NeuroImmune pharmacology and therapeutics最新文献

{"title":"The 30^th Scientific Conference of the Society on NeuroImmune Pharmacology in Annapolis, Maryland, May 3^rd - 6^th, 2026.","authors":"Linda Chang, Susmita Sil, Jerel Adam Fields, Allison Andrews, Servio Ramirez, Richard Noel","doi":"10.1515/nipt-2026-0006","DOIUrl":"https://doi.org/10.1515/nipt-2026-0006","url":null,"abstract":"<p><p>The 30^th Annual Society on Neuroimmune Pharmacology (SNIP) conference will be held on May 3-6^th at the Graduate Hotel by Hilton in Annapolis, Maryland. This 4-day conference will present preclinical, translational, and clinical research in the intersecting fields of neuro-HIV and substance use disorders, as well as related neurodegenerative conditions. The speakers and poster presenters will share cutting-edge research funded by the National Institutes of Health. On the first day, we will have two concurrent preconference symposia. The first is \"Single Cell HIV and SUD Effects on the Brain: SCORCH Consortium Progress\", with an overview and 7 presentations by investigators, highlighting the outstanding work in the Single Cell Opioid Response in the Context of HIV (SCORCH). The second concurrent symposium is \"Catalyzing Interdisciplinary Research on HIV-Associated Co-occurring Conditions.\" In the evening, we will have our first Poster Session with 52 abstracts by early-stage-career investigators (ECIs), including those that received the ECI travel awards. On days 2-4, in addition to a plenary talk and two memorial lectures, we will have 11 symposia, with 62 speakers (including 12 who are early-stage career investigator travel awardees), and 65 additional poster presentations. In total, the 30^th SNIP conference received 185 abstracts for the 70 oral presentations and 115 posters. Topics covered by these symposia and poster presentations include mechanistic and observational studies that evaluate neuronal injury and neuroinflammation associated with HIV brain infection, and how drugs of abuse, including stimulants, opioids, and cannabis, may exacerbate or mitigate neuropathogenesis. In addition, with the aging population of people with HIV and many with substance use disorders, recent work also evaluated how aging and various neurodegenerative disorders could further impact brain health. At the plenary lecture, Dr. Nora Volkow will highlight the priorities of HIV research at the National Institute on Drug Abuse (NIDA), while our banquet speaker, Dr. Avindra Nath will elucidate how viruses, particularly retroviruses, may invade the brain, infect brain cells, and adapt to the local environment for decades or mutate and possibly lead to neurodegenerative disorders. This will be an exciting conference that will continue SNIP's emphasis on the career development of early-stage investigators.</p>","PeriodicalId":74278,"journal":{"name":"NeuroImmune pharmacology and therapeutics","volume":"5 1","pages":"1-77"},"PeriodicalIF":0.0,"publicationDate":"2026-04-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13123886/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147791511","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":"Loss of AMPK potentiates inflammation by activating the infammasome in a preclinical mouse model of TBI.","authors":"Mohammad Ejaz Ahmed, Hamid Suhail, Mohammad Nematullah, Benoit Viollet, Shailendra Giri, Abdullah Shafique Ahmad","doi":"10.1515/nipt-2024-0019","DOIUrl":"10.1515/nipt-2024-0019","url":null,"abstract":"<p><strong>Objectives: </strong>Traumatic brain injury (TBI) is a major cause of mortality and long-term neurological disabilities. Adenosine monophosphate-activated protein kinase (AMPK), a key cellular energy sensor, plays a critical role in maintaining energy homeostasis. Loss of AMPK phosphorylation following TBI impairs the restoration of cellular energy homeostasis and promotes inflammation. In this study, we investigated whether post-TBI loss of AMPK worsens functional impairments, amplifies inflammation, and exacerbates tissue damage in a mouse model of TBI.</p><p><strong>Methods: </strong>Adult male C57BL/6 wild-type (WT) and (AMPKα1-KO) mice were subjected to TBI or sham surgery. Behavioral assessments were performed at 24 h post-TBI, followed by mice were anesthetized, and their brains were rapidly collected for histological and biochemical analyses. To further support our findings, mixed glial cells isolated from WT and AMPKα1-KO pups were treated with lipopolysaccharides and interferon-gamma (LI) (0.1 μg/ml LPS and 20 ng/ml IFNg) for 6 h to induce an inflammatory response.