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Purpose of Review Alzheimer’s disease (AD) is a progressive neurodegenerative disorder characterized by cognitive decline associated with oxidative stress, neuroinflammation, tau neurofibrillary tangles, amyloid-beta plaque deposition, and metabolic dysfunction. Increasing evidence suggests that the gut microbiota plays an important role in AD pathogenesis through the microbiota–gut–brain axis. This review aims to provide a comprehensive overview of the role of the gut microbiota in AD and healthy aging, with a particular focus on microbiota-targeted preventive and therapeutic strategies and their potential to influence disease progression. Recent Findings Recent studies have demonstrated that alterations in gut microbial composition are closely associated with AD. Patients with AD commonly exhibit a reduced abundance of short-chain fatty acid–producing bacteria and an increased prevalence of lipopolysaccharide-producing taxa, supporting a mechanistic link between microbial dysbiosis, systemic inflammation, and neurodegeneration. Emerging evidence indicates that dietary patterns, prebiotics, probiotics, synbiotics, postbiotics, and microbiota-based therapies, including fecal microbiota transplantation (FMT), may beneficially modulate gut microbial composition and influence AD-related pathophysiological processes. In addition, lifestyle factors such as sleep quality and physical activity have been increasingly recognized for their interactions with the gut–brain axis and their potential to affect cognitive health. Summary Current evidence highlights the gut microbiota as a promising therapeutic target in AD prevention and management. Microbiota-directed interventions, together with healthy dietary and lifestyle modifications, may help attenuate neuroinflammation, improve metabolic homeostasis, and delay cognitive decline. Furthermore, given the substantial global economic burden of AD, microbiota-focused preventive strategies may contribute not only to improving clinical outcomes but also to reducing long-term healthcare and societal costs. Future longitudinal and interventional studies are needed to establish causal relationships and determine the efficacy of microbiota-based therapies in AD.

Obsessive-compulsive disorder (OCD) is a psychiatric disorder characterized by obsessions and compulsions that significantly impair functioning, affecting approximately 1–3% of individuals during their lifetime. The persistence of clinically significant symptoms in a sizable percentage of patients necessitates the development of novel treatment strategies despite existing pharmacological and psychotherapy methods. According to recent research, the pathophysiology of OCD may be significantly influenced by the gut-brain-microbiome axis, which characterizes the bidirectional communication between the gut microbiota and the central nervous system. This review examines the relationship between OCD and gut microbiota through the lens of short-chain fatty acids (SCFAs), neurotransmitter modulation, inflammatory pathways, and microbiota-derived metabolites. Through the hypothalamus-pituitary-adrenal (HPA) axis and the vagus nerve, neuroimmune and neurohumoral pathways mediate the reciprocal relationship between gut microbiota and OCD. According to research, OCD may be associated with dysbiosis, reduced microbial diversity, poor formation of SCFAs, and abnormalities in neurotransmitter systems like serotonin, dopamine, glutamate, and GABA. It is also reported that a Western-style diet, which is low in fiber, may contribute to this process by negatively affecting microbiota composition. It has been suggested that microbiota-based interventions, such as probiotics, prebiotics, synbiotics, and micronutrient supplements, may have potential regulatory effects on OCD symptoms. In conclusion, approaches targeting the gut microbiota appear promising for developing new complementary and supportive strategies in the treatment of OCD.

Given the limited knowledge of probiotic effects on clock genes, this study investigated whether probiotics that regulate gut integrity and microbiota balance influence central circadian clock gene expression. In this study conducted on three groups [control group (CG), shifted group (SG), and shifted and probiotic supplement group (SPG)] of eight BALB/c mice each, Clock, Bmal1, and Per2 gene expressions and weight gain were evaluated. Although body weights at baseline, week 8, and week 16 were similar among groups, weight gain over time was significantly higher in the SG and SPG groups ( p p = 0.045). These findings demonstrate the regulatory effect of probiotic supplementation on circadian disruption and weight gain, suggesting a potential role in circadian rhythm management. Nevertheless, the results should be interpreted cautiously because they are based on limited gene expression changes and require confirmation in larger studies.

Obesity is a complex disorder affecting metabolism and immunity, with gut microbiota and vitamin D metabolism playing key roles. This study aimed to evaluate the impact of vitamin D supplementation and probiotics on the vitamin D receptor (VDR) levels and the gut microbiota of rats given a high‐fat diet as an experimental model of obesity. In this study, experimental obese rat models were used to assess the impact of vitamin D and probiotic supplements on lipid profiles, inflammation, obesity, diabetes, VDR, and gut microbiota. 24 Wistar rats (4–6 weeks) were divided into four groups: control, high‐fat diet, high‐fat diet with probiotic supplementation (HFD + P), and high‐fat diet with probiotic and vitamin D supplementation (HFD + P + VD). Blood and fecal samples were collected from rats for analysis. Changes in BMI values, initial and final weights, and weight changes across all groups were found ( p = 0.018, p = 0.006, p = 0.023). HFD + P and HFD + P + VD showed lower levels of insulin, CRP, triglycerides, IL‐6, HOMA‐IR, and leptin. Supplementing probiotics and vitamin D reduced the phylum Bacteroidetes while increasing the phyla Proteobacteria, Firmicutes, and Actinobacteria. The findings suggest that probiotics combined with vitamin D supplementation may be a promising approach for supporting the management of obesity‐related metabolic disorders and microbiota. Furthermore, probiotics may enhance vitamin D's effectiveness by inducing VDR expression.

