Objective: Brain-derived neurotrophic factor (BDNF) and high sensitive C-reactive protein (hs-CRP) have been reported to play roles in depression and bipolar disorder (BD). However, the probable discriminatory properties of these biologic markers are less investigated. We aimed to assess the serum BDNF and hs-CRP levels among Iranian patients with major depressive disorder (MDD) and BD during a depressive episode and investigate the optimum cut-off point for differential diagnosis of BD and MDD.
Methods: We recruited 30 patients with MDD, 30 with BD in depressive mood and 30 healthy comparators. Blood sample was taken from each participant to measure BDNF and hs-CRP levels. We also used receiver operating characteristic (ROC) curve analysis to find an optimal cut-off point for differentiating MDD from BD according to pre-defined variables.
Results: The mean age of total study population was 37.3 ± 5.0 years (males: 49%). BDNF was significantly lower in patients with BD, followed by MDD subjects and healthy controls 541.0 ± 601.0 pg/ml vs. 809.5 ± 433.3 pg/ml vs. 1,482.1 ± 519.8, respectively, < 0.001). The area under curve of ROC curve analysis for BD versus MDD was 0.704 (95% confidence interval: 0.564-0.844, p = 0.007). We also found that the BDNF cut-off value of 504 could appropriately distinguished BD from MDD (sensitivity: 73%, specificity: 70%). No significant association were identified in terms of hs-CRP levels.
Conclusion: Patients suffering from BD had lowest BDNF levels compared to MDD or healthy adults and this biomarker could play a practical role differentiating MDD from BD. Several studies are required confirming our outcomes.
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http://dx.doi.org/10.9758/cpn.2023.21.1.108 | DOI Listing |
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Biotechnology Unit, University of Ribeirão Preto/UNAERP, Ribeirão Preto, SP, Brazil.
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Collegium Medicum, WSB University, Dabrowa Gornicza, Poland.
This study investigated the role of brain-derived neurotrophic factor (BDNF) in patients with degenerative lumbar stenosis, focusing on its expression and correlation with pain intensity. The study examined 96 patients with lumbar stenosis and 85 control participants. BDNF levels in the yellow ligamentum flavum were measured using reverse transcription quantitative polymerase chain reaction (RT-qPCR), enzyme-linked immunosorbent assay (ELISA), and western blot analysis.
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Department of Urology, Beijing Friendship Hospital, Capital Medical University, Beijing 100050, China; Institute of Urology, Beijing Municipal Health Commission, Beijing 100050, China. Electronic address:
We previously established an effective method to ameliorate erectile dysfunction (ED) using intracavernous injection (ICI) of mesenchymal stem cell (MSC) microspheres. However, the expression of a key neurotrophic factor, brain-derived neurotrophic factor (BDNF), was low in both MSCs and MSC microspheres, restricting the associated neural repair. Based on the hypoxia and oxidative stress microenvironments within cell spheroids and lesion areas, BDNF-expressing nanocomplexes that are dual-responsive to hypoxia and reactive oxygen species were designed to modify MSCs, achieving high BDNF expression in MSC spheroids.
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Physiology, Department of Biology, Marvdasht Branch, Islamic Azad University, Marvdasht, Iran.
Intrauterine growth restriction (IUGR) induced by utero-placental insufficiency (UPI) results in delayed neural development and impaired brain growth. This study investigates the effects of Naringin (Nar) on memory, learning, cholinergic activity, oxidative stress markers, hippocampal CREB/BDNF signal pathway and cell damage in offspring of rats exposed to UPI. Twenty pregnant Wistar rats were randomly assigned to four groups: control, sham surgery, UPI + NS (UPI + normal saline as a vehicle), and UPI + Nar (UPI + Nar at 100 mg/kg/day).
View Article and Find Full Text PDFMetab Brain Dis
January 2025
Division of Applied Biomedical Science and Biotechnology, School of Health Science, IMU University, No. 126, Jalan Jalil Perkasa 19, Bukit Jalil, 57000, Kuala Lumpur, Malaysia.
Alzheimer's disease (AD) consists of two main pathologies, which are the deposition of amyloid plaque as well as tau protein aggregation. Evidence suggests that not everyone who carries the AD-causing genes displays AD-related symptoms; they might never acquire AD as well. These individuals are referred to as non-demented individuals with AD neuropathology (NDAN).
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