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OBJECTIVES: We aimed to elucidate the pathogenic mechanisms underlying autosomal dominant adult-onset demyelinating leukodystrophy (ADLD), and to understand the genotype/phenotype correlation of structural variants (SVs) in the LMNB1 locus. BACKGROUND: Since the discovery of 3D genome architectures and topologically associating domains (TADs), new pathomechanisms have been postulated for SVs, regardless of gene dosage changes. ADLD is a rare genetic disease associated with duplications (classical ADLD) or noncoding deletions (atypical ADLD) in the LMNB1 locus. METHODS: High-throughput chromosome conformation capture, RNA sequencing, histopathological analyses of postmortem brain tissues, and clinical and neuroradiological investigations were performed. RESULTS: We collected data from >20 families worldwide carrying SVs in the LMNB1 locus and reported strong clinical variability, even among patients carrying duplications of the entire LMNB1 gene, ranging from classical and atypical ADLD to asymptomatic carriers. We showed that patients with classic ADLD always carried intra-TAD duplications, resulting in a simple gene dose gain. Atypical ADLD was caused by LMNB1 forebrain-specific misexpression due to inter-TAD deletions or duplications. The inter-TAD duplication, which extends centromerically and crosses the 2 TAD boundaries, did not cause ADLD. Our results provide evidence that astrocytes are key players in ADLD pathology. INTERPRETATION: Our study sheds light on the 3D genome and TAD structural changes associated with SVs in the LMNB1 locus, and shows that a duplication encompassing LMNB1 is not sufficient per se to diagnose ADLD, thereby strongly affecting genetic counseling. Our study supports breaking TADs as an emerging pathogenic mechanism that should be considered when studying brain diseases. ANN NEUROL 2024.
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Osteoarthritis (OA) is one of the most common disabling pathologies, characterized by joint pain and reduced function, significantly worsening the quality of life. Even if important progresses have been made in OA research, little is yet known about the precise cellular and molecular mechanisms underlying OA. Understanding dysregulated signaling networks and their crosstalk in OA may offer a strong opportunity for the development of combined targeted therapies. Hence, this review highlights the recent findings on the main pathways involved in OA development, including Wnt, Notch, Hedgehog, MAPK, AMPK, and JAK/STAT, providing insights on current targeted therapies in OA patients' management. The translational potential of this article: The identification of key signaling pathways involved in OA development and the investigation of their signaling crosstalk could pave the way for more effective treatments and improved management of OA patients in the future.
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Pericytes are multipotent cells embedded within the vascular system, primarily surrounding capillaries and microvessels where they closely interact with endothelial cells. These cells are known for their intriguing properties due to their heterogeneity in tissue distribution, origin, and multifunctional capabilities. Specifically, pericytes are essential in regulating blood flow, promoting angiogenesis, and supporting tissue homeostasis and regeneration. These multifaceted roles draw on pericytes' remarkable ability to respond to biochemical cues, interact with neighboring cells, and adapt to changing environmental conditions. This review aims to summarize existing knowledge on pericytes, emphasizing their versatility and involvement in vascular integrity and tissue health. In particular, a comprehensive view of the major signaling pathways, such as PDGFß/ PDGFRß, TGF-ß, FOXO and VEGF, along with their downstream targets, which coordinate the behavior of pericytes in preserving vascular integrity and promoting tissue regeneration, will be discussed. In this light, a deeper understanding of the complex signaling networks defining the phenotype of pericytes in healthy tissues is crucial for the development of targeted therapies in vascular and degenerative diseases.
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Homeostasis , Pericitos , Transducción de Señal , Pericitos/metabolismo , Pericitos/fisiología , Humanos , Animales , Neovascularización Fisiológica , Receptor beta de Factor de Crecimiento Derivado de Plaquetas/metabolismoRESUMEN
Hepatocellular carcinoma (HCC) is a common cancer which unfortunately has poor outcomes. Common anti-cancer treatments such as chemotherapy and targeted therapy have not increased patient survival significantly. A common treatment for HCC patients is transplantation, however, it has limitations and complications. Novel approaches are necessary to more effectively treat HCC patients. Berberine (BBR) is a nutraceutical derived from various fruits and trees, which has been used for centuries in traditional medicine to treat various diseases such as diabetes and inflammation. More recently, the anti-proliferation effects of BBR have been investigated in the treatment of patients with various cancers, especially colorectal cancer, and in non-alcoholic fatty liver disease (NAFLD) and non-alcoholic steatohepatitis (NASH). In this review, we will focus on studies with BBR in liver diseases.
