In the last century, industrial activities increased and caused multiple health problems for humans and animals. At this moment, heavy metals are considered the most harmful substances for their effects on organisms and humans. The impact of these toxic metals, which have no biological role, poses a considerable threat and is associated with several health problems. Heavy metals can interfere with metabolic processes and can sometimes act as pseudo-elements. The zebrafish is an animal model progressively used to expose the toxic effects of diverse compounds and to find treatments for different devastating diseases that human beings are currently facing. This review aims to analyse and discuss the value of zebrafish as animal models used in neurological conditions, such as Alzheimer’s disease (AD), and Parkinson’s disease (PD), particularly in terms of the benefits of animal models and the limitations that exist.

Mercury (Hg) is considered one of the most widespread toxic environmental pollutants, which seems to have multiple effects on organisms even at low concentrations. It has a critical role in many health problems with harmful consequences, with Hg primarily targeting the brain and its components, such as the central nervous system (CNS). Hg exposure was associated with numerous CNS disorders that frequently trigger Alzheimer’s disease (AD). Patients with AD have higher concentrations of Hg in blood and brain tissue. This paper aims to emphasize a correlation between Hg and AD based on the known literature in the occupational field. The outcome shows that all these concerning elements could get attributed to Hg. However, recent studies did not investigate the molecular level of Hg exposure in AD. The present review highlights the interactions between Hg and AD in neuronal degenerations, apoptosis, autophagy, oxidative stress (OS), mitochondrial malfunctions, gastrointestinal (GI) microflora, infertility and altering gene expression.

Background/Objectives: Attention deficit hyperactivity disorder (ADHD) is the most common childhood-onset neurodevelopmental disorder, characterized by difficulty maintaining attention, impulsivity, and hyperactivity. While the cause of this disorder is still unclear, recent studies have stated that heredity is important in the development of ADHD. This is linked to a few comorbidities, including depression, criminal behavior, and anxiety. Although genetic factors influence ADHD symptoms, there are also non-genetic factors, one of which is oxidative stress (OS), which plays a role in the pathogenesis and symptoms of ADHD. This review aims to explore the role of OS in ADHD and its connection to antioxidant enzyme levels, as well as the gut–brain axis (GBA), focusing on diet and its influence on ADHD symptoms, particularly in adults with comorbid conditions. Methods: The literature search included the main available databases (e.g., Science Direct, PubMed, and Google Scholar). Articles in the English language were taken into consideration and our screening was conducted based on several words such as “ADHD”, “oxidative stress”, “diet”, “gut–brain axis”, and “gut microbiota.” The review focused on studies examining the link between oxidative stress and ADHD, the role of the gut–brain axis, and the potential impact of dietary interventions. Results: Oxidative stress plays a critical role in the development and manifestation of ADHD symptoms. Studies have shown that individuals with ADHD exhibit reduced levels of key antioxidant enzymes, including glutathione peroxidase (GPx), catalase (CAT), and superoxide dismutase (SOD), as well as a diminished total antioxidant status (TOS) compared to healthy controls. Additionally, there is evidence of a close bidirectional interaction between the nervous system and gut microbiota, mediated by the gut–brain axis. This relationship suggests that dietary interventions targeting gut health may influence ADHD symptoms and related comorbidities. Conclusions: Oxidative stress and the gut–brain axis are key factors in the pathogenesis of ADHD, particularly in adults with comorbid conditions. A better understanding of these mechanisms could lead to more targeted treatments, including dietary interventions, to mitigate ADHD symptoms. Further research is required to explore the therapeutic potential of modulating oxidative stress and gut microbiota in the management of ADHD.

Tartrazine (TZ, also known as FD&C Yellow No. 5 or E102) is a synthetic, water-soluble yellow food dye widely used in the food and pharmaceutical industries. Some studies have associated TZ with allergic reactions, especially among people with dye sensitivities or pre-existing allergies. Recent research also suggests a possible link between TZ consumption and the worsening of behavioral disorders, especially in children, including symptoms such as hyperactivity, irritability, restlessness, and sleep disturbances. Experimental studies in laboratory animals have highlighted potential risks associated with prolonged or high-dose exposure, including toxic effects on the nervous system and liver function. In addition, increasing evidence indicates that TZ can induce oxidative stress (OS) by increasing the production of reactive oxygen species (ROS), which can contribute to cellular damage and inflammation. Although the evidence remains inconclusive, there are recommendations to limit the intake of synthetic food dyes, especially in children’s diets. The purpose of this review is to examine the potential toxic effects on health of tartrazine by analyzing findings from experimental studies in cell cultures and laboratory animals, as well as correlations observed in humans. We focus on documented adverse reactions, including possible neurotoxic, hepatotoxic, oxidative, and behavioral effects. Through this, we aim to contribute to a more comprehensive understanding of the risks associated with exposure to this synthetic food dye.

Oxidative stress (OS) is a condition in which there is an excess of reactive oxygen species (ROS) in the body, which can lead to cell and tissue damage. This occurs when there is an overproduction of ROS or when the body’s antioxidant defense systems are overwhelmed. Quercetin (Que) is part of a group of compounds called flavonoids. It is found in high concentrations in vegetables, fruits, and other foods. Over the past decade, a growing number of studies have highlighted the therapeutic potential of flavonoids to modulate neuronal function and prevent age-related neurodegeneration. Therefore, Que has been shown to have antioxidant, anticancer, and anti-inflammatory properties, both in vitro and in vivo. Due to its antioxidant character, Que alleviates oxidative stress, thus improving cognitive function, reducing the risk of neurodegenerative diseases. On the other hand, Que can also help support the body’s natural antioxidant defense systems, thus being a potentially practical supplement for managing OS. This review focuses on experimental studies supporting the neuroprotective effects of Que in Alzheimer’s disease (AD), Parkinson’s disease (PD), Huntington’s disease (HD), and epilepsy.

Functional Cognitive Disorder (FCD), a condition marked by significant subjective cognitive complaints in the absence of identifiable neurological disease, is increasingly recognized as a distinct and underdiagnosed entity in clinical practice. This review synthesizes recent findings to clarify its diagnostic features, differentiate it from other cognitive syndromes such as mild cognitive impairment and dementia, and explore its psychological underpinnings. We examined longitudinal studies, meta-analyses, and clinical frameworks to identify patterns of symptom presentation, cognitive performance, and psychosocial factors. Findings reveal that FCD is characterized by inconsistent cognitive deficits, preserved functional independence, and heightened help-seeking behavior, often accompanied by anxiety, metacognitive dysfunction, and maladaptive beliefs about memory. Unlike neurodegenerative conditions, FCD follows a stable, non-progressive course and shows no evidence of conversion to dementia when accurately diagnosed. Enhanced clinical recognition and structured assessment approaches are crucial for improving diagnostic accuracy, minimizing patient distress, and avoiding unnecessary medical interventions. Further research is needed to standardize diagnostic criteria and develop targeted therapeutic strategies.