Neurochemistry international最新文献

{"title":"Increased spinal adenosine after subacute cervical injury correlates with sustained upregulation of CD39 and CD73 in microglia","authors":"Mackenzie R. Berschel ,&nbsp;Maria Nikodemova ,&nbsp;Jose R. Oberto,&nbsp;Alexandria B. Marciante,&nbsp;Alysha Michaelson,&nbsp;Gordon S. Mitchell","doi":"10.1016/j.neuint.2025.106030","DOIUrl":"10.1016/j.neuint.2025.106030","url":null,"abstract":"<div><div>Cervical spinal cord injuries (cSCI) are associated with decreased breathing ability. Although no treatment options are currently available, moderate acute intermittent hypoxia (mAIH) is a promising therapeutic modality to improve breathing function after cSCI. Moderate AIH elicits phrenic motor plasticity <em>via</em> distinct, competing serotonin- or adenosine-driven mechanisms that interact <em>via</em> powerful crosstalk inhibition that constrains or even abolishes plasticity. The dominant mechanism driving plasticity depends on the spinal serotonin/adenosine balance. Shortly after cSCI, repeated AIH exposure elicits plasticity <em>via</em> an adenosine-dependent mechanism but reverts to serotonin-dominance with chronic cSCI. In healthy CNS, microglia regulate AIH-induced phrenic motor plasticity <em>via</em> enzymatic activities of ectonucleotidases (CD39, CD73) by converting extracellular ATP to adenosine. We hypothesized that cSCI increases microglial ectonucleotidase expression, elevating adenosine levels that may alter therapeutic responses to mAIH post-cSCI. We assessed microglial CD39 and CD73 expression at the subacute (1 &amp; 2 weeks) and chronic (8 weeks) stages post C2-hemisection, both at the injury site (C1–C3) and in spinal segments containing phrenic motor neurons below the injury (C3–C6). Both enzymes were upregulated (mRNA &amp; protein) 1- and 2-weeks post injury but returned to baseline by 8 weeks. In association, spinal adenosine increased significantly at 2, but not 8 weeks post-injury. Further, microglial CD39 and CD73 expression strongly correlate with P2Y12 receptor expression. Thus, shifting adenosine levels between subacute and early chronic cSCI may impact mechanism regulating mAIH-induced respiratory motor plasticity and breathing recovery at different times post-cSCI.</div></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"189 ","pages":"Article 106030"},"PeriodicalIF":4.0,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144779560","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Combined supplementation of short-chain fatty acids reduces hyperphosphorylation of Tau at T181,T231 and S396 sites and improves cognitive impairment in a chemically induced AD mouse model via regulation of HDAC and Keap1","authors":"Dan Pu ,&nbsp;Ye Jin ,&nbsp;Longxing Wang ,&nbsp;Renjun Wang ,&nbsp;Lingyu Li ,&nbsp;Yang Song ,&nbsp;Xiaofei Han","doi":"10.1016/j.neuint.2025.106034","DOIUrl":"10.1016/j.neuint.2025.106034","url":null,"abstract":"<div><div>Alzheimer's disease (AD) is characterized by the pathological hallmarks of β-amyloid deposition and Tau protein hyperphosphorylation, with memory loss and cognitive dysfunction as its primary clinical manifestations. The incidence of AD has been progressively increasing in recent years. Short-chain fatty acids (SCFAs), key effector molecules in host-gut microbial interactions, play a crucial role in maintaining central nervous system homeostasis. In this study, AD mouse model was established via AlCl₃/D-gal induction. The effects of mixed SCFA intervention on spatial learning and memory in AD model mice were assessed using behavioral tests, including the Morris Water Maze. Levels of pro-inflammatory cytokines and activities of oxidative stress-related enzymes in brain and colon tissues were quantified using ELISA and commercial kits. Key protein expression levels were analyzed by Western blot, immunohistochemistry, and immunofluorescence. Results demonstrated that SCFAs significantly alleviated cognitive dysfunction in AD model, reduced Tau hyperphosphorylation at T181, T231 and S396 sites, suppressed pro-inflammatory cytokine release, and enhanced antioxidant capacity, but with no reversal in elevated Aβ levels in AD model. Mechanistically, SCFAs inhibited glial cell activation, upregulated MCT-1 and tight junction proteins in the blood-brain barrier and strengthened gut-brain barrier integrity, potentially regulating small molecule <em>trans</em>-barrier transport. Furthermore, examination of relevant protein expressions revealed that SCFAs activated HDAC1 and inhibited overexpressed HDAC3 and Keap-1 in AD mice model. These findings suggest that SCFAs may regulate epigenetic modifications in the brain of AD to exert neuroprotective effects. This study provides novel evidence supporting the potential of symbiotic microbe-derived SCFAs in alleviating AD.