Neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis, currently represent one of the major challenges in contemporary medicine and geriatrics. Progressive degeneration of the nervous system affects not only patients’ physical functioning but also their psychosocial well-being, often leading to social isolation and disruption of interpersonal relationships. These processes are most strongly associated with individuals over 65 years of age, in whom metabolic syndrome is frequently diagnosed and constitutes a significant factor predisposing them to the exacerbation of neuropathological changes. This review analyzes the role of selected vitamins in modulating the course of neurodegenerative disorders, with particular emphasis on their neuroprotective potential. Specific attention is given to their involvement in antioxidant defense mechanisms, regulation of inflammatory pathways, prevention of abnormal protein aggregation, participation in neurotransmitter synthesis, and support of mitochondrial function and cellular energy metabolism. The review also considers key interactions between vitamins and coenzyme Q10, which synergistically enhance neuroprotective mechanisms. Deficiencies in certain vitamins may exacerbate oxidative stress, impair synaptic transmission, and intensify neuroinflammatory responses, thereby contributing to disease progression. The study analyzes the available data on therapeutic doses of vitamins and compares them with the recommended dietary intake and the upper tolerable intake levels (UL). The available evidence suggests that personalized vitamin supplementation, when integrated with a well-balanced and nutrient-dense diet, may constitute a valuable adjunctive therapeutic strategy. Such an approach may help attenuate disease progression, support neuronal integrity, and improve functional outcomes. Ultimately, targeted nutritional interventions may enhance overall well-being and quality of life in patients affected by neurodegenerative diseases.

Background: Atherosclerosis is a chronic inflammatory disease driven by complex interactions between lipid metabolism disorders, oxidative stress, and immune dysregulation. Despite advances in pharmacotherapy, there is growing interest in nutraceutical compounds with multi-target effects. Thymoquinone (TQ), the main bioactive constituent of Nigella sativa, has emerged as a promising candidate due to its anti-inflammatory, antioxidant, and lipid-modulating properties. This review aims to comprehensively evaluate the effects of TQ on the key pathophysiological mechanisms involved in atherosclerosis, with particular emphasis on inflammation, oxidative stress, and lipid metabolism. Methods: A narrative review of preclinical studies, including in vitro and in vivo experimental models, was conducted to assess the biological activity of TQ and its potential anti-atherosclerotic effects. Results: TQ exhibits multi-target activity by modulating several molecular pathways associated with atherogenesis. It reduces oxidative stress by enhancing antioxidant enzyme activity and decreasing reactive oxygen species production. TQ also suppresses inflammatory signaling pathways, including NF-κB, MAPK, and COX-2, leading to decreased expression of pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α. Furthermore, it influences lipid metabolism by lowering total cholesterol and LDL-C levels while improving lipid profiles. TQ has also been shown to inhibit foam cell formation, endothelial dysfunction, and vascular inflammation. Additionally, nanocarrier-based formulations of TQ may improve its bioavailability and therapeutic potential. Conclusions: Current preclinical evidence suggests that TQ may play a significant role in the prevention and modulation of atherosclerosis through its multi-mechanistic action. However, the lack of well-designed clinical trials, limited bioavailability, and insufficient data on long-term safety highlight the need for further research to establish its clinical efficacy and optimal therapeutic use.