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Berberina , Carcinoma Hepatocelular , Suplementos Dietéticos , Neoplasias Hepáticas , Enfermedad del Hígado Graso no Alcohólico , Berberina/uso terapéutico , Berberina/farmacología , Humanos , Enfermedad del Hígado Graso no Alcohólico/tratamiento farmacológico , Enfermedad del Hígado Graso no Alcohólico/metabolismo , Enfermedad del Hígado Graso no Alcohólico/patología , Carcinoma Hepatocelular/tratamiento farmacológico , Carcinoma Hepatocelular/metabolismo , Neoplasias Hepáticas/tratamiento farmacológico , Neoplasias Hepáticas/metabolismo , AnimalesRESUMEN
PURPOSE: Dural ectasia (DE) may significantly impact Marfan syndrome (MFS) patients' quality of life due to chronic lower back pain, postural headache and urinary disorders. We aimed to evaluate the association of quantitative measurements of DE, and their evolution over time, with demographic, clinical and genetic characteristics in a cohort of MFS patients. METHODS: We retrospectively included 88 consecutive patients (39% females, mean age 37.1 ± 14.2 years) with genetically confirmed MFS who underwent at least one MRI or CT examination of the lumbosacral spine. Vertebral scalloping (VS) and dural sac ratio (DSR) were calculated from L3 to S3. Likely pathogenic or pathogenic FBN1 variants were categorized as either protein-truncating or in-frame. The latter were further classified according to their impact on the cysteine content of fibrillin-1. RESULTS: Higher values of the systemic score (revised Ghent criteria) were associated with greater DSR at lumbar (p < 0.001) and sacral (p = 0.021) levels. Patients with protein-truncating variants exhibited a greater annual increase in lumbar (p = 0.039) and sacral (p = 0.048) DSR. Mutations affecting fibrillin-1 cysteine content were linked to higher VS (p = 0.009) and DSR (p = 0.038) at S1, along with a faster increase in VS (p = 0.032) and DSR (p = 0.001) in the lumbar region. CONCLUSION: Our study shed further light on the relationship between genotype, dural pathology, and the overall clinical spectrum of MFS. The identification of protein-truncating variants and those impacting cysteine content may therefore suggest closer patient monitoring, in order to address potential complications associated with DE.
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Duramadre , Fibrilina-1 , Síndrome de Marfan , Humanos , Síndrome de Marfan/genética , Síndrome de Marfan/diagnóstico por imagen , Femenino , Masculino , Adulto , Persona de Mediana Edad , Estudios Retrospectivos , Duramadre/diagnóstico por imagen , Duramadre/patología , Dilatación Patológica/genética , Dilatación Patológica/diagnóstico por imagen , Fibrilina-1/genética , Adulto Joven , AdipoquinasRESUMEN
In the last three decades, the presence of phospholipids in the nucleus has been shown and thoroughly investigated. A considerable amount of interest has been raised about nuclear inositol lipids, mainly because of their role in signaling acting. Here, we review the main issues of nuclear phospholipid localization and the role of nuclear inositol lipids and their related enzymes in cellular signaling, both in physiological and pathological conditions.
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Núcleo Celular , Fosfolípidos , Transducción de Señal , Humanos , Núcleo Celular/metabolismo , Fosfolípidos/metabolismo , AnimalesRESUMEN
Anatomical education is pivotal for medical students, and innovative technologies like augmented reality (AR) are transforming the field. This study aimed to enhance the interactive features of the AEducAR prototype, an AR tool developed by the University of Bologna, and explore its impact on human anatomy learning process in 130 second-year medical students at the International School of Medicine and Surgery of the University of Bologna. An interdisciplinary team of anatomists, maxillofacial surgeons, biomedical engineers, and educational scientists collaborated to ensure a comprehensive understanding of the study's objectives. Students used the updated version of AEducAR, named AEducAR 2.0, to study three anatomical topics, specifically the orbit zone, facial bones, and mimic muscles. AEducAR 2.0 offered two learning activities: one explorative and one interactive. Following each activity, students took a test to assess learning outcomes. Students also completed an anonymous questionnaire to provide background information and offer their perceptions of the activity. Additionally, 10 students participated in interviews for further insights. The results demonstrated that AEducAR 2.0 effectively facilitated learning and students' engagement. Students totalized high scores in both quizzes and declared to have appreciated the interactive features that were implemented. Moreover, interviews shed light on the interesting topic of blended learning. In particular, the present study suggests that incorporating AR into medical education alongside traditional methods might prove advantageous for students' academic and future professional endeavors. In this light, this study contributes to the growing research emphasizing the potential role of AR in shaping the future of medical education.