</div></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"189 ","pages":"Article 106034"},"PeriodicalIF":4.0,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144852112","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circular RNAs from the MAPT and TARDBP genes: Novel players in neurodegeneration?","authors":"Naghme Bagheri ,&nbsp;Giorgi Margvelani ,&nbsp;Tai-Wei Chiang ,&nbsp;Peter T. Nelson ,&nbsp;Trees-Juen Chuang ,&nbsp;Stefan Stamm","doi":"10.1016/j.neuint.2025.106019","DOIUrl":"10.1016/j.neuint.2025.106019","url":null,"abstract":"<div><div>The microtubule associated protein tau (<em>MAPT</em>) and TAR DNA binding protein (<em>TARDBP</em>) genes play crucial roles in neurodegeneration. The tau protein encoded by <em>MAPT</em> is the main component of tau tangles, a pathologic hallmark of “tauopathies” such as Alzheimer's disease (AD). Cytosolic accumulations of TDP-43, encoded by <em>TARDBP</em> are characteristic for LATE (Limbic-predominant age-related TDP-43 encephalopathy) and other TDPopathies. In addition to the well-characterized mRNA splicing isoforms, both genes generate a multitude of circular RNAs (circRNAs). Both <em>MAPT</em> and <em>TARDBP</em> express circular RNA-specific exons characterized by suboptimal splice sites and lengths and are frequently derived from Alu-elements. Most circTau and to date all circTARDBP RNAs expressed in brain are human-specific, suggesting a possible unique contribution to human brain disease. TARDBP and MAPT circRNAs harbor open reading frames and circTau RNAs were shown to be translated into polypeptides in cells. Thus, circRNAs from the <em>MAPT</em> and <em>TARDBP</em> genes should be considered in molecular analysis of AD, LATE and other neurological diseases.</div></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"189 ","pages":"Article 106019"},"PeriodicalIF":4.4,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144599022","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"TRPM8 modulation alters uptake of Transferrin-mediated Fe3+, mitochondrial Fe2+ and intracellular Ca2+-levels in microglia","authors":"Raima Sing ,&nbsp;Deep Shikha ,&nbsp;Chandan Goswami","doi":"10.1016/j.neuint.2025.106031","DOIUrl":"10.1016/j.neuint.2025.106031","url":null,"abstract":"<div><div>Microglia play an important role in the immunity of the central nervous system, crucial in maintaining homeostasis. However, under diseased conditions, this cell accumulates Fe^2+/3+, triggering inflammatory and neurotoxic effects that contribute to neurodegenerative disorders such as Alzheimer's and Parkinson's. Hence, the study of dysregulated microglial activation and overload of Fe^2+/3+ is crucial in the context of neurodegenerative conditions. Emerging research has identified cold-sensitive ion channels, i.e., TRPM8 in microglia, which can regulate key subcellular functions. This study explores the regulatory function of the TRPM8 in Fe^2+/3+ metabolism and its implications for potential ferroptosis in BV2 microglial cells. We used highly specific fluorescence probes, pharmacological modulators of TRPM8 and performed life cell imaging to understand the uptake of Transferrin-488, mitochondrial Fe²⁺-level, cellular Ca²⁺-levels in live BV2 cells under different experimental conditions. Our findings reveal that TRPM8 activation leads to enhanced Transferrin-488-mediated cytosolic Fe³⁺-uptake, disrupts mitochondrial superoxide levels, and promotes cell death. Interestingly, under inflammatory conditions induced by LPS treatment, TRPM8 exhibits a distinct functional role. These results position TRPM8 as an important regulator of microglial Fe^2+/3+ metabolism. This study indicates the involvement of TRPM8 in overload of Fe^2+/3+ leading to ferroptosis and potential for M1-M2 polarization in microglia. These findings impose TRPM8 as a potential therapeutic target for neurodegenerative diseases, and aging.