Chronic stress, even stress of a moderate intensity related to daily life, is widely acknowledged to be a predisposing or precipitating factor in neuropsychiatric diseases. There is a clear relationship between disturbances induced by stressful stimuli, especially long-lasting stimuli, and cognitive deficits in rodent models of affective disorders. Regular physical activity has a positive effect on the central nervous system (CNS) functions, contributes to an improvement in mood and of cognitive abilities (including memory and learning), and is correlated with an increase in the expression of the neurotrophic factors and markers of synaptic plasticity as well as a reduction in the inflammatory factors. Studies published so far show that the energy challenge caused by physical exercise can affect the CNS by improving cellular bioenergetics, stimulating the processes responsible for the removal of damaged organelles and molecules, and attenuating inflammation processes. Regular physical activity brings another important benefit: increased stress robustness. The evidence from animal studies is that a sedentary lifestyle is associated with stress vulnerability, whereas a physically active lifestyle is associated with stress resilience. Here, we have performed a comprehensive PubMed Search Strategy for accomplishing an exhaustive literature review. In this review, we discuss the findings from experimental studies on the molecular and neurobiological mechanisms underlying the impact of exercise on brain resilience. A thorough understanding of the mechanisms underlying the neuroprotective potential of preconditioning exercise and of the role of exercise in stress resilience, among other things, may open further options for prevention and therapy in the treatment of CNS diseases.

A number of case-control studies regarding the association of the polymorphisms in the programmed cell death 1 (PD-1) and programmed cell death ligand 1 (PD-L1) genes with the risk of cancer have yielded inconsistent findings. Therefore, we have conducted a comprehensive, updated meta-analysis study to identify the impact of PD-1 and PD-L1 polymorphisms on overall cancer susceptibility. The findings revealed that PD-1 rs2227981 and rs11568821 polymorphisms significantly decreased the overall cancer risk (Odds Ratio (OR) = 0.82, 95% CI = 0.68–0.99, p = 0.04, TT vs. CT+CC; OR = 0.79, 95% CI = 0.67–0.94, p = 0.006, AG vs. GG, and OR = 0.82, 95% CI = 0.70–0.96, p = 0.020, AG+AA vs. GG, respectively), while PD-1 rs7421861 polymorphism significantly increased the risk of developing cancer (OR = 1.16, 95% CI = 1.02–1.33, p = 0.03, CT vs. TT). The PD-L1 rs4143815 variant significantly decreased the risk of cancer in homozygous (OR = 0.62, 95% CI = 0.41–0.94, p = 0.02), dominant (OR = 0.70, 95% CI = 0.50–0.97, p = 0.03), recessive (OR = 0.76, 95% CI = 0.60–0.96, p = 0.02), and allele (OR = 0.78, 95% CI = 0.63–0.96, p = 0.02) genetic models. No significant association between rs2227982, rs36084323, rs10204525, and rs2890658 polymorphisms and overall cancer risk has been found. In conclusions, the results of this meta-analysis have revealed an association between PD-1 rs2227981, rs11568821, rs7421861, as well as PD-L1 rs4143815 polymorphisms and overall cancer susceptibility.

In this study, we aim to assess and examine cognitive functions in Parkinson’s Disease patients using EEG recordings, with a central focus on characteristics associated with a cognitive decline. Based on neuropsychological evaluation using Mini-Mental State Examination, Montreal Cognitive Assessment, and Addenbrooke’s Cognitive Examination-III, 98 participants were divided into three cognitive groups. All the particpants of the study underwent EEG recordings with spectral analysis. The results revealed an increase in the absolute theta power in patients with Parkinson’s disease dementia (PD-D) compared to cognitively normal status (PD-CogN, $p=0.00997$) and a decrease in global relative beta power in PD-D compared to PD-CogN ($p=0.0413$). An increase in theta relative power in the left temporal region ($p=0.0262$), left occipital region ($p=0.0109$), and right occipital region ($p=0.0221$) were observed in PD-D compared to PD-N. The global alpha/theta ratio and global power spectral ratio significantly decreased in PD-D compared to PD-N (p = 0.001). In conclusion, the increase in relative theta power and the decrease in relative beta power are characteristic changes in EEG recordings in PD patients with cognitive impairment. Identifying these changes can be a useful biomarker and a complementary tool in the neuropsychological diagnosis of cognitive impairment in Parkinson’s Disease.

