Recent research exploring the relationship between the gut and the brain suggests that the condition of the gut microbiota can influence cognitive health. A well-balanced gut microbiota may help reduce inflammation, which is linked to neurodegenerative conditions. Prebiotics, probiotics, and symbiotics are nutritional supplements and functional food components associated with gastrointestinal well-being. The bidirectional communication of the gut–brain axis is essential for maintaining homeostasis, with pre-, pro-, and symbiotics potentially affecting various cognitive functions such as attention, perception, and memory. Numerous studies have consistently shown that incorporating pre-, pro-, and symbiotics into a healthy diet can lead to improvements in cognitive functions and mood. Maintaining a healthy gut microbiota can support optimal cognitive function, which is crucial for disease prevention in our fast-paced, Westernized society. Our results indicate cognitive benefits in healthy older individuals with probiotic supplementation but not in healthy older individuals who have good and adequate levels of physical activity. Additionally, it appears that there are cognitive benefits in patients with mild cognitive impairment and Alzheimer’s disease, while mixed results seem to arise in younger and healthier individuals. However, it is important to acknowledge that individual responses may vary, and the use of these dietary supplements should be tailored to each individual’s unique health circumstances and needs.

Neurodegenerative disorders, including Alzheimer’s disease (AD), Parkinson’s disease (PD), and post-stroke cognitive impairment (PSCI), represent an escalating global health and economic challenge. In the quest for disease-modifying interventions, natural polyphenols—most notably curcumin, the principal bioactive compound of Curcuma longa—have attracted considerable interest due to their pleiotropic neuroprotective effects. This narrative review critically synthesizes findings from a selection of peer-reviewed articles published between 2000 and 2025, chosen for their relevance to curcumin’s molecular mechanisms and translational potential. Curcumin’s complex chemical structure confers antioxidant, anti-inflammatory, and epigenetic modulatory properties; however, its clinical application is limited by poor oral bioavailability. Mechanistically, curcumin attenuates oxidative stress and suppresses key inflammatory mediators, including nuclear factor kappa B (NF-κB), cyclooxygenase-2 (COX-2), and inducible nitric oxide synthase (iNOS). Additionally, it modulates apoptosis, inhibits amyloid-beta aggregation, and enhances cellular quality control processes such as autophagy and mitophagy, while upregulating neurotrophic factors such as brain-derived neurotrophic factor (BDNF). Preclinical studies employing rodent models of AD, PD, and ischemic stroke have demonstrated curcumin’s dose-dependent neuroprotective efficacy, with improved outcomes observed using nanoparticle-based delivery systems. Early-phase clinical trials further support curcumin’s favorable safety profile and potential cognitive benefits, although challenges remain regarding pharmacokinetics, formulation standardization, and therapeutic reproducibility. Future directions include the development of advanced drug delivery platforms, combinatory therapeutic regimens, and personalized medicine approaches integrating curcumin within multifaceted neurotherapeutic strategies. Collectively, this narrative review highlights curcumin as a promising multi-targeted candidate for combating neurodegenerative diseases, while emphasizing the need for further translational and clinical validation.

Background: Neurodegenerative diseases, including Alzheimer’s disease and Parkinson’s disease, are among the leading causes of disability and mortality worldwide. Dietary patterns have emerged as modifiable risk factors that may influence disease onset and progression. The Mediterranean diet (MedDiet), rich in fruits, vegetables, whole grains, legumes, fish, and extra virgin olive oil, has been consistently associated with better cognitive outcomes and reduced risk of neurodegeneration. Aim: This narrative review summarizes current evidence on the role of the MedDiet in slowing the progression of neurodegenerative diseases, with a particular focus on polyphenols such as resveratrol and oleuropein as key bioactive mediators. Methods: We synthesized findings from epidemiological studies, clinical trials, and mechanistic research to provide an integrated overview of how adherence to the MedDiet and its polyphenol components affects neurodegenerative disease trajectories. Results: Epidemiological studies suggest that higher MedDiet adherence is associated with slower cognitive decline, reduced conversion from mild cognitive impairment to Alzheimer’s disease, and better motor and non-motor outcomes in Parkinson’s disease. Mechanistically, the MedDiet modulates oxidative stress, neuroinflammation, mitochondrial function, vascular health, and the gut–brain axis. Polyphenols such as resveratrol and oleuropein exert neuroprotective effects through antioxidant activity, modulation of amyloid aggregation, mitochondrial biogenesis, and activation of signaling pathways (e.g., SIRT1). Clinical studies, although limited, indicate beneficial effects of polyphenol-rich interventions on cognitive and metabolic biomarkers. Conclusions: Current evidence supports the Mediterranean diet as a promising dietary strategy to slow the progression of neurodegenerative diseases. Polyphenols, including resveratrol and oleuropein, may play a role in mediating these effects. Further well-designed, long-term clinical trials are needed to establish causal relationships, optimize dosage, and explore biomarker-driven personalized nutrition approaches.