Aflatoksin B1 (AFB1), hem insan hem de hayvanlarda ciddi sağlık sorunlarına yol açabilen güçlü bir mikotoksindir. Propolisin çeşitli toksinlere karşı koruyucu etkileri üzerine çok sayıda çalışma bulunmasına rağmen, AFB1 maruziyetine bağlı intestinal inflamasyon üzerindeki etkilerine ilişkin veriler sınırlıdır. Bu çalışmada, AFB1’ye maruz bırakılan ratlarda propolis takviyesinin duodenum dokusundaki inflamatuar yanıt ve oksidatif hasar üzerine olası koruyucu etkilerinin değerlendirilmesi amaçlanmıştır. Deney planına göre, 32 erkek Sprague Dawley rat, dört gruba ayrılmıştır: Kontrol, AFB1 (25 μg/kg/gün), Propolis (250 mg/kg/gün) ve AFB1+Propolis (25 μg/kg/gün AFB1+250 mg/kg/gün propolis). Yirmi sekiz günlük uygulama sonunda, duodenum dokusundaki inflamatuar belirteçler enzim bağlı immünosorbent testi ile ölçülmüştür. Veriler GraphPad Prism yazılımı (versiyon 10.0, San Diego, CA, ABD) kullanılarak analiz edilmiştir. AFB1 grubunda interlökin-1β (IL-1β), interlökin-6 (IL-6), tümör nekroz faktör-α (TNF-α) ve nükleer faktör kappa B (NF-κB) düzeyleri, propolis grubuna kıyasla anlamlı olarak daha yüksek bulunmuştur (P<0.05). AFB1+Propolis grubunda IL-6 ve NF-κB düzeyleri, AFB1 grubuna göre anlamlı şekilde düşük olduğu belirlenmiştir (P<0.05). Ayrıca, nükleer faktör eritroid 2 ile ilişkili faktör (Nrf-2) ve hem oksijenaz-1 (HO-1) düzeyleri AFB1 grubunda diğer gruplara kıyasla belirgin olarak daha düşük bulunmuştur (P<0.05). Sonuç olarak, propolisin AFB1 maruziyetinin neden olduğu bağırsak inflamasyonu ve oksidatif stres üzerinde koruyucu etki gösterebileceği; bu etkinin inflamatuar sinyal yollarının modülasyonu ve sitoprotektif mekanizmaların aktivasyonu aracılığıyla gerçekleşebileceği düşünülmektedir.

Backgrounds: Fat mass and obesity‐related gene (FTO) has been associated with glucose homeostasis and insulin sensitivity in some populations. The aim of this study was to evaluate the association of FTO gene rs9939609 and rs17817449 polymorphisms with insulin resistance, some cardiometabolic parameters, and body mass index (BMI) in Turkish children with obesity. Methods: The cross‐sectional observational study included 83 children with obesity genotyped for variants of the FTO gene (rs9939609 and rs17817449). Children were divided into two groups as control and insulin resistant according to the homeostatic model assessment of insulin resistance (HOMA‐IR). The relationship between the genotypes of rs9939609 and rs17817449 polymorphisms and insulin resistance was determined using binary logistic regression analysis. Results: In the control group and insulin‐resistant obese group, the majority of the rs9939609 polymorphism was AT (69.2%) and AA (64%) genotypes, and the majority of the rs17817449 polymorphism was GT (65.4%) and TT (70%) genotypes, respectively. Fasting glucose and insulin values were lower, and quantitative insulin sensitivity calculation index (QUICKI) values were higher in the risk genotype (GG) of rs17817449 polymorphism ( p < 0.05). Additionally, rs9939609 (AT genotype, OR = 0.063; 95% CI: 0.006–0.707, p = 0.025 and AA genotype, OR = 0.111; 95% CI: 0.021–0.576, p = 0.009) and rs17817449 (GT genotype, OR = 12.250; CI: 9.720–84.383, p < 0.001) polymorphisms were strongly associated with insulin resistance. Conclusion: Our study supports that FTO gene rs9939609 and rs17817449 polymorphisms are associated with insulin resistance independently of age, gender, and BMI.

