Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology最新文献

{"title":"Cytokine Blockade Attenuates Inflammation and Improves Depressive Psychopathology After COVID-19: A Naturalistic Observational Study.","authors":"Mariagrazia Palladini, Alessia A Azzalin, Margherita Bessi, Rebecca De Lorenzo, Patrizia Rovere-Querini, Francesco Benedetti, Mario Gennaro Mazza","doi":"10.1007/s11481-025-10247-w","DOIUrl":"10.1007/s11481-025-10247-w","url":null,"abstract":"<p><p>Current insight on inflammation in psychiatry suggests that perturbation of inflammatory set points could foster psychopathology and recent evidence support immune-inflammatory mechanisms as targets for antidepressant pharmacology. In the present naturalistic observational study we evaluated the possible effect of the cytokine-blocking agents in preventing the development of post-COVID depression in a large sample of survivors also exploring the relationship between post-COVID depressive risk, treatment with cytokine-blocking agents, and innate immune response markers. 588 COVID-19 survivors were included, of them 374 received the best available treatment at the time and 131 received standard treatment combined with cytokine-blocking agents (anakinra, tocilizumab, sarilumab, reparixin and mavrilimumab). Post-COVID depressive psychopathology was evaluated at short (34.6 ± 17.39 days) and long term (126.76 ± 61.4 days) follow-ups. The systemic inflammation index as (neutrophils*platelets)/lymphocytes was computed in a subgroup of 274 patients. COVID-19 survivors who were treated with cytokine-blocking agents experienced less severe depressive symptomatology and, simultaneously, less susceptibility to develop clinically relevant depression. Moreover, the longitudinal investigations, revealed that patients treated with cytokine-blocking agents underwent a spontaneous symptoms relief over time. Systemic inflammation index decrease over hospitalization was found to affect the susceptibility to long-term depression. Finally, we observed that cytokine-blocking agents' impact on depression was mediated by lowering of systemic inflammation. Our findings indicate potential efficacy of cytokine-blocking agent treatment during the early stages of COVID-19, mitigating post-COVID depressive symptoms by attenuating systemic inflammation. Further investigation through preclinical and clinical studies is warranted to elucidate immune-inflammatory pathways as viable targets for antidepressant psychopharmacology.</p>","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"20 1","pages":"86"},"PeriodicalIF":3.5,"publicationDate":"2025-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145276715","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sinomenine Hydrochloride Impedes Memory Impairments via Nrf2/HO-1-Mediated Inhibition of Oxidative Stress, Neuroinflammation and Apoptosis in Mice Brain.","authors":"Waqar Ali, Kyonghwan Choe, Inayat Ur Rehman, Hyun Young Park, Sihoon Jang, Safi Ullah, Tae Ju Park, Myeong Ok Kim","doi":"10.1007/s11481-025-10243-0","DOIUrl":"10.1007/s11481-025-10243-0","url":null,"abstract":"<p><p>Oxidative stress is a key factor in the progression of Alzheimer's disease (AD) and other neurodegenerative disorders. We evaluated whether sinomenine hydrochloride (SH) exhibits antioxidant and anti-inflammatory effects against cadmium chloride (CdCl2)-induced neurodegeneration and synaptic impairment in mouse brains. The mice were allowed to undergo Cd injection for two weeks. SH was administered orally for eight consecutive weeks (100 mg/kg/bw/mouse, p.o.). The heavy metal cadmium (Cd) disrupts cellular metabolism in the brain, increasing levels of reactive oxygen species (ROS) and lipid peroxidation (LPO), which affects glutathione (GSH) and the production of regulatory enzymes, such as glutathione reductase (GSH-R). An imbalance in this homeostatic system may lead to the downregulation of nuclear factor erythroid-2-related factor 2 (Nrf2) and the enzyme heme oxygenase 1 (HO-1) expression in the Cd-injected mouse brain. Interestingly, the levels of both Nrf2 and HO-1 increased in the Cd + SH-treated mice. Additionally, toll-like receptor 4 (TLR4), phospho-nuclear factor kappa B (p-NF-kB), and phospho-c-Jun N-terminal kinase (p-JNK) expressions were elevated in the Cd-treated group, but significantly downregulated in the Cd + SH-treated mice brains. Similarly, SH inhibits Cd-induced apoptotic markers in mouse hippocampal tissues. These results suggest that SH may mitigate Cd-induced mitochondrial oxidative stress and inflammatory responses in wild-type mice brain hippocampus by regulating the NRF-2/HO-1 signaling pathways.