</div></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"189 ","pages":"Article 106031"},"PeriodicalIF":4.0,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144815473","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Probing impact of sleep deprivation on hippocampal neurochemistry in rats using CEST imaging and 1H-MRS at 7.0T MRI","authors":"Zhihong Zhao ,&nbsp;Lvhao Wang ,&nbsp;Xiaolei Zhang ,&nbsp;Yue Chen ,&nbsp;Xinhui Zheng ,&nbsp;Renhua Wu","doi":"10.1016/j.neuint.2025.106020","DOIUrl":"10.1016/j.neuint.2025.106020","url":null,"abstract":"<div><h3>Purpose</h3><div>Sleep is a physiological process that plays a crucial role in maintaining cognitive functions. The hippocampus, a key brain region implicated in cognition, is particularly sensitive to sleep deprivation. we aim to investigate impact of sleep deprivation on hippocampal neurochemistry in rats using CEST imaging and ¹H-MRS.</div></div><div><h3>Methods</h3><div>Twelve female Sprague-Dawley rats were randomly divided into sleep deprivation and control groups. All rats experienced Morris water maze training and testing from Day 1 to Day 6 and underwent MRI scans including CEST imaging and ¹H-MRS on Days 1 and Day 3. Lastly, rats were euthanized for Nissl staining.</div></div><div><h3>Results</h3><div>Sleep deprivation led to a significant decrease in CEST signals across various frequency offsets (0.5–3.5 ppm) in the hippocampus (P &lt; 0.05). Meanwhile, sleep deprivation caused an increase in glutamate (P &lt; 0.0001) with no alterations in other metabolites (P &gt; 0.05). Behaviorally, sleep deprivation impaired learning-memory abilities, evidenced by reduced target quadrant distance (P &lt; 0.001) and time (P &lt; 0.01) in the Morris water maze. Histologically, sleep deprivation caused a decline of surviving neurons in the hippocampal CA1 and CA3 regions (P &lt; 0.001). These indicators correlated negatively with the concentrations of glutamate (P &lt; 0.05) and positively with most of the CEST signals (P &lt; 0.05) in the hippocampus.</div></div><div><h3>Conclusion</h3><div>The integration of CEST imaging and ¹H-MRS offers a promising approach for identifying imaging biomarkers that aid in the assessment and management of sleep deprivation's impact on hippocampal neurochemistry.</div></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"189 ","pages":"Article 106020"},"PeriodicalIF":4.4,"publicationDate":"2025-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144658092","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The potentiating activity of benzodiazepine site of the GABA(A) receptor is inhibited by competitive antagonists of orthosteric site","authors":"Elena I. Solntseva,&nbsp;Julia V. Bukanova,&nbsp;Rodion V. Kondratenko","doi":"10.1016/j.neuint.2025.106018","DOIUrl":"10.1016/j.neuint.2025.106018","url":null,"abstract":"<div><div>Benzodiazepines (BDZs) are widely-prescribed drugs that act as positive allosteric modulators of GABA_A receptor, enhancing the GABA-elicited chloride current (<em>I</em>_GABA). In this work, we studied the influence of competitive antagonists of the GABA_A receptor gabazine (GBZ), bicuculline (Bic), and amiloride (Ami) on the potentiating effect of the agonist of BDZ site zolpidem (Zolp). These antagonists bind to their own sites, which partially overlap with the orthosteric site. The experiments were carried out on native GABA_A receptors in isolated Purkinje cells of the rat cerebellum. The <em>I</em>_GABA was measured using the patch-clamp technique and a system of fast application. The effects of the drugs on <em>I</em>_GABA were assessed by the change in the EC₅₀ value for GABA dose-effect curve constructed in the ranges of 0.5–100 μM GABA. Changes in EC₅₀ values as a percentage relative to the control were calculated. 