Journal of Ethnopharmacology, Journal Year: 2023, Volume and Issue: 319, P. 117355 - 117355
Published: Oct. 27, 2023
Language: Английский
Journal of Ethnopharmacology, Journal Year: 2023, Volume and Issue: 319, P. 117355 - 117355
Published: Oct. 27, 2023
Language: Английский
World Journal of Psychiatry, Journal Year: 2022, Volume and Issue: 12(1), P. 77 - 97
Published: Jan. 17, 2022
Major depressive disorder is a debilitating affecting millions of people each year. Brain-derived neurotrophic factor (BDNF) and inflammation are two prominent biologic risk factors in the pathogenesis depression that have received considerable attention. Many clinical animal studies highlighted associations between low levels BDNF or high inflammatory markers development behavioral symptoms depression. However, less known about potential interaction inflammation, particularly within central nervous system. Emerging evidence suggests there bidirectional regulation these with important implications for anti-depressant response. Elevated mediators been shown to reduce expression BDNF, may play an negative regulatory role on brain. Understanding this more fully context neuropsychiatric disease both developing fuller understanding biological identifying novel therapeutic opportunities. Here we review particular focus pathogenic their interaction.
Language: Английский
Citations
113Frontiers in Cellular Neuroscience, Journal Year: 2024, Volume and Issue: 18
Published: March 13, 2024
The blood brain barrier (BBB) plays a crucial role in maintaining homeostasis by selectively preventing the entry of substances from peripheral into central nervous system (CNS). Comprised endothelial cells, pericytes, and astrocytes, this highly regulated encompasses majority brain’s vasculature. In addition to its protective function, BBB also engages significant crosstalk with perivascular macrophages (MΦ) microglia, resident MΦ brain. These interactions play pivotal modulating activation state cells comprising BBB, as well MΦs themselves. Alterations systemic metabolic inflammatory states can promote cell dysfunction, reducing integrity potentially allowing factors leak CNS compartment. This may mediate MΦs, initiate further immune responses within parenchyma, suggesting neuroinflammation be triggered signaling periphery, without primary injury or disease originating CNS. intricate interplay between periphery through highlights importance understanding microglia mediating challenges. Despite recent advancements, our is still early stages, leaving gap knowledge. However, emerging research shedding light on involvement at various conditions, including infections, diabetes, ischemic stroke. review aims provide comprehensive overview current investigating relationship health disease. By exploring these connections, we hope advance challenges their impact pathology. Uncovering hold promise for development novel therapeutic strategies neurological conditions that involve vascular mechanisms.
Language: Английский
Citations
35Molecular Pain, Journal Year: 2025, Volume and Issue: 21
Published: Jan. 1, 2025
This study investigated the role of brain-derived neurotrophic factor (BDNF) in patients with degenerative lumbar stenosis, focusing on its expression and correlation pain intensity. The examined 96 stenosis 85 control participants. BDNF levels yellow ligamentum flavum were measured using reverse transcription quantitative polymerase chain reaction (RT-qPCR), enzyme-linked immunosorbent assay (ELISA), western blot analysis. results showed significantly higher at both messenger ribonucleic acid (mRNA; fold change = +1.35 ± 0.23; p < 0.05) protein (28.98 6.40 pg/mg) compared to controls (4.56 1.98 pg/mg; 0.05). Furthermore, correlated positively intensity reported by patients, observed those experiencing more severe pain. also explored influence lifestyle factors, such as smoking alcohol consumption, related diseases, diabetes, expression. Smoking, use, diabetes associated elevated ( These findings suggest that could serve a biomarker for severity level, although this was not consistently mRNA level; highlights potential BDNF-targeted therapies managing Future research should involve larger longitudinal studies validate these explore therapeutic interventions. underscores importance considering molecular factors treatment aiming improve patient outcomes through comprehensive, targeted approaches.
Language: Английский
Citations
3Frontiers in Psychiatry, Journal Year: 2021, Volume and Issue: 11
Published: Feb. 10, 2021
The prevalence and etiology of COVID-19's impact on brain health cognitive function is poorly characterized. With mounting reports delirium, systemic inflammation, evidence neurotropism, a statement impairment among COVID-19 cases needed. A substantial literature has demonstrated that inflammation can severely disrupt function, suggesting an immune response, cytokine storm, as possible cause neurocognitive impairments. In this light, the aim present study was to summarize available knowledge cognition (i.e., herein, we broadly define reflecting reporting topic in literature) during acute recovery phases disease, hospitalized patients outpatients with confirmed status. systematic review identified six studies which document impairment, one quantifies deficits after recovery. Pooling samples included (total sample n = 644) at three standards quality produced conservative estimates ranging from 43.0 66.8% only, no report met criteria for inclusion main synthesis. most common reported delirium frequent elevated inflammatory markers suggest etiology. Other have disease involves marked increases IL-6, TNFα, IL-1β; cytokines known profound working memory attention. Impairment these functions characteristic aspect suggests key mediators induced Researchers are encouraged assay determine potential role mediating disturbance individuals affected by COVID-19.