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Anatomía , Realidad Aumentada , Educación de Pregrado en Medicina , Evaluación Educacional , Aprendizaje , Estudiantes de Medicina , Femenino , Humanos , Masculino , Adulto Joven , Anatomía/educación , Instrucción por Computador/métodos , Curriculum , Educación de Pregrado en Medicina/métodos , Evaluación Educacional/estadística & datos numéricos , Estudios Interdisciplinarios , Estudiantes de Medicina/psicología , Estudiantes de Medicina/estadística & datos numéricos , Encuestas y Cuestionarios/estadística & datos numéricosRESUMEN
The hierarchical organization of the leukemic stem cells (LSCs) is identical to that of healthy counterpart cells. It may be split into roughly three stages: a small number of pluripotent stem cells at the top, few lineage-restricted cells in the middle, and several terminally differentiated blood cells at the bottom. Although LSCs can differentiate into the hematopoietic lineage, they can also accumulate as immature progenitor cells, also known as blast cells. Since blast cells are uncommon in healthy bloodstreams, their presence might be a sign of cancer. For instance, a 20% blast cutoff in peripheral blood or bone marrow is formally used to distinguish acute myeloid leukemia from myelodysplastic neoplasms, which is essential to plan the patients' management. Many techniques may be useful for blast enumeration: one of them is flow cytometry, which can perform analyses on many cells by detecting the expression of cell surface markers. Leukemic and non-leukemic blast cells might indeed be characterized by the same surface markers, but these markers are usually differently expressed. Here we propose to use CD45, in combination with CD34 and other cell surface markers, to identify and immunophenotype blast cells in patient-derived samples.
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Leucemia Mieloide Aguda , Humanos , Leucemia Mieloide Aguda/genética , Médula Ósea/metabolismo , Antígenos CD34/metabolismo , Citometría de Flujo/métodos , Células Madre Neoplásicas/metabolismo , InmunofenotipificaciónRESUMEN
Myelodysplastic Syndromes, a heterogeneous group of hematological disorders, are characterized by abnormalities in phosphoinositide-dependent signaling, epigenetic regulators, apoptosis, and cytokine interactions within the bone marrow microenvironment, contributing to disease pathogenesis and neoplastic growth. Comprehensive knowledge of these pathways is crucial for the development of innovative therapies that aim to restore normal apoptosis and improve patient outcomes.
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Células Madre Hematopoyéticas , Síndromes Mielodisplásicos , Humanos , Células Madre Hematopoyéticas/metabolismo , Síndromes Mielodisplásicos/genética , Síndromes Mielodisplásicos/metabolismo , Médula Ósea/patología , Citocinas/metabolismo , Transducción de SeñalRESUMEN
Oral cavity defects occur after resection of lesions limited to the mucosa, alveolar gum, or minimally affecting the bone. Aiming at esthetical and functional improvements of intraoral reconstruction, the possibility of harvesting a new galeo-pericranial free flap was explored. The objective of this study was to assess the technical feasibility of flap harvesting through anatomical dissections and surgical procedure simulations. Ten head and neck specimens were dissected to simulate the surgical technique and evaluate the vascular calibers of temporal and cervical vessels. The procedure was therefore reproduced on a revascularized and ventilated donor cadaver. Anatomical dissections demonstrated that the mean cervical vascular calibers are compatible with superficial temporal ones, proving to be adequate for anastomosis. Perforating branches of the superficial temporal vascularization nourishing the pericranium were identified in all specimens. In conclusion, blood flow presence was recorded after anastomosing superficial temporal and facial vessels in the revascularized donor cadaver, demonstrating both this procedure's technical feasibility and the potential revascularization of the flap and therefore encouraging its potential in vivo application.