0.5 μM Zolp shifted the GABA curve to the left and decreased the EC₅₀ by 54 % (from 4.8 μM to 2.2 μM). Competitive antagonists shifted the GABA curve to the right and increased the EC₅₀ to 72.6 μM (0.5 μM GBZ), 25.5 μM (500 μM Ami) and 28.8 μM (5 μM Bic). With the addition of Zolp, these EC₅₀ values decreased by 21–25 % and were 56.8 μM (GBZ), 19.2 μM (Ami), and 22.7 μM (Bic), respectively. The results show that the potentiating effect of Zolp is reduced by half in the presence of competitive GABA_A receptor antagonists (p &lt; 0. 001).</div></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"188 ","pages":"Article 106018"},"PeriodicalIF":4.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144581127","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"DNA methylation and hydroxymethylation dynamics in the aging brain and its impact on ischemic stroke","authors":"Vijay Arruri ,&nbsp;Pallavi Joshi ,&nbsp;Raghu Vemuganti","doi":"10.1016/j.neuint.2025.106007","DOIUrl":"10.1016/j.neuint.2025.106007","url":null,"abstract":"<div><div>DNA methylation and hydroxymethylation patterns at the 5th carbon of cytosine (5mC and 5hmC) in CpG dinucleotides tightly regulate gene transcription in normal physiology, aging, and associated diseases, including ischemic stroke. Resilience to ischemic brain injury depends on the interplay of diverse neural and non-neural cell types, whose gene expression and identity are predominantly regulated by brain-enriched epigenetic mechanisms, particularly the dynamics of 5mC and 5hmC in response to changing transcriptional demands under ischemic stress. In this review, we discussed the role of 5mC and 5hmC in aging and the pathophysiology of stroke. Given the high degree of inter-individual variability in stroke studies and its multifactorial etiology, we emphasize the need for personalized, temporally controlled, epigenome-based therapies to improve stroke outcomes.</div></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"188 ","pages":"Article 106007"},"PeriodicalIF":4.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144279359","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Thiamet-G ameliorates Parkinson's disease-associated cognitive impairment via increasing O-GlcNAcylation of STING in the microglia","authors":"Shanshan Zhu ,&nbsp;Nan Wang ,&nbsp;Shuyang Chen ,&nbsp;Ju Zou ,&nbsp;Sijie Tan","doi":"10.1016/j.neuint.2025.106014","DOIUrl":"10.1016/j.neuint.2025.106014","url":null,"abstract":"<div><div>Microglia activation contributed to the development of Parkinson's disease (PD)-associated cognitive impairment and targeting microglia may be a promising strategy for improving the cognitive function in PD. O-GlcNAclytion is a novel protein post-translational modification with cognitive enhancing effects. This study aimed to investigate the effects of Thiamet-G (TMG), an O-GlcNAcase inhibitor that can increase the intracellular O-GlcNAclytion levels, on PD-associated cognitive impairment and the mechanism related to microglia activation. A PD mouse model was established using rotenone (ROT) and the cognitive functions of these mice were investigated by behavioral tests. The anti-inflammatory effects of TMG were tested in the BV2 microglia cells. TMG treatment significantly improved the cognitive function in the ROT-induced PD mouse model as evidenced by the Y-maze test and objective recognition test. Histological studies showed that TMG decreased the reactive microglia via increasing the total protein O-GlcNAclytion levels in the hippocampus of the PD mice. In the in vitro studies, TMG inhibited ROT-induced inflammation via decreasing the pro-inflammatory cytokines such as TNF-α, IL-1β and IL-6 in BV2 microglia cells. Bioinformatic analysis revealed that STING, a core protein in the innate immunity regulation, might be a novel target of O-GlcNAclytion. The <strong>i</strong>mmunoprecipitation experiments further confirmed that TMG inhibited STING phosphorylation via increasing O-GlcNAcylation. Taken together, <span>TMG</span> might ameliorate PD-associated cognitive impairment via increasing O-GlcNAcylation of STING in microglia, which provided evidence supporting that inhibiting the inflammatory response of microglia by elevating the O-GlcNAclytion levels might be an effective strategy for improving the cognitive function in PD.</div></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"188 ","pages":"Article 106014"},"PeriodicalIF":4.