</p><p><strong>Results: </strong>Our results show that TBI reduces AMPK phosphorylation in WT mice and that AMPK loss correlates with worsened behavioral deficits, enhanced NLRP3 inflammasome activation, and elevated levels of pro-inflammatory mediators, including IL-1β. Similarly, AMPKα1-KO glial cells exhibited greater activation of NLRP3 inflammasome and higher expression of pro-inflammatory markers, such as IL-1β, IL-6, TNF-α, iNOS, and Cox 2, compared with WT cells.</p><p><strong>Conclusions: </strong>Collectively, our results demonstrate that AMPKα1 is a critical endogenous regulator of glial-driven neuroinflammation and secondary tissue damage following TBI. Restoring AMPKα1 activity after TBI may therefore represent a promising therapeutic strategy to attenuate neuroinflammation and limit TBI-associated neurological damage.</p>","PeriodicalId":74278,"journal":{"name":"NeuroImmune pharmacology and therapeutics","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13034800/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147596605","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":"HIV-1 Tat expression drives progressive synaptic decline: evidence from longitudinal [¹¹C]-UCB-J PET imaging.","authors":"Tara Chand Yadav, Isabella C Orsucci, Spencer V Thompson, Zhanhong Wu, Zibo Li, Hong Yuan, Barkha J Yadav-Samudrala, Sylvia Fitting","doi":"10.1515/nipt-2025-0020","DOIUrl":"10.1515/nipt-2025-0020","url":null,"abstract":"<p><strong>Objectives: </strong>In the era of combined antiretroviral therapy (cART), human immunodeficiency virus type 1 (HIV-1) is considered a chronic condition that continues to affect the brain. As synaptodendritic injury occurs early, often years before the onset of clinical symptoms, noninvasive neuroimaging methods such as positron emission tomography (PET) hold promise for early detection.</p><p><strong>Methods: </strong>A doxycycline (DOX)-inducible HIV-1 Tat_1-86 transgenic mouse model was used to examine the longitudinal impact of Tat expression on synaptic density <i>in vivo.</i> PET imaging with [¹¹C]-UCB-J, a radiotracer targeting synaptic vesicle glycoprotein 2A (SV2A), was performed at 0-, 2-, and 12-weeks after Tat induction via DOX to assess progressive changes in synaptic density in the cerebrum. Complementary Western blot analyses were conducted at 12 weeks of Tat induction to measure SV2A and PSD-95 protein levels across the cortex, prefrontal cortex, striatum, and cerebellum.</p><p><strong>Results: </strong>Longitudinal [¹¹C]-UCB-J PET imaging revealed a progressive decline of SV2A in the cerebrum of DOX treated Tat(+) mice compared to Tat(-) controls. Western blot analyses demonstrated a significant genotype x sex interaction in the cortex in which Tat expression reduced SV2A protein levels in females, without affecting males. Further, lower SV2A protein levels were noted overall in males relative to females in the cortex, prefrontal cortex, and cerebellum. No significant effects were detected for PSD-95 protein expression.</p><p><strong>Conclusions: </strong>These findings provide <i>in vivo</i> evidence that HIV-1 Tat expression contributes to progressive synaptic density decline and highlight sex-dependent differences in SV2A regulation, supporting SV2A as a biomarker for synaptic alterations in neuroHIV.</p>","PeriodicalId":74278,"journal":{"name":"NeuroImmune pharmacology and therapeutics","volume":"5 1","pages":"79-92"},"PeriodicalIF":0.0,"publicationDate":"2026-02-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13123889/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147791536","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":"Analyses of astrocyte-neuron lactate shuttle transporter levels in brain tissues from people with HIV-associated neurocognitive impairment and Alzheimer's disease.","authors":"Ali Boustani, Anna Laird, Leeann Shu, Erin E Sundermann, David J Moore, Robert Rissman, Jerel A Fields","doi":"10.1515/nipt-2025-0019","DOIUrl":"10.1515/nipt-2025-0019","url":null,"abstract":"<p><strong>Objectives: </strong>With the success of antiretroviral therapy (ART), people with HIV (PWH) are living longer. As they age, they increasingly face age-related comorbidities, including neurodegenerative conditions. The astrocyte-neuron lactate shuttle (ANLS) is a key mechanism that couples astrocytic glycolysis to neuronal oxidative metabolism, ensuring an adequate energy supply for synaptic activity. Disruption of this system has been implicated in both Alzheimer's disease (AD) and HIV-associated neurocognitive impairment (HIV-NCI), conditions characterized by some overlapping cognitive deficits yet distinct pathological drivers.