Autism spectrum disorder (ASD) is a neurological condition with an increasingly high incidence rate due to more effective diagnostic tools. The symptoms of ASD vary widely, making it difficult to detect. It represents a spectrum of alterations ranging from mild indications to severe impairments. Given this clinical presentation, each patient should be treated on an individual basis. Nevertheless, certain neuropathological changes are common, although the background of this disorder remains still unknown. Therefore, some research aimed at better understanding the pathology of the neurological alterations in ASD, as well as the possibilities for early diagnosis and treatment of this disorder, is urgently needed. This study presents the results of the studies on some selected proteins such as Tau protein, NFL, BDNF as well as IGF-1 that appear to be the best protein candidates for better understanding the causes of autism, as well as for use as fluid biomarkers in diagnosis and monitoring of ASD.

Colorectal cancer (CRC) remains a major global health challenge, primarily due to late-stage diagnosis and high metastatic potential. Effective management requires novel diagnostic and prognostic strategies, with a growing focus on molecular biomarkers. A Disintegrin and Metalloproteinase (ADAM) proteins, characterized by unique proteolytic activity, play a fundamental role in tumorigenesis by regulating tumor growth, epithelial-mesenchymal transition (EMT), and metastasis. Based on recent investigations, among all ADAMs, ADAM8, ADAM9, ADAM12, ADAM15, and ADAM17 have been proved to play an important role in the CRC pathogenesis. Thus, this review underscores the potential of selected ADAM family members as promising candidates for biomarkers of CRC. Elevated ADAM8, ADAM9, ADAM12 and ADAM17 levels were observed in CRC tissues and correlated with more advanced tumor stage, while increased serum ADAM15 concentrations associated with the presence distant metastases. Moreover, ADAM9, ADAM12, ADAM15 and ADAM17 levels were associated with poorer survival, whereas ADAM8 overexpression was found to be independent prognostic factor for CRC patients' survival. In addition, the measurement of serum ADAM15 concentrations, especially in combination with well-established tumor marker-CEA improved the diagnosis of patients with this malignancy. In conclusion, selected ADAM are critical contributors to the development and progression of CRC, affecting tumor growth, EMT, and metastasis. ADAM8, ADAM9, ADAM12, ADAM15 and ADAM17 were identified as promising biomarkers for the assessment of CRC progression and proved to be prognostic indicators for patients' survival. Further validation through large prospective studies and standardized assays is necessary to establish their potential in clinical practice.

Background: Neurofilament light chain (NfL) has emerged as a highly sensitive biomarker of neuroaxonal injury across diverse neurological disorders. This narrative review synthesizes current evidence regarding its diagnostic, prognostic, and therapeutic-monitoring utility, while outlining major clinical limitations and emphasizing the complementary role of glial fibrillary acidic protein (GFAP). Summary: NfL concentrations increase following axonal damage and correlate with inflammatory activity, lesion burden, and long-term disability progression in multiple sclerosis. Elevated levels also reflect neurodegeneration in Alzheimer’s disease, predict disease severity and survival in amyotrophic lateral sclerosis, and are associated with motor and cognitive decline in Parkinson’s disease and multiple system atrophy. In acute neurological conditions, including traumatic brain injury and stroke, NfL serves as a robust indicator of the extent of neuronal injury. Interpretation is constrained, however, by substantial physiological variability related to age, renal function, body mass index, and comorbidities, limiting the utility of absolute cut-off values. GFAP provides complementary information by capturing astrocytic damage, and the GFAP/NfL ratio may aid in differentiating multiple sclerosis from neuromyelitis optica spectrum disorder. Integration of NfL with multimodal biomarkers-such as GFAP, tau proteins, proteomic and metabolomic signatures, and advanced neuroimaging-may enhance diagnostic specificity and prognostic accuracy. Key Messages: Future research priorities include establishing age-adjusted reference intervals, validating longitudinal thresholds, and incorporating NfL into therapeutic monitoring frameworks. Advances in these areas are expected to improve diagnostic precision and support broader clinical implementation of NfL.

