Current Neuropharmacology最新文献

{"title":"In Silico Pharmacogenomic Assessment of Glucagon-like Peptide-1 (GLP1) Agonists and the Genetic Addiction Risk Score (GARS) Related Pathways: Implications for Suicide Ideation and Substance Use Disorder.","authors":"Alireza Sharafshah, Kai-Uwe Lewandrowski, Mark S Gold, Brian Fuehrlein, J Wes Ashford, Panayotis K Thanos, Gene Jack Wang, Colin Hanna, Jean Lud Cadet, Eliot L Gardner, Jag H Khalsa, Eric R Braverman, David Baron, Igor Elman, Catherine A Dennen, Abdalla Bowirrat, Albert Pinhasov, Edward J Modestino, Paul R Carney, Rene Cortese, Rossano Kepler Alvim Fiorelli, Sergio Schmidt, Aryeh R Pollack, Rajendra D Badgaiyan, Kenneth Blum","doi":"10.2174/011570159X349579241231080602","DOIUrl":"https://doi.org/10.2174/011570159X349579241231080602","url":null,"abstract":"<p><strong>Introduction: </strong>Glucagon-Like Peptide-1 Receptor (GLP1R) agonists have become widespread anti-obesity/diabetes pharmaceuticals in the United States.</p><p><strong>Aim: </strong>This article aimed to provide our current knowledge on the plausible mechanisms linked to the role of Ozempic (Semaglutide), which is generalized as one of the anti-addiction compounds.</p><p><strong>Methods: </strong>The effects of GLP1R agonists in Alcohol Use Disorder (AUD) and substance use disorder (SUD) are mediated, in part, through the downregulation of dopamine signaling. We posit that while GLP1R agonism could offer therapeutic advantages in hyperdopaminergia, it may be detrimental in patients with hypodopaminergia, potentially leading to long-term induction of Suicidal Ideation (SI). The alleged posit of GLP1 agonists to induce dopamine homeostasis is incorrect. This study refined 31 genes based on the targets of Ozempic, GLP1R, and related enzymes for SI and 10 genes of the Genetic Addiction Risk Score (GARS) test. STRING-MODEL refined 29 genes, and further primary analyses indicated associations of GLP1R with DRD3, BDNF, CREB1, CRH, IL6, and DPP4.</p><p><strong>Results: </strong>In-depth silico enrichment analysis revealed an association between candidate genes and depressive phenotypes linked with dopaminergic signaling. Finally, through primary and in-depth silico analyses, we demonstrated multiple findings supporting that GLP1R agonists can induce depression phenotypes.</p><p><strong>Conclusion: </strong>Our findings suggest that associated polymorphisms seem to have overlapping effects with addictive behaviors of Reward Deficiency Syndrome (RDS) and dopamine regulation. Consequently, GLP1R agonists may represent a double-edged sword, potentially triggering both antiaddictive effects and SI by exacerbating depressive phenotypes. Thus, we encourage the scientific community to perform further empirical clinical studies to confirm this proposed pathway.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143045859","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Stable Gastric Pentadecapeptide BPC 157 as a Therapy of Severe Electrolyte Disturbances in Rats.","authors":"Marija Medvidovic Grubisic, Sanja Strbe, Ivan Barisic, Dijana Balenovic, Vasilije Stambolija, Marin Lozic, Sanja Barsic Ostojic, Ivana Oreskovic, Helena Zizek, Klara Brcic, Luka Coric, Mario Staresinic, Vladimir Blagaic, Lidija Beketic Oreskovic, Zeljka Belosic Halle, Danijel Matek, Dragan Soldo, Boris Grizelj, Alenka Boban Blagaic, Anita Skrtic, Predrag Sikiric, Sven Seiwerth","doi":"10.2174/011570159X349612241205065330","DOIUrl":"https://doi.org/10.2174/011570159X349612241205065330","url":null,"abstract":"<p><p>This review explores the therapeutic potential of the stable gastric pentadecapeptide BPC 157 in addressing electrolyte imbalances, specifically hyperkalemia, hypokalemia, hypermagnesemia, and hyperlithemia. In hyperkalemia, BPC 157 demonstrated a comprehensive counteractive effect against KCl overdose (intraperitoneally, intragastrically, and in vitro), effectively mitigating symptoms such as muscular weakness, hypertension, sphincter dysfunction, arrhythmias, and lethality. It also counteracted the adverse effects of succinylcholine and magnesium overdose, including systemic muscle paralysis, arrhythmias, and hyperkalemia. In hypokalemia, BPC 157 (administered prophylactically or therapeutically, intraperitoneally or intragastrically) prevented fatal outcomes and addressed furosemide-induced