Neurological disorders are a major public health concern. Notably, the rate of chronic neurological diseases is affected by lifestyle changes, leading to considerable health-care and economic burden worldwide. Considerable interest has emerged on functional foods due to their beneficial health efficacy. Thus, efforts have been made to extract different bioactive phytochemicals or compounds from therapeutic natural-based products, which has led to functional foods referred to as "vitafoods,""medifoods," "pharmafoods," or "medicinal foods." To overcome neurological illness such as obsessive-compulsive disorder (OCD), nutraceuticals have been applied as prophylactic options This review addresses nutraceutical intervention in the OCD treatment.
Mycotoxins pose a serious threat to global food safety, agricultural productivity, and public health. Food contamination with mycotoxins leads to physiological and biochemical abnormalities in humans and livestock. C. elegans, due to its unique characteristics, offers a dependable complementary model for elucidating the cellular and molecular basis of mycotoxin-mediated neurotoxicity and other general toxicological impacts. This chapter covers recent studies on mycotoxin toxicity in C. elegans, examining four classes of mycotoxins, namely aflatoxins (AFB1), fumonisins (FB1), deoxynivalenol (DON), and zearalenone (ZEA). Data in the literature reveal that mycotoxin exposure in C. elegans elicits oxidative stress, mitochondrial dysfunction, DNA damage, neurotoxicity, neuroendocrine alterations, and reproductive impairment. Specifically, FB1 promotes abnormal GABAergic and serotonergic neurotransmission, resulting in behavioral deficits in C. elegans. Mechanistic evidence reveals the central role of conserved transcription factors in stress-response and detoxification pathways, notably SKN-1/Nrf2 and DAF-16/FOXO signaling, in mediating mycotoxin toxicity. Collectively, this chapter highlights the utility of C. elegans in evaluating mycotoxin toxicity at environmentally relevant exposures. C. elegans represents an integrative and complementary model in understanding mechanisms associated with neurobehavioral toxicity resulting from mycotoxin exposure.
Heavy metals pose a profound threat to neurological health across all stages of human life, from prenatal development to old age. Heavy metals such as lead, mercury, cadmium, and arsenic are pervasive environmental pollutants that disrupt neural function through mechanisms including oxidative stress, inflammation, mitochondrial dysfunction, and neurotransmitter system imbalances. During critical developmental windows such as fetal growth and early childhood, exposure can impair neurogenesis, synaptic plasticity, and myelination, leading to lifelong cognitive deficits, behavioral disorders, and increased vulnerability to neurodegenerative diseases in later life. Even in adulthood and aging, chronic exposure exacerbates neurodegeneration, accelerating conditions like Alzheimer's and Parkinson's diseases through persistent oxidative damage and inflammatory cascades. This chapter underscores the dual role of nutrition as both a shield and a therapeutic tool against heavy metal neurotoxicity. Key nutrients, such as polyphenols, vitamins, and essential minerals, counteract heavy metal-induced damage by scavenging free radicals, enhancing antioxidant defenses, modulating inflammation, and promoting neuronal repair. By integrating evidence from epidemiological, preclinical, and clinical studies, this chapter emphasizes actionable strategies, such as fortified infant formulas, plant-based proteins, and micronutrient supplementation to reduce heavy metal bioavailability and bolster neurological resilience. Public health initiatives targeting vulnerable populations, alongside policies regulating environmental pollutants, are critical to curbing this silent epidemic. This chapter advocates for a proactive, nutrition-centered approach to safeguarding brain health, demonstrating that dietary interventions are not merely complementary but foundational in combating the pervasive threat of heavy metal neurotoxicity across generations.
Increased evidence from epidemiological research and pre-clinical studies have presented a correlation between exogenous neurotoxicants (such as aluminum, arsenic, lead, cadmium, mercury and ethanol) and various neurobiological disorders which contribute to cognitive impairments. The existing data demonstrate that nutraceutical supplementation affords neuroprotective effects against neurotoxicity. Nutraceuticals improved learning and memory impairments, anxiety and depressive-like behavior, locomotor activity and neuropathic pain. The most common molecular and cellular mechanisms in nutraceutical therapy include attenuation of oxidative stress (by suppressing lipid peroxidation and increasing antioxidant enzymes and contents), suppression of apoptosis (by increasing B-cell lymphoma 2 (Bcl2) expression, and reduction in Bcl-2-associated X protein (Bax), caspase-3 and cytochrome c expression), suppression of neuroinflammation (by inhibiting inflammatory cytokines), inhibition of amyloid β (Aβ) plaque and neurofibrillary tangles, and increased synaptic plasticity (by increasing Brain-derived neurotrophic factor (BDNF), and regulating cholinergic and neurotransmitter systems.