AflatoxinB1 (AFB1) is a hepatotoxic mycotoxin whose bioactivation by cytochrome P450 (CYP450) enzymes generates reactive metabolites that drive oxidative stress, inflammation, and apoptosis. Propolis is a bee-derived product with antioxidant and immunomodulatory properties. To investigate whether propolis supplementation attenuates AFB1-induced hepatic injury by modulating inflammatory mediators, Nrf2–HO-1 signaling, mitochondrial apoptosis, and CYP450 expression in rats, twenty-four male Sprague-Dawley rats were randomly allocated to four groups (n = 6): control, AFB1 (25 µg/kg/day), propolis (250 mg/kg/day), and AFB1 + propolis. Treatments were given by oral gavage for 28 days. Hepatic IL-1β, IL-6, TNF-α, Nrf2 and HO-1 levels were measured by ELISA. Histopathology was assessed on H&E-stained sections. Bax, Bcl-2, caspase-3, CYP1A2, CYP3A4, CYP2C19 and cytochrome P450 reductase expressions were evaluated immunohistochemically and quantified by ImageJ. Data were analyzed using one-way ANOVA with Tukey’s post hoc test. AFB1 significantly increased hepatic IL-1β and IL-6 and reduced Nrf2 levels, while propolis supplementation restored Nrf2, elevated HO-1 and significantly lowered IL-6 compared with AFB1 alone (p < 0.05). AFB1 induced marked hydropic degeneration, sinusoidal congestion, and mononuclear infiltration, alongside increased Bax and caspase-3 and decreased Bcl-2 expression; these changes were largely reversed in propolis-treated groups. AFB1 upregulated CYP1A2, CYP3A4 and cytochrome P450 reductase, whereas propolis co-treatment significantly suppressed their expression without affecting CYP2C19. Propolis supplementation attenuated AFB1-induced liver injury through coordinated anti-inflammatory, antioxidant, anti-apoptotic and metabolic regulatory effects, notably via restoration of Nrf2–HO-1 signaling and down-regulation of key CYP450 isoenzymes. Propolis may represent a promising natural dietary strategy against AFB1-associated hepatotoxicity, warranting further translational research.

Amaç: Demir eksikliği anemisi düşük doğum ağırlığı, preterm doğum, maternal-perinatal mortalite ve morbitide artışı, yenidoğan ve ileri çocukluk döneminde motor-mental gelişmede gerilik gibi olumsuz sonuçlar ile yakından ilişkilendirilirken, gebelikte hemodilüsyon ve negatif demir dengesi sebebi ile hemoglobin konsantrasyonlarında azalma görülmektedir. Bunun yanında gebelikte B12 vitamini ihtiyacının artması ve B12 vitamini yetersizliği, annelerde riskli gebelik ve megaloblastik anemiye yol açarken; yenidoğanlarda nörogelişimsel gerilik ile ilişkilendirilmektedir. Bu bilgiler ışığında bu çalışmada postnatal dönemde gebelikte serum Hb düzeyleri ile vitamin B12 düzeyleri ile yenidoğanların antropometrik ölçümleri arasındaki ilişkiyi değerlendirmek amaçlanmıştır. Gereç ve Yöntem: Çalışma 19-43 yaş arası 126 birey ile yürütüldü. Gebeliğin ilk trimesterinde serum Hb düzeyleri ve vitamin B12 düzeyleri ile yenidoğanların doğum ağırlığı, doğum uzunluğu ve baş çevresi uzunluğu değerlendirildi. Ayrıca anne yaşı, doğum sayısı ve gebelik haftası değerlendirildi. Sonuç ve Öneriler:Maternal vitamin B12 düzeyleri ile yenidoğan doğum ağırlığı ve baş çevresi uzunluğu arasında istatistiksel olarak anlamlı ilişki bulunmasına rağmen (p 0,05). Çalışmada maternal birinci trimester B12 eksikliğinin yenidoğanda prematürite ve diğer ve antropometrik ölçümleri ile ilişkili olduğu belirlendi.

Background: Intestinal microbiota play a role in the health and performance of athletes, and can be influenced by probiotics. Thus, in this study, we aimed to investigate the effect of the use of probiotics combined with chronic exercise on the thiol/disulfide homeostasis, a novel marker of oxidative stress. Methods: Male Wistar rats were randomly divided into four groups: control (Cn), exercise (Ex), probiotics (P), and probiotics + exercise (PEx). A capsule containing 6 × 10⁸ CFU of L. rhamnosus, L. paracasei, L. acidophilus, and B. lactis was given daily for eight weeks to all the experimental animals. The total thiol (TT, μmol/L) and native thiol (NT, μmol/L) concentrations were measured to determine the oxidative stress parameters. The dynamic disulfide (DD, %), reduced thiol (RT, %), oxidized thiol (OT, %), and thiol oxidation reduction (TOR, %) ratios were analyzed. Results: The TT level was found to be significantly higher in the Ex group (p = 0.047, η² = 0.259). The DD level, a marker of oxidation, was significantly lower in the PEx group (p = 0.042, η² = 0.266); the highest value of this parameter was found in the Ex group. The use of probiotics alone had no effect on thiol/disulfide homeostasis. Conclusions: We showed, for the first time, that probiotics administered “with exercise” decreased dynamic disulfide and significantly reduced oxidative damage. Therefore, we speculate that the use of probiotics in sports involving intense exercise might be beneficial to reduce oxidative stress.