Brain-derived neurotrophic factor as a potential diagnostic marker in minimal hepatic encephalopathy

Stawicka, Agnieszka; Świderska, Magdalena; Zbrzeźniak, Justyna; Sołowianowicz, Natalia; Woszczenko, Aleksandra; Flisiak, Robert; Jaroszewicz, Jerzy

doi:10.5114/ceh.2021.103242

Cited by 5 publications

(4 citation statements)

References 38 publications

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“…Fortythree people completed thorough psychometric testing to assess MHE. Patients with LC had serum BDNF levels that were two times lower than those of healthy individuals (13.6 (7.8-22.6) vs. 33.0 (24.1-40.7) ng/ml, p 0.001, respectively), and this difference was due to a level of liver insufficiency determined by the model for end-stage liver disease (MELD) [28].…”

Section: Discussionmentioning

confidence: 94%

Diagnostic role of serum brain-derived neurotrophic factor in HCV cirrhotic patients with minimal hepatic encephalopathy with and without schistosomiasis

Bedewy,

Elhadidi,

El-Latif

et al. 2024

Egypt Liver Journal

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Background Liver cirrhosis (LC) advances from an asymptomatic phase (compensated cirrhosis) to a symptomatic phase (decompensated cirrhosis). Up to 80% of patients with LC may experience minimal hepatic encephalopathy (MHE), which is the first stage of hepatic encephalopathy (HE). Due to the lack of serum indicators, the diagnosis of MHE is frequently based on neuropsychometric tests. Therefore, this study aimed to evaluate the role of brain-derived neurotrophic factor (BDNF) as a diagnostic marker for MHE in HCV cirrhotic patients with or without hepatic schistosomiasis. Patients and methods The study consisted of 60 patients with divided into 3 groups (20 patients with HCV-related LC with overt HE, 20 patients with HCV-related LC without overt HE, and 20 patients with HCV-related LC and hepatic schistosomiases co-infection without overt HE) as well as 20 healthy controls. Patients without overt HE were evaluated for MHE by psychometric tests (trail making tests A and B). Serum BDNF was measured in all patients as well as healthy controls. Results Serum BDNF was found to be significantly lower in patients with LC regardless of etiology than in healthy controls; however, no statistically significant difference was found between patients with and without overt HE. Upon subdivision of patients without overt HE into “normal” and “deficient” using psychometric tests, serum BDNF was found to be significantly lower in patients with overt as well as those with “deficient” psychometric tests (have MHE). Serum BDNF had a sensitivity of 65.85% and specificity of 84.62%, and positive predictive value (PPV) was 82.0%, and negative predictive value (NPV) was 70.0% for diagnosis of MHE. Conclusion Serum BDNF concentration was found to be significantly lower in patients with deficient psychometric tests having either overt or covert HE which suggests that serum BDNF can be used as a diagnostic marker for MHE.

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Section: Discussionmentioning

confidence: 94%

Diagnostic role of serum brain-derived neurotrophic factor in HCV cirrhotic patients with minimal hepatic encephalopathy with and without schistosomiasis

Bedewy,

Elhadidi,

El-Latif

et al. 2024

Egypt Liver Journal

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“…The level of BDNF was significantly decreased in serum samples of patients with cirrhosis due to biliary atresia and hepatitis. 33 , 34 Recently, a human study by Stawicka et al 35 presented serum levels of BDNF were decreased in cirrhosis patients with HE and introduced it as a diagnostic marker for HE. Furthermore, the protein and expression levels of BDNF were significantly decreased in the brain tissues of hyperammonemic animal models of HE.…”

Section: Discussionmentioning

confidence: 99%

New Insight Into Mechanisms of Hepatic Encephalopathy: An Integrative Analysis Approach to Identify Molecular Markers and Therapeutic Targets