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Lamin B1 is an essential protein of the nuclear lamina that plays a crucial role in nuclear function and organization. It has been demonstrated that lamin B1 is essential for organogenesis and particularly brain development. The important role of lamin B1 in physiological brain development and aging has only recently been at the epicenter of attention and is yet to be fully elucidated. Regarding the development of brain, glial cells that have long been considered as supporting cells to neurons have overturned this representation and current findings have displayed their active roles in neurogenesis and cerebral development. Although lamin B1 has increased levels during the differentiation of the brain cells, during aging these levels drop leading to senescent phenotypes and inciting neurodegenerative disorders such as Alzheimer's and Parkinson's disease. On the other hand, overexpression of lamin B1 leads to the adult-onset neurodegenerative disease known as Autosomal Dominant Leukodystrophy. This review aims at highlighting the importance of balancing lamin B1 levels in glial cells and neurons from brain development to aging.
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Phospholipase C (PLC) enzymes represent crucial participants in the plasma membrane of mammalian cells, including the cardiac sarcolemmal (SL) membrane of cardiomyocytes. They are responsible for the hydrolysis of phosphatidylinositol 4,5-bisphosphate (PtdIns(4,5)P2) into 1,2-diacylglycerol (DAG) and inositol (1,4,5) trisphosphate (Ins(1,4,5)P3), both essential lipid mediators. These second messengers regulate the intracellular calcium (Ca2+) concentration, which activates signal transduction cascades involved in the regulation of cardiomyocyte activity. Of note, emerging evidence suggests that changes in cardiomyocytes' phospholipid profiles are associated with an increased occurrence of cardiovascular diseases, but the underlying mechanisms are still poorly understood. This review aims to provide a comprehensive overview of the significant impact of PLC on the cardiovascular system, encompassing both physiological and pathological conditions. Specifically, it focuses on the relevance of PLCß isoforms as potential cardiac biomarkers, due to their implications for pathological disorders, such as cardiac hypertrophy, diabetic cardiomyopathy, and myocardial ischemia/reperfusion injury. Gaining a deeper understanding of the mechanisms underlying PLCß activation and regulation is crucial for unraveling the complex signaling networks involved in healthy and diseased myocardium. Ultimately, this knowledge holds significant promise for advancing the development of potential therapeutic strategies that can effectively target and address cardiac disorders by focusing on the PLCß subfamily.
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Cardiopatías , Isoenzimas , Animales , Humanos , Fosfolipasa C beta , Miocitos Cardíacos , Biomarcadores , MamíferosRESUMEN
Polyphosphoinositides (PPIns) are signalling messengers representing less than five per cent of the total phospholipid concentration within the cell. Despite their low concentration, these lipids are critical regulators of various cellular processes, including cell cycle, differentiation, gene transcription, apoptosis and motility. PPIns are generated by the phosphorylation of the inositol head group of phosphatidylinositol (PtdIns). Different pools of PPIns are found at distinct subcellular compartments, which are regulated by an array of kinases, phosphatases and phospholipases. Six of the seven PPIns species have been found in the nucleus, including the nuclear envelope, the nucleoplasm and the nucleolus. The identification and characterisation of PPIns interactor and effector proteins in the nucleus have led to increasing interest in the role of PPIns in nuclear signalling. However, the regulation and functions of PPIns in the nucleus are complex and are still being elucidated. This review summarises our current understanding of the localisation, biogenesis and physiological functions of the different PPIns species in the nucleus.
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Núcleo Celular , Fosfatidilinositoles , Fosfatidilinositoles/metabolismo , Núcleo Celular/metabolismo , Fosfatos de Fosfatidilinositol/metabolismo , Nucléolo Celular/metabolismo , Membrana Nuclear/metabolismoRESUMEN
Autosomal dominant leukodystrophy (ADLD) is an ultra-rare, slowly progressive, and fatal neurodegenerative disorder associated with the loss of white matter in the central nervous system (CNS). Several years after its first clinical description, ADLD was found to be caused by coding and non-coding variants in the LMNB1 gene that cause its overexpression in at least the brain of patients. LMNB1 encodes for Lamin B1, a protein of the nuclear lamina. Lamin B1 regulates many cellular processes such as DNA replication, chromatin organization, and senescence. However, its functions have not been fully characterized yet. Nevertheless, Lamin B1 together with the other lamins that constitute the nuclear lamina has firstly the key role of maintaining the nuclear structure. Being the nucleus a dynamic system subject to both biochemical and mechanical regulation, it is conceivable that changes to its structural homeostasis might translate into functional alterations. Under this light, this review aims at describing the pieces of evidence that to date have been obtained regarding the effects of LMNB1 overexpression on cellular morphology and functionality. Moreover, we suggest that further investigation on ADLD morpho-functional consequences is essential to better understand this complex disease and, possibly, other neurological disorders affecting CNS myelination.
