Brain Research最新文献

{"title":"RhoA regulates morphine associated NMDA receptor signaling in the prelimbic region of medial prefrontal cortex pyramidal neurons","authors":"Qiufeng Dong ,&nbsp;Xin Wang ,&nbsp;Yuqi Wen ,&nbsp;Jian Fu ,&nbsp;Liangjun Zhang ,&nbsp;Yile Zhang ,&nbsp;Zhiqiang Yan ,&nbsp;Liang Qu","doi":"10.1016/j.brainres.2026.150184","DOIUrl":"10.1016/j.brainres.2026.150184","url":null,"abstract":"<div><div>Opioid dependence (OD) involves maladaptive neuroplasticity in brain reward circuits, particularly within the medial prefrontal cortex (mPFC). While RhoA and NMDA receptors (NMDARs) are implicated in addiction-related synaptic plasticity, their specific interaction within mPFC subregions remains unclear. Using male Sprague-Dawley rats (6 weeks old), we investigated the role of RhoA signaling in the prelimbic cortex (PLC) via behavioral, molecular biological, and electrophysiological assays. Intra-PLC infusion of the RhoA inhibitor Rhosin significantly attenuated morphine-induced conditioned place preference and locomotor sensitization. Furthermore, repeated morphine administration (RMA) upregulated RhoA expression in layer 5 pyramidal neurons. In vitro whole-cell patch-clamp recordings of layer 5 neurons, stimulated at layer 2/3, revealed that Rhosin reduced the amplitude of synaptic NMDAR-mediated excitatory postsynaptic currents. Additionally, using an activity-dependent MK-801 block to isolate extrasynaptic components, we demonstrated that RhoA inhibition significantly attenuated extrasynaptic NMDAR activation, likely by limiting glutamate spillover during high-frequency stimulation. These findings elucidate a critical mechanism by which RhoA mediates opioid-induced neuroadaptations through the regulation of both synaptic and extrasynaptic NMDAR activity, identifying RhoA in the PLC as a promising therapeutic target for opioid dependence.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1875 ","pages":"Article 150184"},"PeriodicalIF":2.6,"publicationDate":"2026-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146075106","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Inflammation-induced Neuronal Damage in CNS Tuberculosis: Molecular Mechanism and Therapeutic Targets","authors":"Shad Ahmad ,&nbsp;Adil Husain ,&nbsp;Parul Jain ,&nbsp;Firoz Ahmad","doi":"10.1016/j.brainres.2026.150169","DOIUrl":"10.1016/j.brainres.2026.150169","url":null,"abstract":"<div><h3>Background</h3><div>Central nervous system tuberculosis (CNS-TB), most frequently manifesting as tuberculous meningitis, is associated with high mortality and significant long-term neurological morbidity. Increasing evidence suggests that disease severity and neurological damage are driven largely by dysregulated host neuroinflammatory responses rather than direct Mycobacterium tuberculosis–mediated cytotoxicity. However, the mechanistic links between glial activation, inflammatory signaling, and neuronal injury remain incompletely defined.</div></div><div><h3>Materials and Methods</h3><div>A comprehensive literature review was conducted using PubMed, Scopus, and Web of Science databases to identify experimental, clinical, and translational studies investigating neuroimmune mechanisms in CNS-TB. Studies focusing on glial activation, cytokine signaling, oxidative stress, excitotoxicity, mitochondrial dysfunction, and neuronal death were included. Recent advances in single-cell transcriptomics, immunometabolism, and host-directed therapeutic strategies were also analyzed and integrated.</div></div><div><h3>Results</h3><div>The reviewed evidence indicates that CNS invasion by M. tuberculosis leads to sustained activation of microglia and astrocytes, resulting in excessive production of pro-inflammatory cytokines such as TNF-α, IL-1β, and IL-6. This inflammatory milieu disrupts blood–brain barrier (BBB) integrity, promotes leukocyte infiltration, and induces oxidative and nitrosative stress. Astrocyte dysfunction further contributes to excitotoxicity through impaired glutamate clearance. These converging inflammatory, oxidative, and excitotoxic pathways drive mitochondrial dysfunction, synaptic impairment, and activation of regulated neuronal cell death pathways, culminating in neurodegeneration.</div></div><div><h3>Conclusion</h3><div>CNS-TB–associated neuronal injury arises primarily from maladaptive host neuroimmune responses rather than direct mycobacterial effects. A unifying framework centered on glial-driven inflammation and mitochondrial dysfunction provides critical insight into disease pathogenesis. Targeting these convergent pathways through host-directed therapies, alongside antimicrobial treatment, represents a promising strategy to mitigate neuroinflammation and improve long-term neurological outcomes in CNS tuberculosis.