Language: Английский
Citations
100Psychiatry Research, Journal Year: 2022, Volume and Issue: 317, P. 114857 - 114857
Published: Sept. 21, 2022
Language: Английский
Citations
46International Journal of Molecular Sciences, Journal Year: 2022, Volume and Issue: 23(15), P. 8417 - 8417
Published: July 29, 2022
Brain-derived neurotrophic factor (BDNF) is the most abundant neurotrophin in adult brain and functions as both a primary signal neuromodulator. It serves essential roles neuronal development, maintenance, transmission, plasticity, thereby influencing aging, cognition, behavior. Accumulating evidence associates reduced central peripheral BDNF levels with various neuropsychiatric disorders, supporting its potential utilization biomarker of pathologies. Subsequently, extensive research has been conducted to evaluate restoring, or otherwise augmenting, transmission therapeutic approach. Promising results were indeed observed for genetic upregulation exogenous administration using multitude murine models neurological psychiatric diseases. However, varying mechanisms have proposed underlie effects, many findings indicate engagement disease-specific other non-specific mechanisms. This because essentially affects all aspects cellular function through tropomyosin receptor kinase B (TrkB) signaling, disruptions which vary between regions across different pathologies leading diversified consequences on cognition Herein, we review neurophysiology signaling classify converging diverging molecular underlying potentials disorders. These include neuroprotection, synaptic immunomodulation, plasticity facilitation, secondary neuromodulation, preservation neurovascular unit integrity viability. Lastly, discuss several suggesting common mediator actions centrally acting pharmacological agents used treatment illness.
Language: Английский
Citations
42Frontiers in Cellular Neuroscience, Journal Year: 2023, Volume and Issue: 17
Published: June 19, 2023
Microglia are the primary immunocompetent cells that protect brain from environmental stressors, but can also be driven to release pro-inflammatory cytokines and induce a cytotoxic environment. Brain-derived neurotrophic factor (BDNF) is important for regulation of plasticity, synapse formation, general neuronal health. Yet, little known about how BDNF impacts microglial activity. We hypothesized would have direct modulatory effect on cortical (Postnatal Day 1-3: P1-3) microglia (Embryonic 16: E16) cultures in context bacterial endotoxin. To this end, we found treatment following LPS-induced inflammation had marked anti-inflammatory effect, reversing both IL-6 TNF-α microglia. This was transferrable neurons, such LPS-activated media able produce an inflammatory when added separate culture, again, priming attenuated effect. reversed overall impact LPS exposure speculate directly play role regulating state hence, influence microglia-neuron interactions.
Language: Английский
Citations
38Molecular Neurobiology, Journal Year: 2024, Volume and Issue: 61(8), P. 5680 - 5698
Published: Jan. 15, 2024
Abstract Postoperative depression (POD) and postoperative cognitive dysfunction (POCD) have placed heavy burden on patients’ physical mental health in recent years. Sleep disturbance before surgery is a common phenomenon that has been increasingly believed to affect recovery, especially aged patients, while little attention paid sleep disruption the potential mechanism remains ambiguous. Ketamine reported attenuate POCD after cardiac elicit rapid-acting sustained antidepressant actions. The present study aimed clarify effect of esketamine’s (the S-enantiomer ketamine) protective effects possible mechanisms action POD. Our results showed exacerbated microglial M1 polarization BDNF-TrkB signalling induced by surgery, resulting emotional changes impairments. Notably, treatment with esketamine reversed behavioural abnormalities through inhibiting microglia inflammatory response thus improving vivo vitro. In addition, administration also impaired hippocampal synaptic plasticity which perturbed surgery. These findings warrant further investigations into interplay may provide novel ideas for implication preoperative preparations prevention brain-related complications.
Language: Английский
Citations
13Neurobiology of Disease, Journal Year: 2024, Volume and Issue: 198, P. 106561 - 106561
Published: June 9, 2024
Neuroinflammation and mitochondrial dysfunction are closely intertwined with the pathophysiology of neurological disorders. Recent studies have elucidated profound alterations in dynamics across a spectrum Dynamin-related protein 1 (DRP1) emerges as pivotal regulator fission, its dysregulation disrupting homeostasis fueling neuroinflammation, thereby exacerbating disease severity. In addition to role dynamics, DRP1 plays crucial modulating inflammation-related pathways. This review synthesizes important functions central nervous system (CNS) impact epigenetic modification on progression neurodegenerative diseases. The intricate interplay between neuroinflammation microglia astrocytes, contributors is expounded upon. Furthermore, use inhibitors influence activation well their involvement processes such mitophagy, oxidative stress, calcium ion transport CNS-mediated scrutinized. modulation astrocyte crosstalk by inflammatory neurodegeneration also highlighted. Overall, targeting presents promising avenue for ameliorating enhancing therapeutic management
Language: Английский
Citations
10Life, Journal Year: 2025, Volume and Issue: 15(2), P. 263 - 263
Published: Feb. 9, 2025
Diabetic retinopathy (DR), a leading cause of vision impairment worldwide, is characterized by progressive damage to the retina due prolonged hyperglycemia. Despite advances in treatment, current interventions largely target late-stage vascular complications, leaving underlying neurodegenerative processes insufficiently addressed. This article explores crucial role neuronal survival, axonal growth, and synaptic plasticity neuroprotective potential Brain-Derived Neurotrophic Factor (BDNF) as therapeutic strategy for enhancing retinal resilience DR. Furthermore, it discusses innovative delivery methods BDNF, such gene therapy nanocarriers, which may overcome challenges achieving sustained targeted levels retina, focusing on early intervention preserve function prevent loss.
Language: Английский
Citations
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