hypokalemia, ECG changes, AV conduction block, ventricular arrhythmias, and skeletal muscle myoclonus. Following magnesium overdose, BPC 157 alleviated muscle weakness, brain lesions, and hyperkalemia-induced complications. In vitro studies (HEK293 cells) revealed the ability of BPC 157 to counteract hyperkalemia- and hypermagnesemia-induced depolarization and hypokalemia-induced hyperpolarization. In lithium intoxication, BPC 157 promoted collateral pathway activation, resolved vascular and multiorgan failure, and counteracted advanced Virchow triad conditions and occlusion-like syndromes. Collectively, these findings underscore the therapeutic promise of BPC 157 in managing electrolyte imbalances and warrant further investigation.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143045870","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Antiseizure Medications: Advancements, Challenges, and Prospects in Drug Development.","authors":"Yan Hong Ng, Siti Nur Hidayah Jamil, Murni Nazira Sarian, Qamar Uddin Ahmed, Jalifah Latip, Su Datt Lam, Shevin Rizal Feroz","doi":"10.2174/011570159X323666241029171256","DOIUrl":"https://doi.org/10.2174/011570159X323666241029171256","url":null,"abstract":"<p><p>Epilepsy is a neurological disorder affecting millions of people worldwide. Antiseizure medications (ASM) remain a critical therapeutic intervention for treating epilepsy, notwithstanding the rapid development of other therapies. There have been substantial advances in epilepsy medications over the past three decades, with over 20 ASMs now available commercially. Here we describe the conventional and unique mechanisms of action of ASMs, focusing on everolimus, cannabidiol, cenobamate, fenfluramine, and ganaxolone, the five most recently marketed ASMs. Major obstacles in the development of ASMs are also addressed, particularly drug-resistant epilepsy as well as psychiatric and behavioral adverse effects of ASMs. Moreover, we delve into the mechanisms and comparative efficacy of ASM polytherapy, with remarks on the benefits and challenges in their application in clinical practice. In addition, the characteristics of the ideal ASM are outlined in this review. The review also discusses the development of new potential ASMs, including modifying existing ASMs to improve efficacy and tolerability. Furthermore, we expound on the modulation of γ- aminobutyric acid type A receptor (GABAAR) as a strategy for the treatment of epilepsy and the identification of a GABAAR agonist, isoguvacine, as a potential ASM.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143045857","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cortisol Imbalance and Fear Learning in PTSD: Therapeutic Approaches to Control Abnormal Fear Responses.","authors":"Simone Battaglia, Chiara Di Fazio, Sara Borgomaneri, Alessio Avenanti","doi":"10.2174/1570159X23666250123142526","DOIUrl":"https://doi.org/10.2174/1570159X23666250123142526","url":null,"abstract":"<p><p>Post-Traumatic Stress Disorder (PTSD) is mainly characterized by dysregulated fear re- sponses, including hyperarousal and intrusive re-experiencing of traumatic memories. This work delves into the intricate interplay between abnormal fear responses, cortisol dysregulation, and the Hypothalamic-Pituitary-Adrenal (HPA) axis, elucidating their role in the manifestation of PTSD. Giv- en the persistent nature of PTSD symptoms and the limitations of conventional therapies, innovative interventions are urgently needed. One promising avenue of research revolves around the modulation of cortisol through targeting receptors, with dexamethasone emerging as a critical agent capable of reducing cortisol levels, thus potentially aiding in the extinction of fear. In this study, we emphasize the need for innovative interventions in the neuropharmacological treatment of PTSD, focusing on cortisol modulation and its impact on fear regulation mechanisms. The complex interplay between the HPA axis, cortisol modulation, and fear dysregulation not only broadens our comprehension but also reveals promising paths to enhance therapeutic outcomes for individuals struggling with PTSD, under- scoring a crucial need for more effective treatment strategies.