</p>","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"20 1","pages":"85"},"PeriodicalIF":3.5,"publicationDate":"2025-10-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12513979/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145276752","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comparative Study on the Neuroprotective Effects of Perindopril and Benazepril in Experimentally-induced Chronic Mild Stress in Rats.","authors":"Alaa M Badawy, Amany M Gad, Amany E Abdel-Maged, Haidy E Michel, Reem N El-Naga, Samar S Azab","doi":"10.1007/s11481-025-10244-z","DOIUrl":"10.1007/s11481-025-10244-z","url":null,"abstract":"<p><p>Depression remains a major global health issue, characterized by inadequate response rates to conventional antidepressant therapies. This highlights a critical need for novel treatment strategies. Our study investigated the antidepressant effects of benazepril, a non-centrally acting angiotensin-converting enzyme (ACE) inhibitor, and compared it with perindopril, a centrally acting ACE inhibitor. We utilized a rat model of depression induced by chronic unpredictable mild stress (CUMS) to evaluate their efficacy. The CUMS protocol effectively caused several depression-like behaviors and impaired neurobehavioral functions in the rats. Analysis of brain tissues from these animals revealed several key pathological hallmarks: diminished monoamine neurotransmitter levels, heightened oxidative stress, robust inflammatory responses, and increased apoptotic processes. Our findings demonstrated that both perindopril and benazepril significantly reversed these CUMS-induced deficits. Specifically, both ACE inhibitors exhibited potent antioxidant, anti-inflammatory, and anti-apoptotic properties. This was coupled with their effective inhibition of the renin-angiotensin-aldosterone system (RAAS) signaling pathway, a mechanism known to be implicated in stress responses and mood disorders. Notably, while many ACE inhibitors have been extensively studied for their central effects, research on benazepril's direct effects within the brain or central nervous system in rats is notably limited. This study is among the first to highlight the antidepressant potential of benazepril, a non-centrally acting ACE inhibitor, and provides novel insights into its comparative efficacy against perindopril. These results collectively emphasize the broader therapeutic potential of ACE inhibitors in treating depression and underscore the need for further research to fully explore their underlying mechanisms and diverse applications in psychiatric disorders.</p>","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"20 1","pages":"84"},"PeriodicalIF":3.5,"publicationDate":"2025-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12511162/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145253801","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Intranasal Aβ_1-42 Exposure Led To Neurobehavioral Alteration, Neuroinflammatory and Neurodegenerative Molecular Biomarkers in Mice Brain.","authors":"Avtar Singh Gautam, Mohammad Zunaid Akhtar, Lasure Vaibhav Uttamrao, Nisha Kumari, Shivam Kumar Pandey, Mangaldeep Dey, Rakesh Kumar Singh","doi":"10.1007/s11481-025-10246-x","DOIUrl":"10.1007/s11481-025-10246-x","url":null,"abstract":"<p><p>In this study, we aimed to evaluate the AD structural hallmarks along with brain biomarkers and neurobehavioral alterations in a repeated intranasal Aβ_1-42 exposure mouse model. This model is a simple, non-invasive, and less stressful method and may allow direct access of Aβ to the brain. The results of this study showed a dose-dependent increase in the level of Aβ_1-42 deposition, tau phosphorylation, neuroinflammatory and oxidative stress biomarkers in brain tissue, along with learning and memory deficits in mice. This model may be suitable for evaluating the biochemical, structural, functional histological alterations, along with the neurobehavioral deficits mimicking AD.