Neurons require protective systems throughout their entire life course to function prop-erly. However, the brain remains highly susceptible to injury with modern environmental dynamics, when threats, produced naturally and synthetically, can bypass the blood-brain barrier (BBB) and cause neurological damage. Among those toxicants, atrazine (ATZ) has been regarded as a neurotoxic environmental pollutant. Both low-dose exposure and variable courses (short- and long-term) carried out in different experimental models demonstrated that ATZ impairs multiple neurochemical pathways. The resultant disruption leads to oxidative stress, mitochondrial dysfunction, and neuroinflammation, culminating in neuronal injury and impaired function. Despite the limited number of existing studies, bioactive compounds such as lycopene, isoflavones, and biflavanone kolaviron have been shown to be promising neuroprotective agents against ATZ neurotoxicity. These compounds, derived from natural bioactive tomato, soybean, walnut, and bitter kola- Garcinia kola, respectively, possess antioxidant and neuroprotective potentials, thus capable of mitigating the toxic actions of ATZ exposure. Overall, in vitro and in vivo studies accentuate that plant-derived bioactive compounds offer therapeutic benefits in mitigating neurotoxicity from ATZ. However, further research is needed to elucidate the detailed mechanisms by which the plants bioactive compounds mitigate ATZ-induced neurotoxicity, including their interactions with the pathways involved in the neurotoxic effects of ATZ.
Aluminum is a stable but highly reactive element and is one of the most abundant elements in the earth crust. Aluminum application is versatile, and remains indispensable across various industries including electronics, construction, automobile, pharmaceuticals, and in advanced technologies. The growing anthropogenic application of aluminum has however raised public health concern, as exposure to aluminum has been linked to neuronal dysfunction and degeneration. Notably, aluminum exposure has been implicated in the pathogenesis of neurodegenerative diseases in humans. Preclinical evidence showed that aluminum exposure can induce disruption of epigenetic mechanisms in the brain, alter neurotransmission dynamics, disrupt neuronal redox homeostasis, cause acute and chronic inflammation, and impair synaptic plasticity in brain cells. Plant-derived bioactive nutraceuticals have been hypothesized to be potential natural therapeutics against aluminum-induced neurotoxicity. In this chapter, we discuss recent in vitro and in vivo studies on the neurotoxic effect of aluminum exposure and its association with neurodegenerative diseases. Moreover, the neuroprotective effects and mechanisms of plant crude extracts, natural diet-derived oils and purified plant-derived bioactive nutraceuticals on neurotoxicity and neurodegenerative diseases induced by aluminum exposure were extensively clarified.
Despite currently available drugs for neurological disorders, the incidence of these diseases continues to rise with attendant morbidity, mortality and economic losses. The available treatments oftentimes focus more on either slowing down disease progression or ameliorating symptoms. According to the World Health Organization, some of these disorders, including Parkinson's disease and Alzheimer's diseases are among the leading causes of death globally. Identification of new compounds with neuroprotective properties is a fascinating line of research. Berberine, a plant-derived bioactive compound, of the alkaloid family, has been studied extensively for its neuroprotective properties in a wide range of models of neurological disorders such as Alzheimer's disease, Parkinson's disease, Huntington's disease, autism spectrum disorders, traumatic brain injuries and amyloid lateral sclerosis. Studies have shown that the neuroprotective property of berberine is linked to its ability to modulate several critical biochemical pathways and to regulate the concentrations and activities of important biomarkers that are both diagnostic and therapeutic targets for neurological disorders. This chapter provides insight into the biosynthesis, pharmacokinetics and neuroprotective mechanisms of berberine. Furthermore, ways to improve the utilization of berberine for its neuroprotective potentials such as combining it with other compounds or nanoparticle delivery are highlighted.
Selenoneine, an antioxidant molecule analogous to ergothioneine, is not synthesized by vertebrates but can be acquired through the diet. Both selenoneine and ergothioneine contain redox-active groups: selone (-C=Se) and thioketone (-C = S), respectively. However, the reactivity of the selone group with pro-oxidant intermediates is significantly higher than that of the thioketone group. In the presence of oxygen, selenoneine undergoes oxidation to its diselenide form, which can be regenerated by a molar excess of reduced thiol groups. High levels of selenoneine have been detected in carnivorous fish, aquatic mammals, and populations consuming these species. It has been suggested that both selenoneine and ergothioneine possess health-promoting properties in humans. This chapter explores the potential protective effects of selenoneine against electrophilic mercury forms, such as methylmercury (CH3Hg+) and divalent mercury (Hg2 +).