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1875 ","pages":"Article 150169"},"PeriodicalIF":2.6,"publicationDate":"2026-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146008955","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Genetics of Autism Spectrum Disorder underscores the role of altered spontaneous neuronal activity as a catalyst for the neurodevelopmental anomalies","authors":"Sarani Dey,&nbsp;Abhijit Das","doi":"10.1016/j.brainres.2026.150164","DOIUrl":"10.1016/j.brainres.2026.150164","url":null,"abstract":"<div><div>Autism Spectrum Disorder (ASD) represents a diverse set of neurodevelopmental disorders diagnosed in children exhibiting common behavioral impairments in social communication and excessive repetitive behaviors. Genetic approaches and large-scale genomic studies have uncovered hundreds of ASD-associated genes with diverse molecular functions contributing to various biochemical and physiological pathways. Despite the underlying genetic diversity, the convergence of phenotypic features suggests the disruption in shared neurobiological mechanisms contributing to ASD. Spontaneous neuronal activity (SNA), the stimulus-independent firing of neurons, which is observed even during neuronal development, has been known to be crucial for neural circuit maturation. Functional neuroimaging studies have demonstrated that SNA is a central process disrupted in ASD patients and mutation-based animal and cellular models. SNA orchestrates critical developmental programs during neuronal maturation such as dendritic arborization, synaptic pruning, excitatory-inhibitory balance, and activity-dependent transcriptional regulation. Perturbations in these dynamics may provide a unifying mechanistic framework linking genetic mutations to abnormal circuit formation and behavioral anomalies. In this review, we collate the genetic and genomic studies to evaluate the contribution of ASD genes in regulating the spontaneous firing of neurons. We classify ASD genes into generators, sensors, transducers, and responders of activity-induced signals and discuss their roles in regulating membrane excitability, transducing the signal to cytoplasmic or nuclear targets to transform the neuronal gene expression program, eventually impacting neuronal and synaptic development. We attempt to substantiate the contribution of altered SNA as the single major common neurological mediator connecting genetic mutations with the common behavioral irregularities manifested in ASD.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1875 ","pages":"Article 150164"},"PeriodicalIF":2.6,"publicationDate":"2026-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145988252","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Single administration of vitamin C produces rapid antidepressant-like effects in female mice: A possible role of dopamine D2 receptor signalling","authors":"Ming-Lian Luo ,&nbsp;Yi-Heng Li ,&nbsp;Xue-Mei Gao ,&nbsp;Yuan-Jian Yang ,&nbsp;Shu-Zhen Jiang","doi":"10.1016/j.brainres.2026.150181","DOIUrl":"10.1016/j.brainres.2026.150181","url":null,"abstract":"<div><h3>Background</h3><div>The lifetime prevalence of depression is significantly higher in women. But the lack of ideal antidepressant severely limits therapies for female specific depressive disorders like perinatal depression. Herein, we evaluated whether vitamin C (ascorbic acid), a widely used nutritional supplement and perinatal therapeutic agent, could serve as a potential treatment for female-related depressive disorders using a chronic restraint stress (CRS) mouse model.</div></div><div><h3>Methods</h3><div>C57BL/6 adult female mice were submitted to a 14-day CRS paradigm to induce depression-like behaviors. The antidepressant potential of vitamin C (200 mg/kg, i.p., a single dose) were assessed in CRS-exposed female mice that exhibited depression-like phenotype. Furthermore, we explored the underlying mechanisms through RNA sequencing, western blotting, and pharmacological interventions.