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-01-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143032415","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Metabolomic Changes in Major Depressive Disorder Adolescent Females with or without Suicide Attempts.","authors":"Wei-Xi Deng, Xiao-Bo Liu, Tian Guo, Li-Fei Shang, Yi Li, Kuan Zeng, Jing-Yi Long","doi":"10.2174/1570159X23666250122093451","DOIUrl":"https://doi.org/10.2174/1570159X23666250122093451","url":null,"abstract":"<p><strong>Background: </strong>The incidence of Major Depressive Disorder (MDD) is high among adolescent females, and MDD is often accompanied by suicide attempts (SAs), which have a serious negative impact on health. However, changes in lipids, thyroid hormone, and brain metabolism among female adolescents with MDD and the relationships between these three markers and MDD with SA have yet to be elucidated.</p><p><strong>Methods: </strong>This study enrolled 71 MDD patients with SA (MDD+SA), 66 MDD patients without SA (MDD-SA), and 47 healthy controls (HCs). We analysed the lipid and thyroid hormone levels and magnetic resonance spectroscopy results of the subjects.</p><p><strong>Results: </strong>Low levels of social support, high levels of life stress, and high levels of suicidal ideation (SI) were risk factors for SA. In MDD patients, 1) thyroid stimulating hormone was positively correlated with triglyceride (TG) and N-acetyl aspartic acid (NAA)/creatinine in the prefrontal cortex (PFC) and negatively correlated with high-density lipoprotein and the choline/creatinine in the thalamus; 2) free thyroxine was negatively correlated with the choline/creatinine in the thalamus; 3) total cholesterol, TG, low-density lipoprotein, and choline/NAA in the PFC were positively correlated with the severity of SI and suicide risk; and 4) NAA/creatinine in the thalamus was negatively correlated with the severity of SI and suicide risk.</p><p><strong>Conclusion: </strong>In female adolescents with MDD, there are significant synergistic changes in lipids, thyroid hormones, and brain metabolism-related factors, and the changes in these indicators may be related to the pathological mechanism of SA.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143022558","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modulation of in vitro Network Activity by Optogenetic Stimulation of Parvalbumin-positive Interneurons During Estrous Cycle.","authors":"Fei Ran Li, Maxime Lévesque, Siyan Wang, Mia Gemayel, Massimo Avoli","doi":"10.2174/011570159X326861241129093354","DOIUrl":"https://doi.org/10.2174/011570159X326861241129093354","url":null,"abstract":"<p><strong>Background: </strong>Catamenial epilepsy, which is defined as a periodicity of seizure exacerbation occurring during the menstrual cycle, has been reported in up to 70% of epileptic women. These seizures are often non-responsive to medication and our understanding of the relation between menstrual cycle and seizure generation (i.e. ictogenesis) remains limited.</p><p><strong>Methods: </strong>Here, we employed the in vitro 4-aminopyridine model of epileptiform synchronization, to analyze the effects induced by optogenetic activation of parvalbumin (PV)-positive interneurons at 8 Hz during estrous and non-estrous phases in female PV-ChR2 mice.</p><p><strong>Results: </strong>We found that: (i) optogenetic stimulation of PV-positive interneurons induced an initial interictal spike followed by field oscillations occurring more often in estrous (59%) than in non-estrous slices (17%); (ii) these oscillations showed significantly higher power in estrous compared to nonestrous slices (p < 0.001); (iii) significantly higher rates of interictal spikes and ictal discharges were identified in both estrous and non-estrous slices during optogenetic stimulation of PV-positive interneurons compared to periods of no stimulation (p < 0.05); and (iv) ictal events appeared to occur more frequently during optogenetic stimulation in estrous compared to non-estrous slices.</p><p><strong>Conclusion: </strong>Our findings show that optogenetic activation of PV-interneurons leads to more powerful network oscillations and more frequent ictal discharges in estrous than in non-estrous slices. We conclude that during the rodent estrous cycle, PV-interneuron hyperexcitability may play a role in epileptiform synchronization and thus in catamenial seizures.