Sepehrinezhad

Shahbazi

Negah

et al. 2023

Bioinform Biol Insights

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Hepatic encephalopathy (HE) is a set of complex neurological complications that arise from advanced liver disease. The precise molecular and cellular mechanism of HE is not fully understood. Differentially expressed genes (DEGs) from microarray technologies are powerful approaches to obtain new insight into the pathophysiology of HE. We analyzed microarray data sets of cirrhotic patients with HE from Gene Expression Omnibus to identify DEGs in postmortem cerebral tissues. Consequently, we uploaded significant DEGs into the STRING to specify protein-protein interactions. Cytoscape was used to reconstruct the genetic network and identify hub genes. Target genes were uploaded to different databases to perform comprehensive enrichment analysis and repurpose new therapeutic options for HE. A total of 457 DEGs were identified in 2 data sets totally from 12 cirrhotic patients with HE compared with 12 healthy subjects. We found that 274 genes were upregulated and 183 genes were downregulated. Network analyses on significant DEGs indicated 12 hub genes associated with HE. Enrichment analysis identified fatty acid beta-oxidation, cerebral organic acidurias, and regulation of actin cytoskeleton as main involved pathways associated with upregulated genes; serotonin receptor 2 and ELK-SRF/GATA4 signaling, GPCRs, class A rhodopsin-like, and p38 MAPK signaling pathway were related to downregulated genes. Finally, we predicted 39 probable effective drugs/agents for HE. This study not only confirms main important involved mechanisms of HE but also reveals some yet unknown activated molecular and cellular pathways in human HE. In addition, new targets were identified that could be of value in the future study of HE.

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“…[59] There is also some evidence that neurotrophic factors, which are disrupted by chronic alcohol use, [60,61] affect liver steatosis, inflammation, and fibrosis in patients with alcohol-associated liver disease and nonalcohol-associated liver disease [62,63] and has even been explored as a potential diagnostic marker for covert HE. [64] Finally, the alcohol consumption has also been shown to cause intestinal inflammation and gut dysbiosis, which, in turn, affects neurotransmitter signaling in the brain. [65] These observations represent other mechanisms by which the direct effects of alcohol may worsen both the neurological impact of cirrhotic liver disease and the drug's hepatotoxic effects.…”

Section: Altered Brain Pathophysiology In Cirrhosismentioning

confidence: 99%

“…Increased cortisol and corticosterone levels have been shown to exacerbate alcohol-induced gut microbiome changes, tight junction disruption, epithelial barrier dysfunction, and liver injury 59. There is also some evidence that neurotrophic factors, which are disrupted by chronic alcohol use,60,61 affect liver steatosis, inflammation, and fibrosis in patients with alcohol-associated liver disease and nonalcohol-associated liver disease62,63 and has even been explored as a potential diagnostic marker for covert HE 64. Finally, the alcohol consumption has also been shown to cause intestinal inflammation and gut dysbiosis, which, in turn, affects neurotransmitter signaling in the brain 65.…”

Section: Altered Brain Pathophysiology In Cirrhosismentioning

confidence: 99%

Gut microbiome-brain-cirrhosis axis

et al. 2023

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Cirrhosis is characterized by inflammation, degeneration, and fibrosis of liver tissue. Along with being the most common cause of liver failure and liver transplant, cirrhosis is a significant risk factor for several neuropsychiatric conditions. The most common of these is HE, which is characterized by cognitive and ataxic symptoms, resulting from the buildup of metabolic toxins with liver failure. However, cirrhosis patients also show a significantly increased risk for neurodegenerative diseases such as Alzheimer and Parkinson diseases, and for mood disorders such as anxiety and depression. In recent years, more attention has been played to communication between the ways the gut and liver communicate with each other and with the central nervous system, and the way these organs influence each other's function. This bidirectional communication has come to be known as the gut-liver-brain axis. The gut microbiome has emerged as a key mechanism affecting gut-liver, gut-brain, and brain-liver communication.Clinical studies and animal models have demonstrated the significant patterns of gut dysbiosis when cirrhosis is present, both with or without concomitant alcohol use disorder, and have provided compelling evidence that this dysbiosis also influences the cognitive and mood-related behaviors. In this review, we have summarized the pathophysiological and cognitive effects associated with cirrhosis, links to cirrhosis-associated disruption of the gut microbiome, and the current evidence from clinical and preclinical studies for the modulation of the gut microbiome as a treatment for cirrhosis and associated neuropsychiatric conditions.

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Brain-derived neurotrophic factor as a potential diagnostic marker in minimal hepatic encephalopathy

Cited by 5 publications

References 38 publications

Diagnostic role of serum brain-derived neurotrophic factor in HCV cirrhotic patients with minimal hepatic encephalopathy with and without schistosomiasis

Diagnostic role of serum brain-derived neurotrophic factor in HCV cirrhotic patients with minimal hepatic encephalopathy with and without schistosomiasis

New Insight Into Mechanisms of Hepatic Encephalopathy: An Integrative Analysis Approach to Identify Molecular Markers and Therapeutic Targets

Gut microbiome-brain-cirrhosis axis

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