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Enfermedades Desmielinizantes , Enfermedades por Almacenamiento Lisosomal , Enfermedades Neurodegenerativas , Humanos , Enfermedades Raras , Enfermedades Desmielinizantes/metabolismo , Encéfalo/metabolismo , Modelos TeóricosRESUMEN
Phospholipases are essential intermediaries that work as hydrolyzing enzymes of phospholipids (PLs), which represent the most abundant species contributing to the biological membranes of nervous cells of the healthy human brain. They generate different lipid mediators, such as diacylglycerol, phosphatidic acid, lysophosphatidic acid, and arachidonic acid, representing key elements of intra- and inter-cellular signaling and being involved in the regulation of several cellular mechanisms that can promote tumor progression and aggressiveness. In this review, it is summarized the current knowledge about the role of phospholipases in brain tumor progression, focusing on low- and high-grade gliomas, representing promising prognostic or therapeutic targets in cancer therapies due to their influential roles in cell proliferation, migration, growth, and survival. A deeper understanding of the phospholipases-related signaling pathways could be necessary to pave the way for new targeted therapeutic strategies.
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Neoplasias Encefálicas , Glioma , Humanos , Fosfolipasas/metabolismo , Neoplasias Encefálicas/terapia , Encéfalo/metabolismo , Glioma/terapia , FosfolípidosRESUMEN
Due to the limited application of insect meal in giant freshwater prawn (Macrobrachium rosenbergii) culture, the present study aimed to (i) produce spirulina-enriched full-fat black soldier fly (Hermetia illucens) prepupae meal (HM) and (ii) test, for the first time, two experimental diets characterized by 3% or 20% of fish meal and fish oil replacement with full-fat HM (HM3 and HM20, respectively) on M. rosenbergii post-larvae during a 60-day feeding trial conducted in aquaponic systems. The experimental diets did not negatively affect survival rates or growth. The use of spirulina-enriched HM resulted in a progressive increase in α-tocopherol and carotenoids in HM3 and HM20 diets that possibly played a crucial role in preserving prawn muscle-quality traits. The massive presence of lipid droplets in R cells in all the experimental groups reflected a proper nutrient provision and evidenced the necessity to store energy for molting. The increased number of B cells in the HM3 and HM20 groups could be related to the different compositions of the lipid fraction among the experimental diets instead of a nutrient absorption impairment caused by chitin. Finally, the expression of the immune response and stress markers confirmed that the experimental diets did not affect the welfare status of M. rosenbergii post-larvae.
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BACKGROUND: miRNAs are small non-coding RNAs that regulate gene expression and are linked to cancer development and progression. miRNA profiles are currently studied as new prognostic factors or therapeutic perspectives. Among hematological cancers, myelodysplastic syndromes at higher risk of evolution into acute myeloid leukemia are treated with hypomethylating agents, like azacitidine, alone or in combination with other drugs, such as lenalidomide. Recent data showed that, during azacitidine and lenalidomide therapy, the concurrent acquisition of specific point mutations affecting inositide signalling pathways is associated with lack or loss of response to therapy. As these molecules are implicated in epigenetic processes, possibly involving miRNA regulation, and in leukemic progression, through the regulation of proliferation, differentiation and apoptosis, here we performed a new miRNA expression analysis of 26 high-risk patients with myelodysplastic syndromes treated with azacitidine and lenalidomide at baseline and during therapy. miRNA array data were processed, and bioinformatic results were correlated with clinical outcome to investigate the translational relevance of selected miRNAs, while the relationship between selected miRNAs and specific molecules was experimentally tested and proven. RESULTS: Patients' overall response rate was 76.9% (20/26 cases): complete remission (5/26, 19.2%), partial remission (1/26, 3.8%), marrow complete remission (2/26, 7.7%), hematologic improvement (6/26, 23.1%), hematologic improvement with marrow complete remission (6/26, 23.1%), whereas 6/26 patients (23.1%) had a stable disease. miRNA paired analysis showed a statistically significant up-regulation of miR-192-5p after 4 cycles of therapy (vs baseline), that was confirmed by real-time PCR analyses, along with an involvement of BCL2, that was proven to be a miR-192-5p target in hematopoietic cells by luciferase assays. Furthermore, Kaplan-Meier analyses showed a significant correlation between high levels of miR-192-5p after 4 cycles of therapy and overall survival or leukemia-free survival, that was stronger in responders, as compared with patients early losing response and non-responders. CONCLUSIONS: This study shows that high levels of miR-192-5p are associated with higher overall survival and leukemia-free survival in myelodysplastic syndromes responding to azacitidine and lenalidomide. Moreover, miR-192-5p specifically targets and inhibits BCL2, possibly regulating proliferation and apoptosis and leading to the identification of new therapeutic targets.