Vitamin D plays a crucial role in the regulation of the immune system, with immunomodulatory effects that are key in the prevention of colorectal cancer (CRC). Over the past decades, research has shown that this steroid hormone impacts much more than bone health, significantly influencing immune responses. Vitamin D enhances immune organ functions such as the spleen and lymph nodes, and boosts T-cell activity, which is essential in defending the body against tumors. Additionally, vitamin D mitigates inflammatory responses closely linked to cancer development, reducing the inflammation that contributes to CRC. It acts via vitamin D receptors (VDRs) expressed on immune cells, modulating immune responses. Adequate vitamin D levels influence gene expression related to inflammation and cell proliferation, inhibiting tumor development. Vitamin D also activates mechanisms that suppress cancer cell survival, proliferation, migration, and metastasis. Low levels of vitamin D have been associated with an increased risk of CRC, with deficiency correlating with higher disease incidence. Lifestyle factors, such as a diet high in red meat and calories but low in fiber, fruits, and vegetables, as well as physical inactivity, contribute significantly to CRC risk. Insufficient calcium and vitamin D intake are also linked to disease occurrence and poorer clinical outcomes. Maintaining optimal vitamin D levels and adequate dietary intake is crucial in preventing CRC and improving patient prognosis. This review explores the role of vitamin D in immune regulation and summarizes findings from randomized clinical trials assessing the effects of vitamin D supplementation on CRC outcomes.

Background: Chronic obstructive pulmonary disease (COPD) is a progressive, inflammatory airway disorder characterized by a gradual decline in lung function and increased oxidative stress. Both oxidative stress and inflammation are central to its pathophysiology, with trace elements such as zinc, copper, iron, manganese, magnesium, selenium, and calcium playing key roles in various cellular processes. Objective: This article reviews the role of trace elements in COPD, focusing on their involvement in disease pathogenesis and their therapeutic potential. Specifically, we examine the effects of zinc, copper, iron, magnesium, manganese, selenium, and calcium in COPD. Methods: We performed a comprehensive narrative review of the literature across databases including PubMed, Web of Science, Cochrane Library, and Google Scholar, identifying studies that explore the therapeutic effects of trace elements in COPD. The studies included in the review consisted of cohort analyses, randomized controlled trials, and clinical investigations. Results: Zinc, copper, iron, magnesium, manganese, selenium, and calcium are critical to both the pathophysiology and management of COPD. These trace elements contribute to the regulation of inflammation, the modulation of oxidative stress, and the maintenance of lung function. Zinc and copper, for instance, reduce oxidative stress and modulate immune responses, while iron is essential for oxygen transport. Magnesium, manganese, selenium, and calcium are vital for muscle function, respiratory performance, reducing inflammation, and improving pulmonary function. Conclusions: The minerals zinc, copper, iron, magnesium, manganese, selenium, and calcium may contribute to beneficial effects as part of the standard therapeutic management of COPD. Maintaining optimal levels of these trace elements may support the regulation of inflammatory processes, a reduction in oxidative stress, and an improvement in the pulmonary function. However, further clinical research is necessary to confirm their efficacy and establish safe dosage recommendations in COPD treatment.

Background: Accelerated demographic aging in Hungary and across Europe presents significant public health and socioeconomic challenges, particularly in preserving cognitive function and preventing neurodegenerative diseases. Modifiable lifestyle factors—especially dietary habits—play a critical role in brain aging and cognitive decline. Objective: This narrative review explores the mechanisms by which Western dietary patterns contribute to cognitive impairment and neurovascular aging, with specific attention to their relevance in the Hungarian context. It also outlines the rationale and design of the Semmelweis Study and its workplace-based health promotion program targeting lifestyle-related risk factors. Methods: A review of peer-reviewed literature was conducted focusing on Western diet, cognitive decline, cerebrovascular health, and dietary interventions. Emphasis was placed on mechanistic pathways involving systemic inflammation, oxidative stress, endothelial dysfunction, and decreased neurotrophic support. Key findings: Western dietary patterns—characterized by high intakes of saturated fats, refined sugars, ultra-processed foods, and linoleic acid—are associated with elevated levels of 4-hydroxynonenal (4-HNE), a lipid peroxidation product linked to neuronal injury and accelerated cognitive aging. In contrast, adherence to Mediterranean dietary patterns—particularly those rich in polyphenols from extra virgin olive oil and moderate red wine consumption—supports neurovascular integrity and promotes brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF) activity. The concept of “cognitive frailty” is introduced as a modifiable, intermediate state between healthy aging and dementia. Application: The Semmelweis Study is a prospective cohort study involving employees of Semmelweis University aged ≥25 years, collecting longitudinal data on dietary, psychosocial, and metabolic determinants of aging. The Semmelweis–EUniWell Workplace Health Promotion Model translates these findings into practical interventions targeting diet, physical activity, and cardiovascular risk factors in the workplace setting. Conclusions: Improving our understanding of the diet–brain health relationship through population-specific longitudinal research is crucial for developing culturally tailored preventive strategies. The Semmelweis Study offers a scalable, evidence-based model for reducing cognitive decline and supporting healthy aging across diverse populations.