</p>","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"20 1","pages":"83"},"PeriodicalIF":3.5,"publicationDate":"2025-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145240435","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Temporin-1CEa and its Analog LK2(6)A(L) Confer Neuroprotective Effects in Parkinson's Disease Model by Attenuating Neuroinflammation Via the NF-κB and MAPK Signaling Pathways.","authors":"Wenying Zhang, Mingwei Qu, Cui Wang, Dejing Shang","doi":"10.1007/s11481-025-10241-2","DOIUrl":"10.1007/s11481-025-10241-2","url":null,"abstract":"<p><p>The formation of Parkinson's disease is affected by various factors, among which neuroinflammation mediated by microglial activation plays a crucial role in the advancement of neurodegenerative diseases. Antimicrobial peptides temporin-1CEa and its analog LK2(6)A(L) exhibit excellent anti-inflammatory activity. To understand the anti-neuroinflammatory mechanisms of antimicrobial peptides in an immortalized mouse microglial cell line (BV2 cells), and assess neuroprotective effects in a PC12 cell line (rat adrenal pheochromocytoma cell) and Caenorhabditis elegans. Lipopolysaccharide (LPS, 500 ng/mL) was used to induce neuroinflammation in microglial BV2 cells. The effects of antimicrobial peptides on inflammatory cytokines and anti-inflammatory pathways activated by microglia were evaluated using cell counting kit-8 (CCK-8), enzyme-linked immunosorbent assay (ELISA), real-time quantitative PCR(RT-qPCR), and western blotting (WB). An apoptosis model was established by treating PC12 cells with the supernatant of LPS-stimulated BV2 cells, and the influence of antimicrobial peptides on apoptosis was analyzed via flow cytometry (FCM), Western blotting, and caspase-3 and caspase-9 activity assays. In the transgenic nematode BZ555, an LPS (200 μg/mL)-induced model of cephalic dopaminergic neurons (CEPs) injury was developed to explore the protective effects of antimicrobial peptides on dopaminergic neuron damage, food-sensing behavior, body bending, neurotoxicity, and lifespan. Furthermore, NL5901 was employed to evaluate the capacity of antimicrobial peptides to clear the accumulation of alpha-synuclein (α-synuclein) and their impact on body bending, neurotoxicity, and lifespan. Temporin-1CEa and LK2(6)A(L) inhibited the release of pro-inflammatory mediators by downregulating the nuclear factor kappa-B (NF-κB) and mitogen-activated protein kinase (MAPK) signaling pathways. At 3.125 μM, both temporin-1CEa and LK2(6)A(L) inhibited the apoptosis of PC12 cells induced by activated BV2 cells. In vivo experiments in nematodes demonstrated that temporin-1CEa and LK2(6)A(L) alleviated the damage to dopaminergic neurons induced by LPS and mitigated the capability to mitigate the accumulation of α-synuclein. In this study, antimicrobial peptides were shown to control inflammatory factors by downregulating the NF-κB and MAPK signaling pathways, thereby providing valuable insights for the agents in the neuroinflammation model of Parkinson's disease. Additionally, an unexpected finding revealed that these peptides could effectively reduce the accumulation of α-synuclein, which is a critical pathogenic factor, as its aggregated forms significantly contribute to Parkinson's disease progression. Notably, temporin-1CEa and LK2(6)A(L) exerted neuroprotective effects on dopaminergic neurons by inhibiting neuroinflammation and clearing the accumulation of α-synuclein.</p>","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"20 1","pages":"82"},"PeriodicalIF":3.5,"publicationDate":"2025-10-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12500741/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145234359","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Correction to: Inhibition of oxidative stress, neuroinflammatory cytokines, and protein expressions contributes to the antipsychotic effects of geraniol in mice with ketamine-induced schizophrenia.","authors":"Christian I Uruaka, Benneth Ben-Azu, Noah A Omeiza, Emmanuel O Chidebe, Abayomi M Ajayi, Cletus B Lemii, Tamunobarabiye I Nonju, Udeme O Georgewill, Owunari A Georgewill","doi":"10.1007/s11481-025-10239-w","DOIUrl":"https://doi.org/10.1007/s11481-025-10239-w","url":null,"abstract":"","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"20 1","pages":"81"},"PeriodicalIF":3.5,"publicationDate":"2025-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145093199","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Rutin Attenuates Virus Entry and Replication and Exerts Neuroprotection in Experimental Models of Japanese Encephalitis.","authors":"Selamu Kebamo Abate, Rohit Soni, Prasanjit Jena, Arup Banerjee, Debapriya Garabadu","doi":"10.1007/s11481-025-10240-3","DOIUrl":"10.1007/s11481-025-10240-3","url":null,"abstract":"<p><p>Japanese encephalitis virus (JEV), which belongs to the virus family of Flaviviridae, is a threat to more than three billion people globally. There are no antiviral agents against JEV despite the availability of vaccines. This