</div></div><div><h3>Results</h3><div>Vitamin C rapidly ameliorated depression-like phenotypes in CRS-exposed female mice within 24 h. The sucrose preference test indicated that the antidepressant effect of vitamin C lasted for more than 72 h. Transcriptome sequencing analysis revealed that vitamin C reversed CRS-induced transcriptional alterations in 104 genes in the medial prefrontal cortex (mPFC) of female mice, including the dopamine receptor D2 (D2R). Western blotting confirmed that CRS suppressed the D2R-ERK1/2-CREB-BDNF pathway in the mPFC, which was effectively rescued by vitamin C. The antidepressant effect of vitamin C was antagonized by the D2R antagonist sulpiride. Additionally, protein–protein interaction network analysis revealed functional linkages between D2R and other vitamin C-regulated stress-sensitive genes.</div></div><div><h3>Conclusions</h3><div>Our findings suggest that vitamin C may serve as an ideal candidate for the treatment of depression in females, potentially through the restoration of the D2R-BDNF pathway.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1875 ","pages":"Article 150181"},"PeriodicalIF":2.6,"publicationDate":"2026-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146036610","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"From truth to deception: a network control theory perspective on brain connectivity and cognitive dynamics","authors":"Ali Rahimi Saryazdi ,&nbsp;Farnaz Ghassemi ,&nbsp;Fatemeh Parastesh ,&nbsp;Karthikeyan Rajagopal ,&nbsp;Sajad Jafari","doi":"10.1016/j.brainres.2026.150159","DOIUrl":"10.1016/j.brainres.2026.150159","url":null,"abstract":"<div><div>Deception represents a sophisticated mental activity that modifies the brain’s dynamic operations. Understanding how brain activity changes during deceptive behavior is important for both cognitive neuroscience and practical applications such as lie detection. Recently, network control theory (NCT) has emerged as a novel tool that combines principles from network science and control theory, offering a powerful framework for quantifying how easily the brain can transition between different cognitive states. In this study, NCT is applied for the first time to examine the effects of deception on brain functional connectivity (FC). Electroencephalogram signals are recorded from 22 participants during a visual task designed to elicit deception. The phase lag index method is then employed to construct FC networks for both truthful and deceptive conditions. The brain is modeled as a linear dynamical system, and two control metrics, average controllability and modal controllability, are computed across five frequency bands: delta, theta, alpha, beta, and gamma. The results reveal significant differences in brain dynamics between the two conditions. In the delta and beta bands, average controllability is significantly higher during truthful responses (p-value &lt; 0.005), while in the gamma band, it is elevated during deception. Additionally, in the beta and gamma bands, modal controllability is significantly higher during deceptive responses (p-value &lt; 0.005). It is observed that during deception, the control energy spectrum shifts from predominance in lower frequencies, which is more evident in truthful responses, toward higher frequencies where energy increases during deception. The outcomes imply that brain connectivity patterns are affected by deceptive behavior and highlight the potential of NCT in advancing deception-related investigations.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1875 ","pages":"Article 150159"},"PeriodicalIF":2.6,"publicationDate":"2026-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145951490","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Tauroursodeoxycholic acid alleviates depression-like behavior induced by chronic unpredictable mild stress through amelioration of catecholamine imbalance","authors":"Natasa Spasojevic,&nbsp;Bojana Stefanovic,&nbsp;Harisa Ferizovic,&nbsp;Milica Jankovic,&nbsp;Kristina Virijevic,&nbsp;Andrea Contos,&nbsp;Sladjana Dronjak","doi":"10.1016/j.brainres.2026.150188","DOIUrl":"10.1016/j.brainres.2026.150188","url":null,"abstract":"<div><div>Depression is thought to emerge as a result of monoamine neuromodulators’ deficiency in a specific central nervous system site. Tauroursodeoxycholic acid (TUDCA) has been found to have a protective role against diseases affecting the central nervous system. The potential effects of TUDCA on brain monoamine neurotransmitters in a stress-induced depression model have not been reported. We investigated the effects of TUCDA treatment on serotonin, norepinephrine and dopamine, catecholamine biosynthesis enzyme tyrosine hydroxylase (TH) and degrading enzyme monoamine oxidase A (MAO-A), NLRP3 