Health Science Inquiry (Journal)
Not a member yet
406 research outputs found
Sort by
A Multi-Omics Therapeutic Approach using SAHA, SP600125, and Exercise to Modulate BDNF levels in Major Depressive Disorder
Get PDFMajor depressive disorder (MDD) is a serious mental health condition associated with decreased quality of life and is correlated with other medical comorbidities like diabetes and hypertension. Despite its widespread impact, there is not an objective method of diagnosis or treatment. However, many studies have outlined the potential of exercise in altering Brain-derived neurotrophic factor (BDNF) to alleviate MDD symptoms. To investigate this association, a targeted literature search was conducted on databases such as OVID, PubMed and Science Direct, including studies published in the past 10 years.
BDNF exists in two forms, pro-BDNF and mature BDNF, with its mature form more involved in improving cognitive function. Pro and mature BDNF can be regulated through the enzyme histone deacetylase 2 (HDAC2), an epigenetic silencer preventing its transcription. Consistent evidence was found for BDNF being regulated by multiple molecular pathways influenced by exercise and that BDNF is a potential target in MDD, playing a role in synaptic plasticity, neurogenesis, and mood regulation. As such, a multi-omics approach was explored to examine the mechanism behind exercise and BDNF, within metabolomics, epigenomics, transcriptomics, and proteomics in the context of MDD.
Our proposed experiment ties together the multi-omics approach by exploring the effects of exercise metabolite β-hydroxybutyric (BHB), and pharmacological agents including SAHA and SP600125 on BDNF levels in mice models. Vorinostat (SAHA), a BHB mimic, is an HDAC2 inhibitor that upregulates both forms of BDNF. To minimize the pro-apoptotic response triggered by excess pro-BDNF binding to P75NTR and activating c-Jun N-terminal kinase (JNK), SP600125 (a JNK inhibitor) can be coupled with SAHA to inhibit pro-BDNF-JNK pathways. These markers can be further analyzed through ChIP-seq and ELISA. This research holds promise in informing novel therapies for MDD and furthering current knowledge in BDNF multi-omics interactions. 
Cracking Cancer’s Drug Resistance Code: How Omics is Shaping the Future of Precision Medicine
Get PDFLocation, Location, Location: Spatial-omics helps map the heterogenous landscape of triple-negative breast cancer to predict response to immunotherapy
No full text
Interview with Dr. Catrina Loucks: Unravelling Genomic Factors Behind Opioid Side Effects in Children
Get PDF
Rethinking bacterial testing: How host-mimicking conditions are transforming antibiotic research with Dr. Eric Brown
No full text
From Correlation to Causation: How Omics Technologies Illuminate the Role of INHBC in Cardiometabolic Disease
Get PDFThe integration of omics technologies, such as genomics, proteomics, and metabolomics, has enabled researchers to uncover complex biological mechanisms underlying disease. In a recent study, Loh et al. used a multi-omics approach to investigate the liver-derived protein INHBC and its role in cardiometabolic health. Through bidirectional Mendelian Randomization and phenome-wide analysis, they identified INHBC as both a driver and consequence of metabolic dysfunction, including obesity, dyslipidemia, and inflammation.
The study revealed that INHBC contributes to coronary artery disease risk by altering lipid levels and is associated with renal and liver traits. Functional assays demonstrated that INHBC, via activin C, signals through the ALK7 receptor to suppress fat breakdown in adipose tissue. These findings position INHBC as a potential biomarker and therapeutic target. Overall, this work illustrates how omics tools can move beyond correlation to reveal causality and provide mechanistic insights with translational relevance in complex disease pathways
Albumin as a Marker of Ascites: The Role of Proteomics in Uncovering Novel Diagnostic Biomarkers: Albumin as a marker of ascites: the role of proteomics
No full textLiver cirrhosis is a major global health concern, often progressing to ascites, which worsens prognosis and increases healthcare costs. Current diagnostic approaches rely on albumin-based markers like the serum-ascites albumin gradient, but these have limitations. Emerging biomarkers such as kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin show promise in identifying acute kidney injury in cirrhotic patients. Integrating multi-omics approaches may improve early detection and management of cirrhosis-related complications. Using kidney injury molecule-1 and neutrophil gelatinase-associated lipocalin alongside traditional markers could enhance risk stratification and patient outcomes