Daily restricted environmental enrichment (REE) refers to limited, structured periods of enrichment aimed at improving both physical and cognitive well-being in animals and humans. This review explores the significance of REE, focusing on studies that investigate 2 and 3 h daily enrichment protocols. Through an analysis of 21 key studies, this paper highlights how even brief periods of REE can lead to substantial improvements in brain plasticity, cognitive function, and stress resilience. The review tracks the evolution of environmental enrichment from early research on enriched environments in animals to modern applications in human rehabilitation, particularly for stroke recovery and mental health treatment. While the traditional approach to environmental enrichment often involves continuous exposure, recent research suggests that restricted daily enrichment can yield comparable benefits, offering a practical, scalable solution for clinical settings. This review underscores the importance of adapting REE for individual needs and developing flexible, home-based programs for broader application.

Background and Objectives: Depression is a multifactorial mental health disorder involving inflammation, oxidative stress, neuroplasticity deficits, and metabolic dysfunction. Emerging research suggests that vitamin K, beyond its classical roles in coagulation and bone metabolism, may influence neurobiological processes relevant to mood regulation. This systematic review evaluates the association between vitamin K and depressive symptoms and explores potential underlying mechanisms. Materials and Methods: A systematic search was conducted across PubMed, Scopus, Cochrane Library, ScienceDirect, and Google Scholar, following PRISMA 2020 guidelines. Eligible studies included human or animal research examining associations between vitamin K status (dietary intake or serum levels) and depression-related outcomes. Fourteen studies met the inclusion criteria: eleven observational studies, one randomized controlled trial (RCT), and two preclinical animal studies. Results: Most observational studies reported an inverse association between vitamin K intake or serum levels and depressive symptoms across diverse populations. One small RCT demonstrated modest improvements in depression scores following vitamin K2 (menaquinone-7) supplementation in women with polycystic ovary syndrome. Two preclinical studies using non-depression models reported behavioral improvements and reduced oxidative stress following vitamin K2 administration. Conclusions: While preliminary findings suggest a potential role for vitamin K in pathways relevant to depression, the current evidence is limited by cross-sectional designs, lack of isoform-specific analyses, and the absence of depression-focused preclinical models. Mechanisms including inflammation reduction, oxidative stress modulation, sphingolipid regulation, and vitamin K-dependent protein signaling (e.g., GAS6 and osteocalcin) were discussed based on indirect evidence and require further investigation in depression-specific contexts.

Background and Objectives: Depression is a growing global health burden, underscoring the need for preventive strategies that complement existing treatments. Environmental enrichment (EE), incorporating physical, cognitive, sensory, and social stimulation, enhances neuroplasticity and stress resilience. Menaquinone-7 (MK-7), a form of vitamin K2, may also support brain health through osteocalcin, a bone-derived hormone involved in cognition and neuroplasticity. This study examined the protective effects of EE and MK-7 preconditioning, alone and combined, against chronic social defeat stress (CSDS), focusing on the osteocalcin-mediated bone–brain axis and structural plasticity. Materials and Methods: Male C57BL/6N mice received MK-7 (100 µg), EE, or both for four weeks before a 10-day CSDS protocol. Depressive-like behavior was assessed using the forced swim and tail suspension tests, while cognition was evaluated using novel object recognition and Y-maze tests. Serum osteocalcin, brain undercarboxylated osteocalcin (ucOC), brain gene expression of Bdnf, Gpr158, and Rbbp4, and protein levels of BDNF, MAP2, and GAP43 were measured. Results: CSDS induced depressive-like behavior and cognitive impairment, accompanied by reductions in serum and brain ucOC, Bdnf expression, BDNF, GAP43, and MAP2. Both MK-7 and EE showed significant main effects on behavioral and cognitive outcomes, while MK-7 exerted broader effects on osteocalcin- and neuroplasticity-related molecular markers. Significant MK-7 × EE interactions were limited to selected outcomes, including FST and brain ucOC, indicating outcome-specific rather than generalized synergy. Conclusions: CSDS disrupts the osteocalcin-mediated bone–brain axis and neuroplasticity-related pathways. MK-7 and EE both improved behavioral and cognitive outcomes, but MK-7 exerted broader effects on ucOC- and BDNF-related molecular markers, whereas their combination produced selective interactions rather than generalized synergy.