Psoriasis is a complex, chronic, inflammatory condition which affects skin, nails and joints. In our study, we enrolled fifty patients with psoriasis and twenty-eight healthy individuals. Serum samples were collected both from the psoriatic patients (study group) and patients with an inguinal hernia (control group). The level of chemerin in the serum was measured by enzyme-linked immunosorbent assay. In the current research we noticed that serum chemerin concentration was significantly higher in the patients suffering from psoriasis in comparison to the controls. Importantly, we observed a positive, statistically significant correlation between the serum chemerin levels and C-reactive protein, as well as chemerin levels and platelets in the serum of patients affected by psoriasis. However, we did not observe a significant correlation between chemerin level and the Psoriasis Area and Severity Index score. To sum up, our results revealed that chemerin levels vary significantly in the serum of patients with psoriasis in contrast to the control group.

Tight junctions (TJs) are essential for preserving cell polarity and controlling permeability. It has been disclosed that TJ proteins, especially specific claudins (CLDNs), are linked to inflammation and contribute to the emergence of diverse cancers, including brain malignancies. Aggressive gliomas, including glioblastoma multiforme (GBM), remain among the most common and deadly central nervous system (CNS) tumors worldwide, despite considerable advances in diagnostic and therapeutic approaches. These types of tumors are characterized by high rates of recurrence and metastasis, resulting in poor outcomes and prognosis. The pathophysiology of brain cancer is closely linked to CLDNs, as these specific proteins play critical roles in tumor cell proliferation, invasion, and disruption of the blood-brain barrier (BBB). Some studies reported the potential role of CLDNs in glioma progression and other neurological disorders. The purpose of this review is to highlight the significance of CLDNs in CNS tumors, especially their participation in the formation of malignant gliomas. Additionally, the diagnostic and prognostic importance of selected CLDNs has been assessed. Selected CLDNs, such as CLDN3 and CLDN4 promote GBM growth, proliferation and migration. Moreover, overexpression of CLDN3 support progression and metastasis of these malignancies, while reduced expression of CLDN1 and CLDN5 is observed in advanced gliomas. Presented results suggest that CLDNs may serve as biomarkers for diagnosis and prognosis as well as therapeutic targets in CNS tumors. Further investigation is essential to clarify their clinical relevance and therapeutic potential.

Psoriasis is a chronic, immune-mediated inflammatory disease that affects the skin, nails, joints, and cardiovascular system. In this study, involving 50 psoriatic patients and 28 healthy controls (patients with inguinal hernia), serum elafin levels were measured using enzyme-linked immunosorbent assay (ELISA). The results revealed significantly higher serum elafin levels in the psoriatic group compared to healthy individuals. Moreover, we observed a statistically significant positive correlation between serum elafin levels and the Psoriasis Area and Severity Index (PASI) scores. These findings indicate that elafin-a protein involved in psoriasis pathogenesis-is significantly altered in the serum of psoriatic patients and may be associated with disease severity.

Alzheimer's disease is the most common cause of dementia and one of the greatest challenges of current medicine. Its pathophysiology is complex, involving β-amyloid deposition, tau hyperphosphorylation, chronic neuroinflammation, and progressive neuronal loss. Despite the introduction of novel therapies, treatment efficacy remains limited, prompting the search for alternative therapeutic targets. One promising area of research focuses on matrix metalloproteinases-proteolytic enzymes involved in tissue remodeling, synaptic plasticity, and inflammatory responses. In the context of AD, MMPs may exert both protective effects, through amyloid degradation, and detrimental effects such as blood-brain barrier disruption and amplification of neuroinflammatory damage. Understanding the dual and context-dependent roles of MMPs may help explain past translational failures and enable the development of more selective, stage-dependent therapeutic strategies. This article is a narrative review summarizing current evidence on the roles of MMPs in AD, with a particular focus on their therapeutic modulation and potential implications for future clinical research. Insights into MMP biology may ultimately guide the design of interventions with improved efficacy and safety for patients with AD.

