Amyotrophic lateral sclerosis is a devastating neurodegenerative disease characterized by the gradual loss of motor neurons in the brain and spinal cord, leading to progressive motor function decline. Unfortunately, there is no effective treatment, and its increasing prevalence is linked to an aging population, improved diagnostics, heightened awareness, and changing lifestyles. In the gastrointestinal system, the gut microbiota plays a vital role in producing metabolites, neurotransmitters, and immune molecules. Short-chain fatty acids, of interest for their potential health benefits, are influenced by a fiber- and plant-based diet, promoting a diverse and balanced gut microbiome. These fatty acids impact the body by binding to receptors on enteroendocrine cells, influencing hormones like glucagon-like peptide-1 and peptide YY, which regulate appetite and insulin sensitivity. Furthermore, these fatty acids impact the blood–brain barrier, neurotransmitter levels, and neurotrophic factors, and directly stimulate vagal afferent nerves, affecting gut–brain communication. The vagus nerve is a crucial link between the gut and the brain, transmitting signals related to appetite, inflammation, and various processes. Dysregulation of this pathway can contribute to conditions like obesity and irritable bowel syndrome. Emerging evidence suggests the complex interplay among these fatty acids, the gut microbiota, and environmental factors influences neurodegenerative processes via interconnected pathways, including immune function, anti-inflammation, gut barrier, and energy metabolism. Embracing a balanced, fiber-rich diet may foster a diverse gut microbiome, potentially impacting neurodegenerative disease risk. Comprehensive understanding requires further research into interventions targeting the gut microbiome and fatty acid production and their potential therapeutic role in neurodegeneration.

Brain tumours are a serious concern among both physicians and patients. The most feared brain tumour is glioblastoma (GBM) due to its heterogeneous histology, substantial invasive capacity, and rapid postsurgical recurrence. Even in cases of early management consisting of surgery, chemo-, and radiotherapy, the prognosis is still poor, with an extremely short survival period. Consequently, researchers are trying to better understand the underlying pathways involved in GBM development in order to establish a more personalised approach. The latest focus is on molecular characterisation of the tumour, including analysis of extracellular vesicles (EVs), nanostructures derived from both normal and pathological cells that have an important role in intercellular communication due to the various molecules they carry. There are two types of EV based on their biogenesis, but exosomes are of particular interest in GBM. Recent studies have demonstrated that GBM cells release numerous exosomes whose cargo provides them the capacity to facilitate tumour cell invasion and migration, to stimulate malignant transformation of previously normal cells, to increase immune tolerance towards the tumour, to induce resistance to chemotherapy, and to enhance the GBM vascular supply. As exosomes are specific to their parental cells, their isolation would allow a deeper perspective on GBM pathogenesis. A new era of molecular manipulation has emerged, and exosomes are rapidly proving their value not only as diagnostic and prognostic markers, but also as tools in therapies specifically targeting GBM cells. Nonetheless, further research will be required before exosomes could be used in clinical practice. This review aims to describe the structural and functional characteristics of exosomes and their involvement in GBM development, diagnosis, prognosis and treatment.

Amyotrophic lateral sclerosis (ALS) is a grievous neurodegenerative disease whose survival is limited to only a few years. In spite of intensive research to discover the underlying mechanisms, the results are fairly inconclusive. Multiple hypotheses have been regarded, including genetic, molecular, and cellular processes. Notably, oxidative stress has been demonstrated to play a crucial role in ALS pathogenesis. In addition to already recognized and exhaustively studied genetic mutations involved in oxidative stress production, exposure to various environmental factors (e.g., electromagnetic fields, solvents, pesticides, heavy metals) has been suggested to enhance oxidative damage. This review aims to describe the main processes influenced by the most frequent genetic mutations and environmental factors concurring in oxidative stress occurrence in ALS and the potential therapeutic molecules capable of diminishing the ALS related pro-oxidative status.