study considered the need for an effective drug against JEV by evaluating the antiviral and neuroprotective potentials of Chicoric Acid (CA) and Rutin in the in vitro and in vivo models of JE. In the in vitro study, CA and Rutin exhibited variable antiviral potency with IC₅₀ values ranging from 11.03 to 24.04 µM and 16.45 to 26.84 µM in different treatment approaches. These agents demonstrated significant antiviral effects via viricidal activity and inhibiting the virus's entry into the host cells. In addition, treatment of JEV-infected SH-SY5Y cells with these compounds significantly reduced the intracellular viral load, the proportion of apoptotic cells, and the ROS level in a dose-dependent manner. In the in vivo studies, Rutin (50 mg/kg) significantly increased the survival rate and attenuated the encephalitis symptoms in the JEV-infected mice compared to other doses. Rutin (25 and 50 mg/kg) significantly reduced infectious viral particles, viral RNA, and viral NS3 protein expression in the mice's brains. Additionally, Rutin significantly mitigated JEV-induced neuroinflammation by decreasing microglial activation, inflammasome formation, proinflammatory cytokine, and ROS levels. In conclusion, Rutin exhibits non-specific viricidal activity, reduced viral load, and inflammatory cytokines; thus, it could be a potential therapeutic option in managing JE, subject to future investigations.</p>","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"20 1","pages":"80"},"PeriodicalIF":3.5,"publicationDate":"2025-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145042123","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Emerging Role of Oligodendrocytes Malfunction in the Progression of Alzheimer's Disease.","authors":"Kinga Tylek, Agnieszka Basta-Kaim","doi":"10.1007/s11481-025-10236-z","DOIUrl":"https://doi.org/10.1007/s11481-025-10236-z","url":null,"abstract":"<p><p>Alzheimer's disease (AD), the most prevalent form of dementia, is characterized by hallmark pathologies such as amyloid-beta (Aβ) plaque accumulation, tau hyperphosphorylation, and progressive neuronal dysfunction. While much attention has focused on neurons and microglia, recent studies underscore the significant yet understudied roles of oligodendrocytes (OL) and oligodendrocyte precursor cells (OPC) in AD pathology. OL, responsible for myelin production and maintenance, are impaired early in AD, contributing to demyelination, synaptic dysfunction, and cognitive decline. Emerging evidence reveals that Aβ and tau pathology disrupt OPC differentiation and induce senescence, exacerbating neuroinflammation and reducing remyelination potential. Demyelination precedes overt AD symptoms, positioning it as a potential early biomarker. Furthermore, animal models reveal that OPC density and function deteriorate with age, particularly in the presence of Aβ plaques, highlighting their vulnerability in the AD environment. Transcriptomic studies also link cholesterol biosynthesis and lipid metabolism dysregulation in OPC to AD progression, emphasizing the intricate relationship between OL, metabolic processes, and amyloid toxicity. Additionally, the identification of disease-associated oligodendrocytes (DAO), characterized by altered gene expression and proximity to Aβ plaques, highlights their involvement in neuroinflammation and APP processing. This review synthesizes recent insights into OL and OPC dysfunction in AD, focusing on their roles in neuroinflammation, Aβ clearance, and myelin integrity. It discusses the potential of targeting OL and OPC pathways, such as enhancing remyelination and mitigating senescence, as novel therapeutic strategies. By addressing gaps in our understanding of OL dynamics, this work sheds light on their critical contributions to AD pathology and sets the stage for future research and intervention.</p>","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"20 1","pages":"79"},"PeriodicalIF":3.5,"publicationDate":"2025-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12399730/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144981205","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Telitacicept Inhibits the Maturation and Differentiation of B Lymphocytes in NMOSD.","authors":"Jie Ding, Chunran Xue, Xinxin Zhao, Xuzhong Pei, Haojun Yu, Qiuju Li, Yi Chen, Xiying Wang, Wendi Yu, Yong Hao, Ye Sun, Zengai Chen, Chong Xie, Yangtai Guan","doi":"10.1007/s11481-025-10237-y","DOIUrl":"10.1007/s11481-025-10237-y","url":null,"abstract":"<p><p>Telitacicept, a novel recombinant fusion protein