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.

Magnesium is an essential mineral involved in hundreds of biochemical reactions, with particular relevance to maintaining neural homeostasis, modulating neurotransmitter systems, and regulating inflammatory and oxidative stress mechanisms. This comprehensive review aims to evaluate the potential role of magnesium in the pathophysiology and treatment of three prevalent neurological and psychiatric disorders—depression, migraine, and Alzheimer’s disease—as well as its broader implications for cognitive health. Current research suggests that magnesium deficiency is associated with the development of depression, as magnesium influences glutamatergic and GABAergic neurotransmission, as well as the activity of the hypothalamic–pituitary–adrenal (HPA) axis, both of which play critical roles in stress responses and mood regulation. Additionally, magnesium’s anti-inflammatory properties may contribute to the alleviation of depressive symptoms. In the context of migraine’s pathophysiology, magnesium plays a role in regulating cerebral vascular tone, modulating the trigeminovascular system, and reducing neuronal hyperexcitability, which may explain the observed correlation between magnesium levels and the incidence of migraines. Regarding Alzheimer’s disease, preclinical and epidemiological studies suggest that magnesium may contribute to modulating neurodegenerative processes and preserving cognitive function; however, due to the heterogeneity of the current findings, further longitudinal and interventional studies are necessary to determine its precise clinical relevance. This review aims to enhance the understanding of the relationship between magnesium and these disorders through a narrative review of relevant clinical studies. The findings may provide insights into the potential therapeutic applications of magnesium and guide the future directions of the research into the prevention and treatment of depression, migraine, and Alzheimer’s disease and overall cognitive health.

Introduction: The biological effects of dietary polyphenols have gained increasing attention due to their roles in regulating oxidative stress, inflammatory processes, and mitochondrial function. Human studies suggest that polyphenol intake may support aspects of post-exercise recovery, neuromuscular function, and selected aspects of physical performance. However, most investigations have been conducted in young or metabolically healthy populations, limiting direct clinical translation to older adults. Objective: This narrative review aims to synthesize current mechanistic and human evidence on the physiological and recovery-related effects of dietary polyphenols in the context of exercise adaptation and skeletal muscle function, and to examine their potential relevance to muscle aging and sarcopenia. Methods: A structured, non-systematic literature search was conducted to integrate findings from human intervention trials, preclinical studies, and mechanistic research addressing polyphenols, exercise adaptation, muscle recovery, and muscle aging. Evidence was synthesized narratively with emphasis on shared physiological pathways and functional outcomes. Results: Human intervention studies suggest that polyphenol intake may attenuate biomarkers of exercise-induced muscle damage, modulate inflammatory responses, and accelerate recovery of muscle strength and functional performance. Mechanistic evidence supports the involvement of redox homeostasis, mitochondrial regulation, and inflammatory signaling as central mediators of these effects. While clinical data in older populations remain limited, converging evidence suggests biological overlap between recovery-related pathways and mechanisms implicated in age-related muscle decline. Conclusions: Current evidence is consistent with a biologically plausible role for polyphenols in modulating exercise-related physiological and recovery processes. By aligning recovery-focused evidence with pathways central to muscle aging, this review proposes a translational framework that may inform the design of future targeted clinical trials in older and clinical populations.

Background: Body mass index (BMI) is widely used as a proxy of nutritional status and related lifestyle risk patterns in public health, yet it does not capture body composition–related heterogeneity in cardiometabolic risk. Evidence on whether a more detailed body composition assessment improves population-level screening efficiency remains inconsistent, particularly in Central European populations. Methods: We conducted a cross-sectional analysis of 868 Hungarian adults participating in a nationwide mobile screening program. Locally weighted regression identified sex-specific BMI inflection points for cardiometabolic risk. Stratified receiver operating characteristic (ROC) analyses compared BMI with bioelectrical impedance-derived parameters across five outcomes. Cost- and time-effectiveness of scalable screening strategies were modeled at the population level. Results: Cardiometabolic risk increased at BMI levels below current WHO thresholds (females: 21.8–22.3 kg/m²; males: 23.8–24.3 kg/m²). Overall, body composition parameters did not outperform BMI in the full population. Subgroup-specific differences were observed, particularly among men with BMI 24–36 kg/m² for atherosclerosis risk, suggesting limited and outcome-specific added value rather than broad superiority over BMI. Together, non-linear risk patterns, stratified performance, and population-level modeling converged on mid-range BMI intervals (females: 22–30 kg/m²; males: 24–30 kg/m²) as likely screening windows of phenotypic heterogeneity. Within these ranges, targeted InBody assessment may help refine risk assessment for selected individuals. A mixed screening strategy covering 52% of the population would cost 178.4% of BMI-only screening, while reducing throughput by 24.3%. Conclusions: Population-specific BMI thresholds may more accurately reflect early deviations in nutritional and cardiometabolic risk than current universal cutoffs. BMI remains a useful first-line marker, and body composition assessment may add complementary information in selected BMI ranges. Overall, these findings support a potentially useful, subgroup-specific screening approach, but the modeled cost and time trade-offs should be considered hypothesis-generating and require further validation.

Population aging, the rising burden of chronic non-communicable diseases, and environmental degradation are increasingly recognized as interconnected global challenges, underscoring the need for integrated strategies that simultaneously promote human and planetary health. The Planetary Health Diet (PHD), originally proposed to address these challenges, has emerged as a promising dietary framework for supporting healthy aging. Although its health benefits are increasingly supported by epidemiological and clinical evidence, the biological mechanisms underlying these effects remain incompletely understood. This narrative review synthesizes evidence on the interplay among the PHD, the gut microbiome, and biological aging, with emphasis on microbiome-mediated pathways connecting sustainable nutrition with healthspan. Adherence to PHD-consistent dietary patterns is associated with greater microbial diversity and functional capacity, increased production of bioactive microbial metabolites, and more favorable intestinal barrier, immune, and metabolic profiles. These adaptations may modulate several hallmarks of aging and contribute to the preservation of physiological resilience. Evidence from prospective cohort studies, randomized controlled trials, and systematic reviews further indicates that dietary patterns consistent with the PHD are associated with lower risks of cardiometabolic diseases, frailty, cognitive decline, and premature mortality. By integrating findings from nutritional science, microbiome research, geroscience, and public health, this review positions the gut microbiome as an important, although not exclusive, biological interface through which sustainable dietary patterns may support healthspan while contributing to environmental sustainability.