Tight junctions (TJs) are essential for preserving cell polarity and controlling permeability. It has been disclosed that TJ proteins, especially specific claudins (CLDNs), are linked to inflammation and contribute to the emergence of diverse cancers, including brain malignancies. Aggressive gliomas, including glioblastoma multiforme (GBM), remain among the most common and deadly central nervous system (CNS) tumors worldwide, despite considerable advances in diagnostic and therapeutic approaches. These types of tumors are characterized by high rates of recurrence and metastasis, resulting in poor outcomes and prognosis. The pathophysiology of brain cancer is closely linked to CLDNs, as these specific proteins play critical roles in tumor cell proliferation, invasion, and disruption of the blood-brain barrier (BBB). Some studies reported the potential role of CLDNs in glioma progression and other neurological disorders. The purpose of this review is to highlight the significance of CLDNs in CNS tumors, especially their participation in the formation of malignant gliomas. Additionally, the diagnostic and prognostic importance of selected CLDNs has been assessed. Selected CLDNs, such as CLDN3 and CLDN4 promote GBM growth, proliferation and migration. Moreover, overexpression of CLDN3 support progression and metastasis of these malignancies, while reduced expression of CLDN1 and CLDN5 is observed in advanced gliomas. Presented results suggest that CLDNs may serve as biomarkers for diagnosis and prognosis as well as therapeutic targets in CNS tumors. Further investigation is essential to clarify their clinical relevance and therapeutic potential.

Introduction:Gestational diabetes mellitus (GDM) is among the most common metabolic disorders during pregnancy, and early detection is key to reducing complications for both mother and child. Mass spectrometry-based metabolomics enables detailed metabolite profiling, offering opportunities not only for early diagnosis and risk prediction but also for understanding the pathophysiological mechanisms that drive the development of GDM. Methods:For the first time, an analysis of such a large number of metabolites was conducted: over 1,000 metabolites across 39 biochemical classes, including 912 lipids and 107 small molecules, were measured in first-trimester plasma from women with abnormal or normal fasting plasma glucose who later developed GDM, as well as from controls with normal glucose tolerance. Statistical analyses included Kruskal-Wallis ANOVA with Conover-Iman post hoc tests, Wilcoxon signed-rank tests for longitudinal changes, and ROC analysis to assess predictive and diagnostic performance. Spearman's rank correlations were used to examine relationships between metabolites and clinical parameters. Results:Distinct metabolic signatures in the first trimester were associated with later GDM development. A prognostic panel, including TG (18:1_36:6), Hex2Cer(d18:1/14:0), valine, PS(36:1), TG (17:2_36:3), p-cresol sulfate, and PC(O-42:4), accurately predicted GDM (AUC = 0.934). A diagnostic panel comprising PE (P-18:0/22:4), glycine-conjugated cholic acid, LPC (20:3), carnitine esters, and arginine detected early signs of carbohydrate metabolism issues (AUC = 0.821). Women with normal fasting glucose who later developed GDM exhibited significant lipid alterations, whereas those with early fasting irregularities showed a partially GDM-like profile. Correlation analyses revealed distinct inflammatory and hormonal networks, with TNF-α-induced lipid remodelling linked to early dysglycaemia. Conclusion:First-trimester metabolomic signatures hold significant promise for early prediction, diagnosis, and understanding of GDM, enabling personalised risk assessment and timely intervention during pregnancy.

Invasive cervical cancer is a very common cause of cancer death in women worldwide, primarily due to late detection of this cancer. The clinical manifestations of cervical cancer vary significantly and are difficult to predict. Finding new effective biomarkers for the early detection of cervical cancer is essential to reducing mortality. Small microRNA molecules have also recently emerged as potential biomarker candidates in the diagnosis of cervical cancer. Despite analytical limitations in microRNA assays and the lack of automated and standardized tests, validated and prospective systematic evaluation of this new parameter in cervical cancer deserves further development. This review describes the importance and potential usefulness of microRNAs in detecting cervical cancer at an early stage, monitoring the course of the disease, and assessing the effectiveness of treatment. The diagnostic importance of microRNAs is well documented in many publications, suggesting that, as microRNA research progresses, they may become a useful diagnostic tool for cervical cancer.

