Research suggests that physical exercise is associated with prevention and management of chronic diseases. The influence of physical exercise on brain function and metabolism and the mechanisms involved are well documented in the literature. This review provides a comprehensive overview of the potential implications of physical exercise and the molecular benefits of exercise in Parkinson's disease, Alzheimer's disease, and epilepsy. Here, we present an overview of the effects of exercise on various aspects of metabolism and brain function. To this end, we conducted an extensive literature search of the PubMed, Web of Science, and Google Scholar databases to identify articles published in the past two decades. This review delves into key aspects including the modulation of neuroinflammation, neurotrophic factors, and synaptic plasticity. Moreover, we explored the potential role of exercise in advancing therapeutic strategies for these chronic diseases. In conclusion, the review highlights the importance of regular physical exercise as a complementary non-pharmacological treatment for individuals with neurological disorders such as Alzheimer's, Parkinson's disease, and epilepsy.

Recent studies have suggested that therapies with stem cells and amniotic membrane can modulate the inflammation following an ischemic injury in the heart. This study evaluated the effects of bone-marrow mononuclear cells (BMMC) and acellular human amniotic membrane (AHAM) on cardiac function and NLRP3 complex in a rat model of heart failure.On the 30th day,the echocardiographic showed improvements on ejection fraction and decreased pathological ventricular remodeling on BMMC and AHAM groups.Oxidative stress analysis was similar between the three groups,and the NLRP3 inflammasome activity were not decreased with the therapeutic use of both BMMC and AHAM,in comparison to the control group.

Glioblastoma (GBM) is an aggressive, common brain cancer known to disrupt redox biology, affecting behavior and DNA integrity. Past research remains inconclusive. To further understand this, an investigation was conducted on physical training’s effects on behavior, redox balance, and genomic stability in GBMA models. Forty-seven male C57BL/6J mice, 60 days old, were divided into GBM and sham groups (n = 15, n = 10, respectively), which were further subdivided into trained (Str, Gtr; n = 10, n = 12) and untrained (Sut, Gut; n = 10, n = 15) subsets. The trained mice performed moderate aerobic exercises on a treadmill five to six times a week for a month while untrained mice remained in their enclosures. Behavior was evaluated using open-field and rotarod tests. Post training, the mice were euthanized and brain, liver, bone marrow, and blood samples were analyzed for redox and genomic instability markers. The results indicated increased latency values in the trained GBM (Gtr) group, suggesting a beneficial impact of exercise. Elevated reactive oxygen species in the parietal tissue of untrained GBM mice (Gut) were reduced post training. Moreover, Gtr mice exhibited lower tail intensity, indicating less genomic instability. Thus, exercise could serve as a promising supplemental GBM treatment, modulating redox parameters and reducing genomic instability.

Background: Rheumatoid arthritis-associated interstitial lung disease (RA-ILD) is heterogeneous. Forced vital capacity (FVC) decline and high-resolution CT (HRCT) pattern are widely used as prognostic markers, but the natural history of RA-ILD identified in rheumatology clinics, particularly in mild disease, remains insufficiently described. Methods: We conducted a prospective, multicentre cohort study across three Brazilian centres. Adults with RA-ILD were followed every 6 months for 24 months. Pulmonary function tests, HRCT, 6 min walk test and King’s Brief Interstitial Lung Disease health-related quality-of-life questionnaire were performed at baseline, 12 and 24 months. Blood biomarkers were assessed at baseline, 6 and 18 months. HRCT scans were independently reviewed by two chest radiologists and analysed using densitometry-based quantitative CT (QCT). Pulmonary fibrosis was qualitatively defined by unequivocal traction bronchiectasis and/or honeycombing on HRCT. Results: Ninety-five subjects were included (mean age 63±10 years; 81% female). Pulmonary fibrosis was present in 80%, although only 20% were classified as definite or probable usual interstitial pneumonia (κ=0.52). Individuals with fibrosis had lower FVC (75%±17 vs 86%±15, p=0.02) and worse QCT measures (%high-attenuation areas −600 to −250 HU 12.1±6.6 vs 5.5±0.8, p<0.001; lung volume 3407±958 mL vs 4077±923 mL, p=0.015). In 24 months, FVC and QCT measures remained stable. Eight subjects (8%) died. Deaths were not preceded by measurable functional or radiological decline. Health-related quality-of-life scores and blood biomarkers remained unchanged. Conclusions: In this predominantly mild RA-ILD cohort, pulmonary function and QCT metrics remained stable over 2 years despite an 8% mortality rate. The absence of preceding decline in conventional prognostic markers suggests potential limitations of current monitoring strategies, although our findings should be interpreted as hypothesis-generating. Trial registration number: NCT04136223 .

Glioblastoma is a very aggressive and common brain cancer. Previous studies have shown that changes in the brain's redox biology interfere with behavioral patterns and DNA damage. The results of these studies, however, have been inconclusive. To evaluate the effects of a physical training program on behavioral aspects, redox and genomic stability parameters in animals exposed to an experimental model of GBM. Forty-seven male C57BL/6J mice aged sixty days were randomly selected and divided into two groups (GBM and sham/placebo surgery), which were subsequently divided into four groups: untrained sham (Sut, n = 10), untrained GBM (Gut, n = 15), trained sham (Str, n = 10), and trained GBM (Gtr, n = 12). The trained animals performed 3 sessions, followed by a rest day, of moderate aerobic exercise on a treadmill for four consecutive weeks, while the untrained animals were kept in boxes during the experimental period. Behavioral indicators were evaluated with open field and rota rod tests. After the last training session, the animals were euthanized and brain, liver, bone marrow, and blood were collected for analysis of redox and genomic instability markers. The results showed higher latency values were sustained by the exercise in Gtr. The elevated levels of total reactive oxygen species in the parietal tissue of Gut animals were reversed after physical training. The Gtr group had a lower tail intensity. Physical exercise is a promise as an adjunctive therapy for the management of GBM by modulating redox parameters in the parietal tissue and reduces the genomic instability in liver and blood.