Physical activity impacts brain functions, but the direct mechanisms of this effect are not fully recognized or understood. Among multidimensional changes induced by physical activity, brain fatty acids (FA) appear to play an important role; however, the knowledge in this area is particularly scarce. Here we performed global metabolomics profiling of the hippocampus and the frontal cortex (FC) in a model of voluntary running in mice. Examined brain structures responded differentially to physical activity. Specifically, the markers of the tricarboxylic acid (TCA) cycle were downregulated in the FC, whereas glycolysis was enhanced in the hippocampus. Physical activity stimulated production of myristic, palmitic and stearic FA; i.e., the primary end products of de novo lipogenesis in the brain, which was accompanied by increased expression of hippocampal fatty acid synthase (FASN), suggesting stimulation of lipid synthesis. The changes in the brain fatty acid profile were associated with reduced anxiety level in the running mice. Overall, the study examines exercise-related metabolic changes in the brain and links them to behavioral outcomes.

Anthropometric measurements and indices are a simple and inexpensive method to assess normal physical development and quickly identify the risk of diseases. The aim of the study was to verify the sensitivity (Se) and specificity (Sp) of selected anthropometric indices in a group of women over 40 years. The study included 87 women (group I—40 to 49 years, group II—50 to 59 years, group III—60 to 69 years, and group IV—70 to 79 years). Anthropometric characteristics were measured: body mass (BM), body height (BH), waist circumference (WC), and hip circumference (HC). Body mass index (BMI), body adiposity index (BAI), waist-hip ratio (WHR), and waist-to-height ratio (WHTR) were calculated. The percentage of fat tissue (FT) and visceral fat volume (FV) were evaluated using DEXA. A decrease in mean BH with an increase in the mean WC, WHR, and WHTR in subsequent decades. There were strong statistically significant correlations between FT and most indicators (except for WHR). FV was correlated at a strong or moderate level with most parameters. In the group of women aged 40 to 80 years, the most favorable AUC was obtained for WC, followed by BMI. BAI can be recommended as a complementary indicator to BMI.

Physical activity (PA) is a factor that may have an influence on the symptoms of Parkinson’s disease (PD). The aim of this study was to identify the potential determinants of spontaneous PA in a PD patient group. A total of 134 PD patients aged 65.2 ± 9.2 years with a Hoehn–Yahr scale score ≤4 and a Mini Mental State Examination (MMSE) score ≥24 were examined. For the study’s purposes, the authors analyzed age, sex, education, history of PD, dopaminergic treatment, the severity of PD symptoms using Unified Parkinson’s Disease Rating Scale (UPDRS), and Hoehn–Yahr scale. Additionally, all participants were evaluated through a set of scales for specific neuropsychiatric symptoms including depression, anxiety, apathy, fatigue, and sleep disorders. A linear regression analysis was used with backward elimination. In the total explanatory model, for 12% of the variability in activity (R² = 0.125; F(16.133) = 2.185; p < 0.01), the significant predictor was starting therapy with the dopamine agonist (DA) (β= 0.420; t= 4.068; p = 0.000), which was associated with a longer duration of moderate PA. In the total explanatory model, for more than 13% of the variance in time spent sitting (R² = 0.135; F(16.130) = 2.267; p < 0.01), the significant predictors were secondary education and the results of the UPDRS. The patients with secondary and vocational education, those starting treatment with DA and those with a less severe degree of Parkinson’s symptoms (UPDRS), spent less time sitting in a day. It is possible to identify determinants of spontaneous PA. It may elucidate consequences in terms of influence on modifiable conditions of PA and the proper approach to patients with unmodifiable PA factors.