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144502576","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of NLRP6 inflammasome on neuroinflammation in temporal lobe epilepsy","authors":"Yiming Guo ,&nbsp;Jiaqi Song ,&nbsp;Yingxi Chen ,&nbsp;Yang Lü ,&nbsp;Weihua Yu","doi":"10.1016/j.neuint.2025.105994","DOIUrl":"10.1016/j.neuint.2025.105994","url":null,"abstract":"<div><div>Epilepsy is one of the most common and severe chronic brain diseases, affecting up to 70 million people worldwide. Neuroinflammation plays a central role in the progression of the disease. The Nod-Like Receptor Protein 6 (NLRP6) inflammasome assembles with apoptosis-associated speck-like protein (ASC) to cleave pro-caspase-1 into caspase-1, thus forming the NLRP6 inflammasome. This process promotes the maturation and release of downstream interleukins (IL)-18 and IL-1β, exacerbating pathological processes in various diseases. In this study, we demonstrated significantly enhanced NLRP6 expression in the cortex and hippocampus of epileptic mice, suggesting a role for the inflammasome in epilepsy. Immunofluorescence staining further revealed that NLRP6 was predominantly expressed in hippocampal neurons of these mice. Additionally, knockdown of NLRP6 reduced susceptibility to epilepsy, alleviated post-seizure neuronal damage, and decreased levels of pro-inflammatory cytokines, including IL-18, IL-1β, and IL-6. Conversely, NLRP6 overexpression produced opposite effects, which were effectively reversed by treatment with the caspase-1 inhibitor VX765. To the best of our knowledge, this is the first study to demonstrate a link between NLRP6 and the activation of the caspase-1/IL-1β/IL-18 signaling pathway in a kainic acid (KA)-induced epilepsy mouse model. Administration of VX765 alleviated pathological alterations and exerted neuroprotective effects. These findings suggest that NLRP6 plays a critical role in the initiation and progression of epilepsy.</div></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"188 ","pages":"Article 105994"},"PeriodicalIF":4.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144106394","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Repetitive transcranial magnetic stimulation as a universal modulator of synaptic plasticity: Bridging the gap between functional and structural plasticity","authors":"Danica Popovic ,&nbsp;Milorad Dragic","doi":"10.1016/j.neuint.2025.106021","DOIUrl":"10.1016/j.neuint.2025.106021","url":null,"abstract":"<div><div>Repetitive transcranial magnetic stimulation (rTMS) is a painless and non-invasive technique for neuromodulation that has shown great potential in therapy of several neurodegenerative and neuropsychiatric disorders both in patients and animal models. In addition to its non-invasiveness, the main rationale for using it for these disorders is that the positive effects extend beyond the stimulation period and can last up to several minutes, hours or even days after the last application. While the mechanisms underlying these long-lasting positive effects have not yet been fully deciphered, current literature supports hypothesis of modulation of both functional and structural plasticity. Dendritic spines are structures on dendritic branches that regulate synaptic transmission at the level of postsynapse and represent one of the structural and functional carriers of synaptic plasticity. Since rTMS has been proposed to induce long-term potentiation/long-term depression-like effects, based on the existing literature in animal studies, we suggest several molecular mechanisms which could underpin rTMS-induced structural plasticity manifested at the level of dendritic spines that include processes starting from spinogenesis to gradual spine maturation and eventual spine shrinkage and loss. The results gathered in this review postulate rTMS as a universal modulator of synaptic plasticity, which could guide future research and help in optimizing appropriate protocols of transcranial magnetic stimulation for adequate disorders and pathologies.</div></div>","PeriodicalId":398,"journal":{"name":"Neurochemistry international","volume":"188 ","pages":"Article 106021"},"PeriodicalIF":4.4,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144597494","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}