Background/Objectives: Adipokines and cytokines, secreted by adipocytes and immune cells, play key roles in metabolic and inflammatory processes. This study aimed to assess the association between salivary visfatin levels and metabolic dysfunction-associated steatotic liver disease (MASLD), determine a salivary visfatin cutoff associated with increased risk of this disease, and examine correlations among selected adipokines, cytokines, and gelatinases in serum and saliva of obese patients. Methods: The study included 65 participants (40 women and 25 men) with a body mass index (BMI) ranging from 30.0 to 39.9 kg/m2, who were divided into groups based on whether the salivary visfatin concentration exceeded the quantification limit (1.229 ng/mL). Body composition analysis was performed using the bioelectrical impedance method, quantitative assessment of hepatic steatosis was carried out using transient elastography, and the concentrations of selected adipokines, cytokines, and gelatinases were determined in serum and saliva. Results: A relationship was observed between lower BMI and salivary visfatin concentrations below the quantification limit (p = 0.017), and between the absence of MASLD and visfatin levels below the quantification threshold in saliva (p = 0.05). Higher concentrations of interleukin-1β (p = 0.003) and matrix metalloproteinase-2 (p = 0.019) in saliva, as well as interleukin-6 (p = 0.002) in serum, were observed in the group with salivary visfatin levels above the quantification limit. Correlations were found between salivary and serum IL-6 concentrations (r = 0.30; p = 0.016) and between serum resistin and salivary IL-6 levels (r = 0.24; p = 0.056), as well as between serum IL-6 and salivary MMP-2 concentrations (r = 0.24; p = 0.059). Conclusions: In this pilot study, salivary visfatin levels were found to differ between obese individuals with and without MASLD and to be associated with selected anthropometric parameters and inflammatory markers, but the observed associations are exploratory and require confirmation.

Psoriasis is a chronic inflammatory disorder with immunological, metabolic, and environmental components. It affects not only the skin but also the nails, joints, and vascular system. A total of 50 patients with psoriasis and 28 healthy controls took part in this study. Serum samples were gathered both from the psoriatic group and the control group. Serum zyxin concentrations were measured via enzyme-linked immunosorbent assay (ELISA). Our results revealed that serum zyxin amounts were significantly higher in patients with psoriasis compared with the controls. However, no statistically significant correlations were found between serum zyxin levels and inflammatory or metabolic parameters in the psoriasis group. Similarly, there was no significant correlation between zyxin level and disease severity as assessed by the Psoriasis Area and Severity Index (PASI) score. To sum up, our study demonstrates that serum zyxin levels are significantly elevated in patients with psoriasis compared with controls. Nevertheless, the precise role of zyxin in the aetiology of psoriasis remains unclear. Further research is needed to clarify the function of this protein in the disease process and to explore its potential as a therapeutic target.

Autism spectrum disorder (ASD) is classified as a neurodevelopmental disorder with an increasingly high incidence rate. Increasing awareness, changing diagnostic criteria and social attitudes, as well as financial considerations, will affect the prevalence of diagnosis. The symptoms of ASD vary widely, making it difficult to detect. It represents a spectrum of alterations ranging from mild indications to severe impairments and diagnosis is based on a very rigorous behavioral assessment. Nevertheless, certain neuropathological changes are common, although the background of this disorder remains still unknown. Therefore, some research aimed at better understanding the pathology of the neurological alterations in ASD, as well as the possibilities for early diagnosis and treatment of this disorder, is urgently needed. This review summarizes the current evidence on some selected proteins such as tau protein, NFL, and BDNF as well as IGF-1 that appear to be the best protein candidates for better understanding the causes of autism, as well as for use as fluid biomarkers in the diagnosis and monitoring of ASD.

Breast cancer (BC) is the most common type of cancer found in women. Detection of this cancer at an early stage is essential for effective treatment and a favorable prognosis. Potential early breast cancer biomarkers useful for diagnosing these tumors are microRNAs. These are small single-stranded RNA chains that can regulate the post-transcriptional expression of many different oncogenes. Cancer cells contain miRNAs that play a special role in the etiology of cancer development. The role of microRNAs in the initiation and development of breast cancer gives us great hope for the creation of molecular tools for early cancer detection. MicroRNAs are characterized by a high stability due to RNase, which protects them from degradation and enables their detection in various biological fluids. Researchers have described multiple serum microRNA signatures useful for detecting breast cancer. This review discusses the importance and potential usefulness of microRNAs in detecting breast cancer at an early stage, predicting the course of the disease, and assessing the effectiveness of treatment.

