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    Can Environmental Enrichment Mitigate Cell Apoptosis in the Central Nervous System Under Adverse Health Conditions? A Systematic Review
    (Wiley, 2026) de Sousa Fernandes, Matheus Santos; Ferreira, Diorginis Jose Soares; Yagin, Fatma Hilal; Badicu, Georgian; Santos, Gabriela Carvalho Jurema; Guedes, Maria Carolina Santos; Ardigo, Luca Paolo
    To summarize the available evidence in the literature regarding the effects of exposure to an enriched environment (EE) on the modulation of apoptotic markers in central tissue of rodents under unfavorable conditions. Searches were conducted in three databases: PubMed/Medline (70 articles), Scopus (65 articles), and EMBASE (128 articles), all of which were subjected to eligibility criteria. Of the 263 articles found, 95 duplicates were removed. After evaluating the title and abstract, 147 studies were excluded, leaving 21 articles, 16 of which were included in this systematic review. EE was implemented using various inanimate objects. The disruptive event/condition included social isolation, cerebral ischemia, stroke, postpartum depression, accelerated aging, ischemia/reperfusion, high altitude, Alzheimer's disease, hypobaric hypoxia, infrasound exposure, sepsis, and exposure to sevoflurane. Regarding the expression of apoptotic markers, after EE exposure, there was a reduction in the expression of p-IKK beta/IKK beta and p-P65/P65 in the hippocampus, a reduction in Bax, as well as cleaved Caspase-3, Cytochrome C, a reduction in the Bax/Bcl-2 ratio, and p53. As for anti-apoptotic markers, increased expression of Bcl-2 was observed following EE exposure. This systematic review concludes that the benefits of EE can reduce apoptosis through the modulation of both pro-apoptotic and anti-apoptotic genes. In this regard, EE has been shown to be an important neuroprotective tool in various adverse conditions, mitigating cognitive deficits by reducing apoptosis related to cellular stress.
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    Is environmental enrichment effective in modulating autophagy markers in the brain exposed to adverse conditions? A systematic review
    (Frontiers Media Sa, 2025) Silva, Clarice Beatriz Goncalves; de Sousa Fernandes, Matheus Santos; Cerqueira, Debora Dantas Nucci; Santos, Gabriela Carvalho Jurema; Yagin, Fatma Hilal; Aygun, Yalin; Tabnjh, Abedelmalek Kalefh
    Autophagy is a key regulator of cellular homeostasis and neuronal survival, particularly under adverse physiological conditions. Environmental enrichment (EE), a non-pharmacological intervention providing enhanced sensory, cognitive, and motor stimulation, may modulate autophagic processes in the brain. This systematic review aimed to synthesize preclinical findings on the effects of EE on autophagy markers in rodent models subjected to diverse adverse conditions. A literature search across PubMed, Scopus, ScienceDirect, and embase yielded eight eligible studies meeting inclusion criteria. EE was found to be generally associated with upregulation of key autophagic markers such as Beclin-1, LC3-II/LC3-I ratio, cathepsins, p62, p-TFEB, and LAMP-1 across brain regions including the cortex, hippocampus, and penumbral area. However, reductions in some markers were also observed, indicating that the modulatory effects of EE are context-dependent and may vary with disease model, brain region, or EE protocol duration. These findings suggest that EE holds promise as an adjunctive strategy to modulate autophagy and mitigate neurodegeneration, though heterogeneity in study design and outcomes warrants caution during interpretation. Further mechanistic and sex-specific studies are needed to clarify the therapeutic relevance of EE-induced autophagic modulation.
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    Serotoninergic modulation in the brainstem and hypothalamus of female overnourished rats: impact on mitochondrial markers, oxidative stress and BDNF mRNA levels
    (Frontiers Media Sa, 2025) Rodrigues, Thyago de Oliveira; dos Santos Junior, Osmar Henrique; Beltrao de Lemos, Maria Daniele Teixeira; de Sousa Fernandes, Matheus Santos; Yagin, Fatma Hilal; Yagin, Burak; Lagranha, Claudia J.
    Introduction Obesity is a global epidemic identified by the World Health Organization, and its complexity involves genetic, cultural, socioeconomic, and behavioral factors.Methods In this study, we used female Wistar rats, with litters standardized to nine female pups, which were divided into two groups: normally nourished or overnourished. The groups were further subdivided into control and fluoxetine-treated groups, with the pharmacological treatment maintained until the 21st day of life. At 30 days of age, euthanasia was performed, and tissues from the hypothalamus and brainstem were collected.Results We observed an increase in body weight and the Lee index in the overnourished group, but fluoxetine treatment reduced these indices. Additionally, overnourished rats consumed more palatable food. Biochemically, NADH content in the hypothalamus was altered by overnutrition but restored by fluoxetine treatment. Citrate synthase activity was reduced in the overnourished group in the hypothalamus but increased in the brainstem of fluoxetine-treated rats. The production of reactive oxygen species was higher in the overnourished group, and oxidative stress biomarkers showed increased levels of MDA and protein carbonylation in these rats. Overnutrition impaired the antioxidant activity of enzymes in both the hypothalamus and brainstem, whereas fluoxetine treatment improved this activity. BDNF expression was higher in the fluoxetine-treated groups compared to the overnourished group.Discussion These results demonstrate the detrimental effects of maternal overnutrition on the development of female offspring and the therapeutic potential of serotonergic manipulation to mitigate the early effects of obesity, with tissue-specific variations.