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143022559","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Integrating Forensic Autopsies with Proteomic Profiling for Suicide Risk Assessment: A Comprehensive Review of Literature.","authors":"Ibrahim H Al-Habash, Asma Mahmoud Alshaeb, Viktorija Belakaposka Srpanova, Djordje Alempijevic, Milica Keckarevic-Markovic, Monica Concato, Davide Radaelli, Stefano D'Errico","doi":"10.2174/011570159X344453241129073214","DOIUrl":"https://doi.org/10.2174/011570159X344453241129073214","url":null,"abstract":"<p><strong>Background: </strong>Suicide is a major global public health concern that affects people of all ages, with over 700000 individuals intentionally ending their lives every year. Suicide is a multifactorial event related to multiple risk factors interlocking with each other, among which neurobiological factors are considered to be an objective measure of the incidence of this phenomenon and can be used as a measurable tool for evaluating suicidal tendencies.</p><p><strong>Objective: </strong>The aim of this study is to thoroughly examine available data and assess candidate proteins as prospective biomarkers for predicting suicides and ascertaining the manner of death in forensic cases.</p><p><strong>Methods: </strong>An electronic search was conducted on PubMed, Science Direct Scopus, and the Excerpta Medica Database. The systematic review adhered to PRISMA guidelines and encompassed case series, prospective and retrospective studies, and short communications published in English. The focus was on proteomics and suicide, specifically, those studies where researchers conducted human proteomic analyses on specimens obtained from individuals who completed or attempted suicide.</p><p><strong>Results: </strong>A total of 14 studies met the inclusion criteria, resulting in a dataset of numerous candidate protein biomarkers. These include tenascin-C, potassium voltage-gated channel subfamily Q member 3, vimentin-immunoreactive astrocytes, glutathione S-transferase theta 1, iron transport proteins, Acrystallin chain B, manganese superoxide dismutase, glial fibrillary acidic protein, various glycolytic pathway proteins, 14-3-3 eta and 14-3-3 theta proteins, specific cytoskeleton proteins, C-reactive protein, serum amyloid A protein 1, extrinsic coagulation pathway proteins, the vacuolar-type proton pump ATPase subunit, plasma apolipoprotein A-IV, and ER stress proteins. These proteins are proposed as a panel of biomarkers to be evaluated in conjunction with other clinical predictors of suicide.</p><p><strong>Conclusion: </strong>This review aims to provide a comprehensive summary of all proteomic studies conducted on cases of attempted or completed suicide. By doing so, it seeks to bridge existing gaps in knowledge and pave the way for future investigations. The ultimate goal is to potentially identify a suicide biomarker.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143001651","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Myelin Repair as a Novel Mechanism for Ketamine's Sustained Antidepressant Effects.","authors":"Sen Wang, Chaoli Huang, Mengyu Wang, Lingxiao Di, Cunming Liu, Kenji Hashimoto, Chun Yang","doi":"10.2174/011570159X349856241213144902","DOIUrl":"https://doi.org/10.2174/011570159X349856241213144902","url":null,"abstract":"<p><p>Depression is a prevalent mental disorder, affecting approximately 300 million people worldwide. Despite decades of research into the underlying mechanisms of depression, a consensus remains elusive. Recent studies have implicated changes in oligodendrocytes and myelin in the pathogenesis of depression. Conventional antidepressants may alleviate symptoms within weeks of use, but approximately one-third of patients do not respond to them. Ketamine exhibits rapid and sustained antidepressant effects in treatment-resistant patients with depression. Given the association between reduced myelination and depression pathology, alterations in myelination may be a key mechanism underlying ketamine's prolonged antidepressant effects. However, the exact role of myelination in ketamine's sustained antidepressant effects remains unclear. In this review, we summarize the relationship between demyelination and depression and discuss the potential mechanisms by which ketamine may exert its antidepressant effects by repairing myelin damage, offering new insights into the role of myelination in antidepressant mechanisms.