In the last decades, an important role of cerebrospinal fluid (CSF) biomarkers for Alzheimer disease (AD) diagnosis has emerged. The evaluation of the triad consisting of 42 aminoacid-long amyloid-beta peptide (Aβ42), total Tau (tTau) and Tau phosphorylated at threonine 181 (pTau) have been recently integrated into the research diagnostic criteria of AD. For a long time, the enzyme-linked immunosorbent assay (ELISA) has represented the most commonly used method for the measurement of CSF biomarkers levels. This study aimed to assess the diagnostic accuracy of CSF biomarkers, namely Aβ42, tTau and pTau and their ratio, measured by fully automated CLEIA assay (Lumipulse). We included 96 patients clinically diagnosed as AD (48) and non-AD (48). All CSF biomarkers levels were measured on Lumipulse G1200 fully automated platform (Fujirebio Inc. Europe, Gent, Belgium). Aβ42 levels, 42/40 ratio, 42/tTau ratio, 42/PTau ratio were significantly reduced, and tTau and PTau levels were significantly increased in AD patients in comparison with non-AD patients. The receiving operator curve (ROC) analysis showed good diagnostic accuracy of all CSF biomarkers and their ratios for discriminating AD patients from non-AD patients, with 42/40 ratio having the best AUC (0.724, 95%CI 0.619–0.828; p < 0.001). Our findings support the use of CSF biomarkers measured by CLEIA method on a fully automated platform for AD diagnosis.

: Chronic neuroinflammation is a common feature of the pathogenic mechanisms involved in various neurodegenerative age-associated disorders, such as Alzheimer's disease, multiple sclerosis, Parkinson’s disease, and dementia. : In particular, persistent low-grade inflammation may disrupt the brain endothelial barrier and cause a significant increase of pro-inflammatory cytokines and immune cells into the cerebral tissue that, in turn, leads to microglia dysfunction and loss of neuroprotective properties. : Nowadays, growing evidence highlights a strong association between persistent peripheral inflammation, as well as metabolic alterations, and neurodegenerative disorder susceptibility. The identification of common pathways involved in the development of these diseases, which modulate the signalling and immune response, is an important goal of ongoing research. : The aim of this review is to elucidate which inflammation-related molecules are robustly associated with the risk of neurodegenerative diseases. Of note, peripheral biomarkers may represent direct measures of pathophysiologic processes common of aging and neuroinflammatory processes. In addition, molecular changes associated with the neurodegenerative process might be present many decades before the disease onset. Therefore, the identification of a comprehensive markers panel, closely related to neuroinflammation, could be helpful for the early diagnosis, and the identification of therapeutic targets to counteract the underlying chronic inflammatory processes.

Microplastics (MPs), emerging contaminants of significant global concern, have a substantially increased environmental impact due to their biological persistence and accumulation in the body. Exposure to MPs has been associated with oxidative stress, systemic inflammation, and cellular dysfunction, notably affecting critical tissues such as the stomach, colon, and brain. This review explores the correlation between MPs and cancer risk along the gastric–colon–brain axis, identifying the signaling pathways altered by MP exposure. Furthermore, it highlights the role of functional nutrition and bioactive flavonoids—including chlorogenic acid, coumaric acid, and naringin—as well as the use of highly bioavailable combined polyphenol nanoparticles as potential detoxifying agents. Functional nutrients are effective in enhancing cellular resilience against reactive oxygen species (ROS) production and MP-induced toxicity, offering protective effects at the gastric, intestinal, and brain barriers. Activation of the Nrf2 pathway by bioactive compounds promotes the expression of detoxifying enzymes, suggesting a promising nutritional strategy to mitigate MP-related damage. This review underscores how functional nutrition may represent a viable therapeutic approach to reduce the harmful effects of MP exposure. The integration of advanced technologies—such as microfluidic systems, organ-on-a-chip platforms, and machine learning—and the identification of key molecular targets lay the foundation for developing preventive and personalized medicine strategies aimed at lowering the risk of environmentally induced carcinogenesis.

Sepsis is one of the most dangerous post-operative complications. Recently, Monocyte Distribution Width (MDW), a blood test parameter able to measure morphological changes in monocytes, has been proposed and investigated as a new promising biomarker of sepsis. The aim of our study was to evaluate if MDW can be influenced by surgery to better understand if it could be use as a sepsis marker. All clinical and laboratories data were collected of all patients admitted from April to August 2021 to the Unit of Urology of our Department for elective kidney and ureteral stones surgery. The blood samples collected to evaluate MDW of each patient were analyzed on the UniCel DxH 900 analyzer (Beckman Coulter, Inc., USA), with an MDW value of 23 considered as significative value. Times of collection of blood samples were before surgery (BS), after surgery (AS) and at discharge time (DT) In all 66 patients enrolled in this study, while White Blood Cells (WBC) significantly increased after surgery (BS:7.95x109/L vs AS:11.4x109/L; p<0.001) with a trend to normalization at discharge (AS:11.40x109/L vs DT:9.90x109/L; p:0.021), there were no statistically significative differences for MDW (BS:17.6 vs AS:18.1; p:1) before and after surgery, as well comparing before surgery and at the time of discharge (BS:17.6 vs DT:18.5; p:0.237). In conclusion, MDW is not affected by surgical procedures and is easily measurable when compared to other biomarkers, considering that is part of a routine CBC. For these reasons, MDW could be a valid, cost-effective and fast biomarker to predict the risk of post-operative sepsis in elective surgery

Rare genetic ocular diseases represent a heterogeneous group of disorders that significantly impair visual function and quality of life. Despite their clinical relevance, many of these conditions remain insufficiently characterized due to complex molecular mechanisms and diagnostic limitations. Recent advances in molecular diagnostics, particularly Next-Generation Sequencing (NGS), have enabled comprehensive and accurate identification of pathogenic variants, offering novel insights into genotype–phenotype correlations and supporting precision medicine approaches. In parallel, the use of alternative biological matrices such as tear fluid has emerged as a promising non-invasive strategy for biomarker discovery and disease monitoring. Tear-based omics, including proteomics and transcriptomics, have identified diagnostic signatures and pathogenic mediators such as non-coding RNAs, microRNAs, and tRNA-derived fragments (tRFs). Among these, tRF-1001 has shown potential both as a biomarker and therapeutic target in ocular neovascular conditions through its modulation of angiogenic pathways. The objective of this review is to show the integration of two rapidly advancing yet frequently isolated fields: next-generation sequencing-based genomics and tear-fluid molecular profiling, positioning them as complementary foundations of precision ophthalmology for rare inherited retinal and optic nerve disorders. Previous reviews have mainly concentrated on either genetic diagnosis or ocular surface biomarkers separately; however, we have introduced a convergent model wherein genomic data furnish diagnostic and prognostic clarity, while tear-omics deliver dynamic, minimally invasive assessments of disease activity, treatment efficacy, and persistent neurovascular stress. By explicitly connecting these two aspects, we have delineated how multi-matrix, multi-omics approaches can expedite early diagnosis, facilitate personalized longitudinal monitoring, and direct focused treatment interventions in rare ocular genetic illnesses.