The role of amyloid beta peptide (Aβ) in memory regulation has been a subject of substantial interest and debate in neuroscience, because of both physiological and clinical issues. Understanding the dual nature of Aβ in memory regulation is crucial for developing effective treatments for Alzheimer’s disease (AD). Moreover, accurate detection and quantification methods of Aβ isoforms have been tested for diagnostic purposes and therapeutic interventions. This review provides insight into the current knowledge about the methods of amyloid beta detection in vivo and in vitro by fluid tests and brain imaging methods (PET), which allow for preclinical recognition of the disease. Currently, the priority in the development of new therapies for Alzheimer’s disease has been given to potential changes in the progression of the disease. In light of increasing amounts of data, this review was focused on the diagnostic and therapeutic employment of amyloid beta in Alzheimer’s disease.

Alzheimer’s disease (AD), a prevalent neurological illness, is the most common form of dementia worldwide. Given that AD symptoms manifest gradually, it is imperative to discover new biomarkers that support early diagnosis of this diseases. Some research indicates that Neutrophil gelatinase-associated lipocalin (NGAL) may influence a number of neurobiological processes, including inflammation occurring in the central nervous system. Moreover, this protein was discovered in brains of AD patients. Literature data suggests that NGAL could be a potential biomarker of severity of Alzheimer’s disease. Therefore, the purpose of our research was to assess the usefulness of the measuring of the concentration of soluble NGAL in cerebrospinal fluid in the diagnosis of AD patients as well as compare it with classical AD biomarkers. The concentrations of NGAL were measured in cerebrospinal fluid (CSF) of 20 AD patients and 20 non-demented controls using ELISA method. Classical biomarkers, such as Aβ-42, Aβ-42/Aβ-40, tau and pTau181 were assessed by immunoenzyme assays. NGAL concentrations were significantly higher in AD patients in comparison to non-demented controls. Additionally, increased CSF levels of NGAL correlated positively with Tau and pTau181 proteins as well as negatively with Aβ-42/Aβ-40 ratio in the whole study group. Findings of our research suggest a potential role of NGAL in pathology of AD. However, follow-up studies on larger study group are needed.

Neurodegenerative diseases, contributing to the significant socioeconomic burden due to aging society, are gaining increasing interest. Despite each disease having different etiologies, neuroinflammation is believed to play a crucial role in Alzheimer’s disease (AD), Parkinson’s disease (PD), and multiple sclerosis (MS). In addition to the pathogenic function of inflammation in the brain there is growing evidence that immune responses are essential for neuroregeneration. This review compares and contrasts the neuroinflammatory pathways that selected neurodegenerative diseases share and have in common. In AD, tau tangles and beta-amyloid plaques cause microglia and astrocytes to become activated in an inflammatory response. Alpha-synuclein aggregation stimulate neuroinflammation in Parkinson’s disease, especially in the substantia nigra. In Multiple Sclerosis an autoimmune attack on myelin is connected to inflammation via invading immune cells. Commonalities include the release of pro-inflammatory mediators like cytokines and activation of signaling pathways such as NF-κB and MAPK. Comprehending these common routes is essential for discovering early diagnostic possibilities for the diseases and possible tailored treatments. Our work underscores the potential for insights into disease mechanisms. Identifying common targets offers promise for advancing our understanding and potential future treatment approaches across these debilitating disorders.

Despite the availability of conventional serum markers for colorectal cancer (CEA, CA 19-9), there remains a need for more sensitive and specific biomarkers, particularly for early-stage detection. This study evaluated the diagnostic usefulness of serum Relaxin-2 (RLN2) and Chitinase-3-like protein 1 (YKL-40) as potential adjunct markers in patients with CRC. Serum concentrations of all the proteins were measured using a multiplexing assay and CMIA and were subsequently compared using non-parametric statistical tests. The concentrations of YKL-40, CEA, and CA 19-9 were elevated in CRC patients relative to controls (p < 0.05), but not so for RLN2. The concentrations of YKL-40 were also significantly elevated in patients undergoing chemotherapy or preoperative radiotherapy referral. Kruskal-Wallis and post-hoc testing found that YKL-40 and CEA were associated with tumor progression, but RLN2 and CA 19-9 were increased primarily in advanced, metastatic disease. No statistically significant differences in marker levels were observed between cancer subtypes or between histologic grades. Performance analysis for diagnostic purposes showed YKL-40 was moderately sensitive (65%) but very specific (77.5%), and its AUC was 0.702, higher than CA 19-9 (AUC = 0.632) but lower than CEA (AUC = 0.869) (all p < 0.05). RLN2 did not reach statistical significance (AUC = 0.593, p = 0.09). Correlation analysis demonstrated the best correlation with disease stage for CEA and weaker positive correlations for YKL-40, CA 19-9, and RLN2. These findings suggest that YKL-40 may serve as a useful adjunct serum biomarker for CRC diagnosis, especially when combined with conventional markers such as CEA.