Amyotrophic lateral sclerosis (ALS) is a devastating neurodegenerative disease characterized by progressive loss of motor neurons. Emerging evidence suggests a potential link between metabolic dysregulation and ALS pathogenesis. This study aimed to investigate the relationship between metabolic hormones and disease progression in ALS patients. A cross-sectional study was conducted involving 44 ALS patients recruited from a tertiary care center. Serum levels of insulin, total amylin, C-peptide, active ghrelin, GIP (gastric inhibitory peptide), GLP-1 active (glucagon-like peptide-1), glucagon, PYY (peptide YY), PP (pancreatic polypeptide), leptin, interleukin-6, MCP-1 (monocyte chemoattractant protein-1), and TNFα (tumor necrosis factor alpha) were measured, and correlations with ALSFRS-R, evolution scores, and biomarkers were analyzed using Spearman correlation coefficients. Subgroup analyses based on ALS subtypes, progression pattern of disease, and disease progression rate patterns were performed. Significant correlations were observed between metabolic hormones and ALS evolution scores. Insulin and amylin exhibited strong correlations with disease progression and clinical functional outcomes, with insulin showing particularly robust associations. Other hormones such as C-peptide, leptin, and GLP-1 also showed correlations with ALS progression and functional status. Subgroup analyses revealed differences in hormone levels based on sex and disease evolution patterns, with male patients showing higher amylin and glucagon levels. ALS patients with slower disease progression exhibited elevated levels of amylin and insulin. Our findings suggest a potential role for metabolic hormones in modulating ALS progression and functional outcomes. Further research is needed to elucidate the underlying mechanisms and explore the therapeutic implications of targeting metabolic pathways in ALS management.

Background: Glioblastoma multiforme (GBM) is the most aggressive brain tumor that occurs in adults. In spite of prompt diagnosis and rapidly administered treatment, the survival expectancy is tremendously poor. Extensive research has been performed in order to establish factors to predict the outcome of GBM patients; however, worldwide accepted prognostic markers are still lacking. Methods: We retrospectively assessed all adult patients who were diagnosed with primary GBM and underwent surgical treatment during a three-year period (January 2017–December 2019) in the Neurosurgery Department of the Emergency Clinical County Hospital of Târgu Mureș, Romania. Our aim was to find any statistically relevant connections between clinical, imagistic, and histopathological characteristics and patients’ survival. Results: A total of 75 patients were eventually included in our statistical analysis: 40 males and 35 females, with a median age of 61 years. The mean tumor dimension was 45.28 ± 15.52 mm, while the mean survival rate was 4 ± 6.75 months. A univariate analysis demonstrated a statistically significant impact of tumor size, pre-, and postoperative KPSI on survival rate. In addition, a Cox multivariate assessment strengthened previous findings regarding postoperative KPSI (regression coefficient −0.03, HR 0.97, 95% CI (HR) 0.96–0.99, p = 0.002) as a favorable prognostic factor and GBM size (regression coefficient 0.03, HR 1.03, 95% CI (HR) 1.01–1.05, p = 0.005) as a poor prognostic marker for patients’ survival. Conclusions: The results of our retrospective study are consistent with prior scientific results that provide evidence supporting the importance of clinical (quantified by KPSI) and imagistic (particularly tumor dimensions) features as reliable prognostic factors in GBM patients’ survival.

Objective : Peripheral blood mononuclear cells (PBMC) are extremely important in the body’s immune response. Their isolation represents a major step in many immunological experiments. In this two phase study, we aimed to establish an optimum protocol for PBMC isolation by density-gradient centrifugation. Methods : During Phase-1, we compared two commercially available PBMC isolation protocols, Stemcell Technologies (ST) and Miltenyi Biotec (MB), in terms of PBMC recovery and purity. Twelve blood samples were assigned to each protocol. Each sample was divided in three subsamples of 1ml, 2ml and 3ml in order to assess the influence of blood sample volume on isolation performance. During Phase-2, a hybrid protocol was similarly tested, processing six blood samples. Additionally, we performed a flow cytometric analysis using an Annexin-V/Propidium-Iodide viability staining protocol. Results : Phase-1 results showed that, for all subsample volumes, ST had superior PBMC recovery (mean values: 56%, 80% and 87%, respectively) compared to MB (mean values: 39%, 54% and 43%, respectively). However, platelet removal was significantly higher for MB (mean value of 96.8%) than for ST (mean value of 75.2%). Regarding granulocyte/erythrocyte contamination, both protocols performed similarly, yielding high purity PBMC (mean values: 97.3% for ST and 95.8% for MB). During Phase-2, our hybrid protocol yielded comparable results to MB, with an average viability of 89.4% for lymphocytes and 16.9% for monocytes. Conclusions : ST yields higher cell recovery rates and MB excels at platelet removal, while the hybrid protocol is highly similar to MB. Both cell recovery and viability increase with blood sample volume.