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143001661","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Partial Dopamine D2/3 Agonists and Dual Disorders: A Retrospective-Cohort Study in a Real-World Clinical Setting on Patients with Schizophrenia Spectrum Disorders and Cannabis Use Disorder.","authors":"Giada Trovini, Ginevra Lombardozzi, Georgios D Kotzalidis, Ilaria Pagano, Emanuela Amici, Valeria Giovanetti, Filippo Perrini, Andrea Fagiolini, Sergio De Filippis","doi":"10.2174/011570159X350599241214042724","DOIUrl":"https://doi.org/10.2174/011570159X350599241214042724","url":null,"abstract":"<p><strong>Introduction/objective: </strong>Schizophrenia with substance use disorder is a complex clinical condition that may increase treatment resistance. Cannabis use disorder is frequently associated with psychosis and the causal link has still to be defined. Partial D2/3 agonists may ensure limbic dopamine release normalization while avoiding reduced frontocortical dopamine release, which would contribute to negative symptoms. We aimed to observe the clinical course of patients with schizophrenia comorbid with cannabis use disorder while being treated with oral or long-acting injectable D2/3 partial agonists.</p><p><strong>Methods: </strong>We observed 96 young adults with schizophrenia/schizoaffective disorder comorbid with cannabis use disorder during 18 months of treatment with aripiprazole long-acting injectable or oral aripiprazole or brexpiprazole. The assessment comprised Clinical Global Impressions-Severity, Positive and Negative Syndrome Scale, Brief Psychiatric Rating Scale, Barratt Impulsiveness Scale, and Visual Analog Scale for Craving.</p><p><strong>Results: </strong>Included were 17 women and 79 men (mean age = 26.89 ± 4.74 years). The sample responded favorably to treatment as assessed by all clinical scales, save for the impulsiveness scale which showed no significant change. The four treatment samples responded well without differences, but employing a general linear model, long-acting injectable aripiprazole and brexpiprazole were better and similar on all clinical and craving scales compared to oral aripiprazole and to other antipsychotics. Long-acting injectable aripiprazole fared better than brexpiprazole on general psychopathology, negative symptoms, and craving, while the reverse was true for global severity. However, the sample size imbalance did not allow for drawing strong conclusions. We found no significant treatment resistance in our 96-patient sample.</p><p><strong>Conclusion: </strong>Partial D2/3 agonists may treat comorbid schizophrenia/schizoaffective disorder and cannabis use disorder, improving the symptoms of both disorders and substance craving.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143001688","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Modulating Ferroptosis: A Novel Approach to Promote Neural Repair in Brain Injury.","authors":"Yanlin Liu, Ying Guo, Huixin Zhou, Yuxin Liu, Yuting Jin, Kaitao Luo, Xiaobing Dou","doi":"10.2174/011570159X343096241209040135","DOIUrl":"https://doi.org/10.2174/011570159X343096241209040135","url":null,"abstract":"<p><p>The increasing prevalence of brain injuries resulting in cognitive and motor function impairments poses a substantial global medical challenge. Nerve repair therapies offer promise for addressing brain injury-related disorders. Ferroptosis, as a cell death mechanism associated with oxidative stress and inflammation. Certain ferroptosis inhibitors, such as iron chelators and antioxidants, exhibit therapeutic potential for brain injury-related conditions. This review explores the fundamental processes and associated mechanisms that regulate neural repair by inhibiting ferroptosis, thereby alleviating brain injury and promoting neuroregeneration. Furthermore, it examines the action mechanisms and potential therapeutic applications of ferroptosis inhibitors in neural repair, aiming to provide novel insights for treating brain injuries.</p>","PeriodicalId":10905,"journal":{"name":"Current Neuropharmacology","volume":" ","pages":""},"PeriodicalIF":4.8,"publicationDate":"2025-01-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143001656","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}