Asthma is a complex airway disorder driven by diverse immunological pathways. While type 2 (T2)-mediated inflammation is well characterized, the mechanisms underlying T2-low (also referred to as mixed inflammatory phenotype) or non-T2-mediated asthma, often associated with Th1/Th17-driven immune responses and high pulmonary neutrophilic inflammation, remain poorly understood. This study investigates airway remodeling in acute and chronic experimental asthma models induced by house dust mite extract to elucidate inflammatory and structural changes. Two acute T2-low models demonstrated pronounced airway inflammation characterized by goblet cell hyperplasia, collagen deposition, and significant upregulation of extracellular matrix remodeling and fibroblast activation. In contrast, the chronic Th17-mediated model exhibited reduced ECM deposition, increased matrix metalloproteinase (MMP) activity, and a distinct molecular signature dominated by IL-17A-driven pathways, indicative of ECM degradation and structural instability. Furthermore, the acute models showed immune cell apoptosis as the predominant cell death mechanism. In contrast, the chronic inflammation model was marked by necroptosis localized to structural lung cells, contributing to persistent inflammation and remodeling. Our findings provide new insights into the distinct immunopathological mechanisms underlying airway remodeling and fibrosis in T2-low and Th17-mediated asthma phenotypes. The study emphasizes the need for advanced preclinical models and targeted therapeutic strategies to address ECM dysregulation and chronic inflammation to progress in airway remodeling treatment in asthma.

Cognitive disorders are a growing cause of morbidity and mortality worldwide. Diagnostic approaches to improve early diagnosis of cognitive disorders are constantly being sought. The pathogenesis of cognitive impairment is multifactorial and complex. It is believed that microglial activation and synaptic disturbance are crucial mechanisms leading to disease progression thus study of the interrelationships of the proteins involved in these processes appears to be important. Chemokine CX3CL1 seems to play a pivotal role in the central nervous system and it is involved in microglia-neuron communication, neuronal survival, synaptic plasticity, as well as neuronal excitability. Findings from preclinical studies on AD models have reported the crucial role of CX3CL1 in microglial activation, regulation of plaque load, and cognition. Neurogranin is considered, as a biomarker of early synaptic dysfunction in AD. Additionally, it may serve as a marker to predict disease progression. Therefore, we aimed to investigate and compare CX3CL1 and neurogranin (Ng) levels in CSF patients with mild cognitive decline (MCI) and cognitively normal subjects from the control group. We also assessed an association between CSF concentrations of CX3CL1, Ng, and neurochemical dementia biomarkers. The concentrations of CX3CL1, neurogranin as well as neurochemical dementia biomarkers, including amyloid beta 1-42 (Aß-42), amyloid beta 1-40, Tau, as well as pTau181 were measured in cerebrospinal fluid patients with mild cognitive impairment and individuals without cognitive decline by multiplexing and enzyme-linked immunosorbent techniques. Significantly higher CSF concentrations of CX3CL1 and neurogranin were found in MCI patients in comparison to subjects without cognitive decline. Furthermore, in the group of patients with MCI the CSF levels of CX3CL1 and Ng significantly correlated with Aβ-42, and pTau181 proteins. Similarly, a significant association between neurogranin and Tau protein was observed. Additionally, a positive correlation between CSF levels of Ng and CX3XL1 was noticed. Our findings indicate that both proteins CX3CL1, as well as neurogranin, could be applied as complementary early biomarkers for more accurate diagnosing and stratification of patients with cognitive decline.