and pro-inflammatory IL-1β in the hippocampus and mPFC of male rats subjected to chronic unpredictable mild stress (CUMS). Behavioral results demonstrated that TUDCA exhibits antidepressant and anxiolytic properties. TUDCA treatment markedly reduced the stress-increased the levels of IL-1β and NLRP3 in the hippocampus and mPFC of CUMS rats. Results showed that TUDCA treatment failed to alter serotonin levels in the hippocampus and mPFC, whereas it restored reduced dopamine and norepinephrine in the hippocampus and ameliorated dopamine imbalance in the mPFC of stressed rats. Further analysis showed that TUDCA treatment increases TH expression in the hippocampus and reduces the increased the protein levels of MAO-A in both brain areas. Our research suggests that TUDCA mitigated depressive-like behavior, and the mechanism appeared to be related to the regulation of catecholamine levels and their synthetic and degrading enzymes in both brain areas.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1875 ","pages":"Article 150188"},"PeriodicalIF":2.6,"publicationDate":"2026-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146096976","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Loss of hepaCAM inhibits cholesterol biosynthesis and impairs learning and memory in mice","authors":"Ziyu Qiu ,&nbsp;Qiang Liu ,&nbsp;Juan Zhang","doi":"10.1016/j.brainres.2026.150183","DOIUrl":"10.1016/j.brainres.2026.150183","url":null,"abstract":"<div><div>Cholesterol is a major astrocyte-derived substance that reprograms neuronal lipid metabolism and regulates neuronal function upon uptake by neurons. However, the mechanisms controlling cholesterol biosynthesis and secretion in astrocytes remain poorly understood. Here, we show that hepaCAM, an astrocytic membrane protein, is essential for normal memory function in mice by maintaining synaptic protein levels and synaptic spine density. Mechanistically, hepaCAM promotes neuronal function by modulating SREBP2-dependent cholesterol biosynthesis in astrocytes and facilitating its subsequent secretion. Furthermore, we identify the interaction of hepaCAM and ClC-2 is required for hepaCAM’s regulatory role in cholesterol biosynthesis. Knockdown of hepaCAM in the hippocampus leads to reduced synaptic protein levels, decreased spine density, and impaired memory in mice. Collectively, our findings demonstrate that astrocytic hepaCAM regulates memory function through modulation of the astrocytic cholesterol biosynthesis pathway.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1875 ","pages":"Article 150183"},"PeriodicalIF":2.6,"publicationDate":"2026-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146100027","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Audio-tactile association improves pitch perception in listeners with and without cochlear implants","authors":"Aaron Hodges ,&nbsp;Matthew B. Fitzgerald ,&nbsp;Lloyd May ,&nbsp;Richard T. Lee ,&nbsp;Raymond L. Goldsworthy ,&nbsp;Takako Fujioka","doi":"10.1016/j.brainres.2026.150182","DOIUrl":"10.1016/j.brainres.2026.150182","url":null,"abstract":"<div><div>Auditory perception can improve when accompanied by somatosensory information, with beneficial effects for hard-of-hearing individuals. Further enhancement could occur by mapping discrete musical pitch information onto tactile spatial patterns across four fingertips. Unlike previous studies, we used tactile stimuli that marked only the sound onsets via light pressure from air-inflated plastic membranes. Pre- and post-learning pitch discrimination tests used vocoded-audio only, vocoded-audio with tactile, and tactile-only conditions. The learning phase was a 10-minute nursery song melody listening task with the audio-tactile condition. In Exp. 1, normal-hearing listeners heard melodies in the original audio; in Exp. 2, normal-hearing listeners heard melodies with vocoded-audio; and cochlear implant (CI) users listened to the original audio. All groups performed best in the audio-tactile condition before the learning phase, and these immediate benefits were maximal at intermediate pitch intervals. Furthermore, CI users showed greater improvement in the audio-only condition after exposure, indicating the rapid transfer effect.