision regarding whether to supplement with neuraminic acid, as well as the dosage and method of supplementation, should be made by a physician based on a comprehensive evaluation of the pregnant or breastfeeding woman’s specific circumstances.
When used in combination with anticoagulants, coagulation parameters should be closely monitored. Neuroaminic acid may interact with anticoagulants, affecting their efficacy or increasing the risk of bleeding. Anticoagulants inhibit blood clotting and prevent thrombosis, but certain mechanisms of action of neuraminic acid may interfere with the effects of anticoagulants. For example, neuraminic acid may affect platelet function, resulting in either synergistic or antagonistic effects with anticoagulants. Therefore, when neuraminic acid and anticoagulants are used together, regular monitoring of coagulation parameters, such as prothrombin time (PT) and international normalized ratio (INR), is essential to facilitate timely dosage adjustments and ensure safe use.
Before using neuraminic acid, individuals with allergies are advised to check for polymorphisms in genes involved in erucic acid metabolism (FADS1/FADS2). Individuals with allergies have a more sensitive immune system and may experience allergic reactions to certain substances. Erucic acid is a metabolite of neuraminic acid, and polymorphisms in the FADS1/FADS2 genes can affect the body’s ability to metabolize erucic acid. Certain mutations in the FADS1/FADS2 genes may lead to abnormal erucic acid metabolism, increasing the risk of allergic reaction to neuraminic acid. Through genetic testing, we can understand the individual’s genetic condition, assess the risk of allergies in advance, avoid allergic reactions caused by the use of neuraminic acid, and ensure the safe use of neuraminic acid.
Research Progress and Future Outlook
Currently, research interest in neurological diseases continues to grow, offering broad prospects for its future clinical applications and the development of the health industry. In Parkinson’s disease research, researchers are focusing on the protective mechanisms of neuratomic acid on dopaminergic neurons in the substantia nigra. Numerous studies in cell models and animal models have demonstrated that neuratomic acid can significantly inhibit oxidative stress and reduce the apoptosis rate of dopaminergic neurons. In cell experiments, treatment with neuratomic acid increased the survival rate of dopaminergic neurons under oxidative stress by 30%. In animal models, supplementation with neuratomic acid significantly improved behavioral symptoms in Parkinson’s disease models, with their time spent in the rotarod test increased by 25%, demonstrating that neuratomic acid can effectively alleviate motor symptoms of Parkinson’s disease and improve motor function.
For amyotrophic lateral sclerosis (ALS), research focuses on neuratomic acid’s protective effects on motor neurons and its ability to slow disease progression. In a preclinical study, neuratomic acid treatment of ALS mice demonstrated a 15% increase in survival and a slowed rate of motor decline. Further mechanistic studies have revealed that neuraminic acid can regulate neurotransmitter balance, reduce glutamate excitotoxicity, and mitigate motor neuron damage. This research provides a potential new strategy for the treatment of ALS, potentially improving patients’ quality of life and prolonging survival.
The combined use of neuraminic acid and stem cell therapy is also a hot topic in current research. Stem cell therapy possesses powerful regenerative and repair capabilities, capable of differentiating into various types of neural cells to replace damaged neurons. Neuroaminic acid, on the other hand, provides a favorable microenvironment for stem cell differentiation and neural cell growth, promoting stem cell differentiation into neurons and enhancing neural cell survival and function. In animal studies, the combination of neuraminic acid and stem cells in a brain injury model demonstrated significantly greater neurological recovery compared to stem cell therapy alone, with neurological function scores increasing by 20%. This finding demonstrates that the combined use of neuraminic acid and stem cell therapy has a synergistic effect, further promoting neurological recovery and offering new hope for the treatment of neurological diseases.
In the future, neuraminic acid has the potential to be developed as a “neuroregenerative nutrient” for precision medicine. With the advent of the era of precision medicine, in-depth research into the mechanism of action of neuraminic acid will provide a solid theoretical foundation for its precise application. By analyzing individual genetic, metabolic, and other multi-omics data, neuratomic acid supplementation regimens can be customized to improve therapeutic efficacy and minimize adverse reactions. For example, for patients with neurodegenerative diseases carrying specific gene mutations, the dosage and duration of neuratomic acid supplementation can be precisely determined based on their genetic profile, enabling targeted treatment.
Nervonic acids may also become an important strategy for early intervention in neurodegenerative diseases. Early intervention is crucial for the treatment of neurodegenerative diseases, slowing disease progression and improving patients’ quality of life. Due to its favorable safety profile and neuroprotective properties, neuratomic acid supplementation in the early stages of disease can effectively delay neuronal damage and death, providing patients with more time for treatment. However, the long-term safety and efficacy of neuratomic acid still require further high-quality clinical data. Large-scale, multicenter, long-term clinical trials are needed to further clarify the optimal dosage, duration, and safety of neuratomic acid and provide a solid scientific basis for its widespread use.
Nervonic acids regulate neural structure and function through multiple targets, demonstrating a lifelong protective effect on the nervous system, from early myelin formation in development to neuroprotection during aging. Scientifically supplementing with neuraminic acid is becoming a cutting-edge option for proactively maintaining brain health. We believe that in the future, with continued in-depth research and technological advancements, neuraminic acid will play an even more important role in the prevention, treatment, and health management of neurological diseases, making greater contributions to human health and well-being.