comprising the ligand-binding domain of the TACI receptor and the Fc component of human IgG, has rarely been studied for the treatment of neuromyelitis optica spectrum disorders (NMOSD). This study aimed to explore the effects of telitacicept in NMOSD mice. An NMOSD mouse model was constructed. Fifty microliters of 0.8 mg/mL telitacicept was injected intravenously on Days 4, 8, 12 and 16 postimmunization (p.i.). Behavioral scoring, magnetic resonance imaging and histopathological evaluation were conducted on Day 19. B lymphocytes and their subgroups were analyzed by flow cytometry. Concentration of serum IgM was measured using an ELISA kit. Concentrations of B lymphocyte stimulator (BLyS) and IL-6 were measured via LEGENDplex. Differentially expressed genes of B lymphocytes were screened via mRNA sequencing and verified by qPCR. Behavioral score of telitacicept-treated NMOSD mice significantly decreased (p < 0.0001). Inflammation, demyelination, loss of AQP4 and GFAP in the spinal cord were markedly alleviated (p < 0.05). B lymphocytes and their subsets were reduced to varying degrees (p < 0.05). Telitacicept treatment significantly reduced serum IgM levels (p < 0.01), as well as BLyS and IL-6 concentrations (p < 0.05). Telitacicept induced differential gene expression in B lymphocytes, inhibiting the expression of transcription factors related to B lymphocyte maturation, such as IRF8, BLIMP1, and Pou2af1, as well as cell surface receptors such as CD19 and CD21. Telitacicept has a therapeutic effect on NMOSD mice by regulating the differentiation of B lymphocyte subsets and inhibiting the production of pathogenic antibodies.</p>","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"20 1","pages":"78"},"PeriodicalIF":3.5,"publicationDate":"2025-08-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144981163","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oscillatory Dynamics Serving Verbal Working Memory Differ in People with HIV and Are Linked To Disease Duration.","authors":"Kellen M McDonald, Seth D Springer, Mikki Schantell, Ryan Glesinger, Lucy K Horne, Hannah J Okelberry, Jason A John, Anna T Coutant, Madelyn P Willett, Hallie J Johnson, Rachel K Spooner, Tony W Wilson","doi":"10.1007/s11481-025-10235-0","DOIUrl":"10.1007/s11481-025-10235-0","url":null,"abstract":"<p><p>BACKGROUND: Medical advances have greatly improved the quality of life and extended the longevity of people with HIV (PWH). However, many PWH still develop neurocognitive deficits even in the presence of effective viral suppression, with impairments in verbal working memory (VWM) being among the most common. While previous neuroimaging studies have demonstrated altered neural responses during VWM, the underlying temporal dynamics and their relation to clinical indices of HIV remain poorly understood. HYPOTHESIS: PWH will have altered neural oscillatory dynamics in brain regions supporting VWM compared to controls, above and beyond the effect of age, and these oscillatory differences will scale with clinical indices of HIV. METHODS: 166 participants (77 virally-suppressed PWH, 89 demographically-matched controls) completed a VWM task during magnetoencephalography, which was separated into encoding and maintenance phases. Whole-brain, mixed-model ANCOVAs were performed to assess the effects of HIV status on neural dynamics controlling for age. RESULTS: PWH performed significantly worse on the task compared to controls. During encoding, there was a significant interaction of group-by-time window, such that PWH had significantly weaker alpha/beta oscillations in the left inferior frontal, superior temporal, and anterior cingulate relative to controls. Further, weaker activity in the anterior cingulate scaled with increased disease duration. PWH also displayed weaker alpha/beta oscillations during maintenance in frontal, temporal, parietal, anterior cingulate, and cerebellar cortices. CONCLUSIONS: PWH exhibited weaker task-related oscillatory activity during VWM, which was associated with disease duration in the anterior cingulate. Overall, these findings suggest that HIV modulates the neural dynamics underlying VWM, with progressive effects in some areas. </p>","PeriodicalId":73858,"journal":{"name":"Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology","volume":"20 1","pages":"77"},"PeriodicalIF":3.5,"publicationDate":"2025-08-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12364757/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144877159","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}