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1875 ","pages":"Article 150182"},"PeriodicalIF":2.6,"publicationDate":"2026-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146117745","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Therapeutic potential of iPSC-exosomes and miR-7 in Targeting Glioblastoma","authors":"Beyza Yilmaz ,&nbsp;Altay Savalan ,&nbsp;Ayyub Ebrahimi","doi":"10.1016/j.brainres.2026.150185","DOIUrl":"10.1016/j.brainres.2026.150185","url":null,"abstract":"<div><div>Exosomes play a vital role in intercellular communication, significantly influencing cell behavior and fate. Their influence is particularly evident in diseases like glioblastoma, one of the most challenging cancers to treat. Due to glioblastoma’s high resistance to conventional therapies, novel treatment strategies are urgently needed. Exosomes, being nano-sized vesicles capable of crossing the blood–brain barrier, can deliver bioactive molecules, including nucleic acids, proteins, and metabolites, to suppress tumor-promoting activities in cancer cells. Induced pluripotent stem cells (iPSCs), known for their unlimited proliferation potential and lack of ethical concerns compared to embryonic sources, present a valuable source of exosomes for therapeutic purposes. Although embryonic stem cell-derived exosomes have shown anti-tumor effects against glioblastoma, the therapeutic potential of iPSC-derived exosomes remains largely unexplored. In this study, we demonstrate that exosomes derived from iPSCs exert anti-tumorigenic effects on glioblastoma cells. We also focused on microRNAs (miRNAs), key regulators of cellular proliferation and apoptosis, which are considered promising therapeutic targets in glioblastoma. Specifically, we observed that microRNA-7 (miR-7) significantly inhibits glioblastoma cell proliferation, migration, and invasion. Our findings show that treatment with a miR-7-5p mimic reduces glioblastoma cell proliferation, and its combination with iPSC-derived exosomes leads to either additive or synergistic anti-cancer effects. These results highlight iPSC-derived exosomes and miR-7 as promising therapeutic candidates for glioblastoma and potentially other malignancies.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1875 ","pages":"Article 150185"},"PeriodicalIF":2.6,"publicationDate":"2026-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146075107","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The oral-gut-brain axis in periodontitis: microbial signaling in systemic and neuroinflammatory disease","authors":"V. Pravin,&nbsp;Chitra Vellapandian,&nbsp;V. Naveen Kumar","doi":"10.1016/j.brainres.2026.150168","DOIUrl":"10.1016/j.brainres.2026.150168","url":null,"abstract":"<div><div>Periodontitis, a chronic inflammatory disease of the oral cavity, has been identified as a modifiable risk factor of the development of systemic and neurological disorders via a complicated interplay of microbiological, immunological, and neural interactions. Periodontal pathogens breach local immune homeostasis, are translocated to the gut and brain, and trigger a cascade of immune deregulation, leaky gut, and blood–brain barrier, thereby forming a tri-directional communication network that links local oral inflammation to systemic and neurovascular conditions. This review synthesizes existing evidence on how oral dysbiosis, can spread to the gut and trigger systemic inflammation, leading to neuroinflammation and neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, and multiple sclerosis. Mechanistically, the OGB axis acts through various processes, such as hematogenous spread, retrograde axonal transport, immune cell trafficking (Trojan horse mechanism), and extracellular vesicle-based signaling corresponding to the causes of neuroinflammation, microglial activation, and the pathology of tau and amyloid. The diagnostic and therapeutic implications of the OGB axis provide new pathways toward early intervention with precision medicine, microbiome remodeling, immune-based therapy, and neuroprotective approaches. Emerging technologies, including AI-based diagnostics and biosensing technologies, offers noninvasive tools to track host-microbial interactions and inflammatory biomarkers. This integrative view underscores the central importance of oral health in systemic homeostasis and the development of neurodegenerative conditions, necessitating collaborative approaches between dentistry, neurology, and immunology to cooperate to deliver efficacy in disease elimination and mitigation.</div></div>","PeriodicalId":9083,"journal":{"name":"Brain Research","volume":"1875 ","pages":"Article 150168"},"PeriodicalIF":2.6,"publicationDate":"2026-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145988307","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}