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Leucemia Mieloide Aguda , MicroARNs , Síndromes Mielodisplásicos , Humanos , Azacitidina/farmacología , Azacitidina/uso terapéutico , Lenalidomida/farmacología , Lenalidomida/uso terapéutico , MicroARNs/genética , Metilación de ADN , Síndromes Mielodisplásicos/tratamiento farmacológico , Síndromes Mielodisplásicos/genética , Leucemia Mieloide Aguda/genética , Proteínas Proto-Oncogénicas c-bcl-2RESUMEN
In the present study, an organic substrate (coffee silverskin) enriched with spirulina (Arthrospira platensis; 15% w/w), as a source of lipids and bioactive molecules, was used to rear the black soldier fly (Hermetia illucens) prepupae. Three grossly isonitrogenous, isoproteic, isolipidic and isoenergetic experimental diets for rainbow trout (Oncorhynchus mykiss) juveniles were then produced: a control diet (HM0) mostly including fish meal and fish oil, and two other test diets named HM3 and HM20, in which 3 or 20% of the marine ingredients were substituted with full fat black soldier fly prepupae meal (HM), respectively. Experimental diets were provided for 6 weeks, and at the end of the trial the physiological responses and marketable traits of the fish were investigated using a multidisciplinary approach. Generally, all test diets were well accepted, and fish growth, gut and liver health status, and marketable characteristics were not impaired by the experimental diets. However, an increased immuno-related gene expression along with a slight reduction of fillet redness and yellowness was evident in fish from the HM20 group.
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Aberrant signaling pathways regulating proliferation and differentiation of hematopoietic stem cells (HSCs) can contribute to disease pathogenesis and neoplastic growth. Phosphoinositides (PIs) are inositol phospholipids that are implicated in the regulation of critical signaling pathways: aberrant regulation of Phospholipase C (PLC) beta1, PLCgamma1 and the PI3K/Akt/mTOR pathway play essential roles in the pathogenesis of Myelodysplastic Syndromes (MDS) and Acute Myeloid Leukemia (AML).
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Leucemia Mieloide Aguda , Síndromes Mielodisplásicos , Humanos , Fosfatidilinositol 3-Quinasas/metabolismo , Transducción de Señal/fisiología , Leucemia Mieloide Aguda/metabolismo , Fosfatidilinositoles/metabolismo , Síndromes Mielodisplásicos/metabolismoRESUMEN
BACKGROUND: The gastrointestinal tract and the central nervous system are distinct because of evident morpho-functional features. Nonetheless, evidence indicates that these systems are bidirectionally connected through the gut-brain axis, defined as the signaling that takes place between the gastrointestinal tract and central nervous system, which plays in concert with the gut microbiota, i.e., the myriad of microorganisms residing in the lumen of the human intestine. In particular, it has been described that gut microbiota abnormalities, referred to as dysbiosis, may affect both central nervous system development and physiology. OBJECTIVE: Starting from the possible mechanisms through which gut microbiota variations were found to impact several central nervous system disorders, including Autism Spectrum Disorder and Alzheimer's Disease, we will focus on intriguing, although poorly investigated, aspects such as the epithelial and vascular barrier integrity. Indeed, several studies suggest a pivotal role of gut microbiota in maintaining the efficiency of both the intestinal barrier and blood-brain barrier. In particular, we report evidence indicating an impact of gut microbiota on intestinal barrier and blood-brain barrier homeostasis and discuss the differences and the similarities between the two barriers. Moreover, to stimulate further research, we review various tests and biochemical markers that can be used to assess intestinal and blood-brain barrier permeability. CONCLUSION: We suggest that the evaluation of intestinal and blood-brain barrier permeability in neurological patients may not only help to better understand central nervous system disorders but also pave the way for finding new molecular targets to treat patients with neurological impairment.