</p><p><strong>Methods: </strong>We investigated the expression of major ANLS transporters, including glucose transporters (GLUT1, GLUT3) and monocarboxylate transporters (MCT1, MCT2, MCT4), in postmortem frontal cortex from individuals with AD and PWH. There were two HIV cohorts based on viral suppression (suppressed/non-suppressed), and both were stratified by neurocognitive status (neurocognitively normal/neurocognitively impaired), while AD participants were compared to cognitively healthy participants. Quantitative immunoblotting and immunofluorescence imaging characterized disease-specific alterations.</p><p><strong>Results: </strong>In AD, both endothelial (GLUT1_{55 kDa}) and astrocytic (GLUT1_{45 kDa}) isoforms were significantly reduced, along with MCT1, indicating widespread impairment of glucose and lactate transport. GLUT3, the neuronal glucose transporter, also showed a marked reduction. In contrast, in virally non-suppressed (VNS) PWH, GLUT1_{45 kDa} and MCT4 were downregulated, while virally suppressed (VS) PWH maintained preserved expression. Correlation analyses revealed strong GLUT3-MCT1 coupling in AD, suggestive of coordinated neuronal-astrocytic adaptation, but disrupted GLUT1-MCT4 relationships in VNS PWH, reflecting ANLS uncoupling under viremia.</p><p><strong>Conclusions: </strong>These findings identify shared and distinct patterns of metabolic disruption: degeneration-driven ANLS failure in AD versus inflammation-driven uncoupling in HIV-NCI.</p>","PeriodicalId":74278,"journal":{"name":"NeuroImmune pharmacology and therapeutics","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2026-02-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12945393/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147328380","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":"CEST MRI assessment of HIV-1-associated neurometabolic impairments in a humanized mouse model.","authors":"Gabriel C Gauthier, Micah Summerlin, Balasrinivasa R Sajja, Mariano G Uberti, Emma G Foster, Manjeet Kumar, Matthew Thiele, Santhi Gorantla, Aditya N Bade, Yutong Liu","doi":"10.1515/nipt-2025-0017","DOIUrl":"10.1515/nipt-2025-0017","url":null,"abstract":"<p><strong>Objectives: </strong>Human immunodeficiency virus 1 (HIV-1)-associated neurocognitive disorders (HAND) persist despite antiretroviral therapy (ART), driven by ongoing neuroinflammation and metabolic dysfunction. This study assesses whether chemical exchange saturation transfer (CEST) MRI can detect HIV-1-induced neurometabolic impairments and ART-mediated improvements in a humanized mouse model.</p><p><strong>Methods: </strong>HIV-1-infected CD34-NSG mice underwent CEST MRI at baseline (Week 0), 6 weeks post-infection (6 WPI), and after 6 weeks of ART or vehicle treatment (12 WPI). CEST contrast was quantified at 2 ppm (creatine-related), 3 ppm (glutamate-related), and -3.5 ppm (nuclear Overhauser effect, NOE). Neuroinflammation and infection were evaluated using immunohistochemistry and qPCR.</p><p><strong>Results: </strong>At 6 WPI, HIV-1 infection reduced 2-ppm CEST contrast in the cortex and hippocampus and increased NOE in the cortex. By 12 WPI, vehicle-treated mice showed decreased 3-ppm contrast in the cortex, hippocampus, and piriform cortex, whereas ART restored contrast in the cortex and hippocampus. Vehicle-treated mice also showed reduced 2-ppm contrast in the cortex, hippocampus, piriform cortex, and thalamus; ART restored this in the hippocampus, piriform cortex, and thalamus. Increased NOE at -3.5 ppm was observed but did not show measurable improvement following ART. CEST alterations corresponded with decreased HIV-1 p24+ cells and reduced neuroinflammatory markers in ART-treated brains.</p><p><strong>Conclusions: </strong>CEST MRI detects region-specific metabolic abnormalities during HIV-1 infection and region-specific metabolic recovery with ART, consistent with reduced viral burden and neuroinflammation. These findings support CEST MRI as a promising non-invasive biomarker for monitoring treatment response and disease progression in neuroHIV.</p>","PeriodicalId":74278,"journal":{"name":"NeuroImmune pharmacology and therapeutics","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12920017/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147273443","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":"S-Equol: a novel therapeutic for HIV-1-associated gastrointestinal dysbiosis.","authors":"Mason T Rodriguez, Sarah J Olmstead, Kristen A McLaurin, Charles F Mactutus, Rosemarie M Booze","doi":"10.1515/nipt-2024-0024","DOIUrl":"10.1515/nipt-2024-0024","url":null,"abstract":"<p><strong>Objective: </strong>HIV-1 infection affects approximately 38.4 million people around the world. The advent of combination anti-retroviral therapy (cART) has greatly improved the quality of life of infected individuals; however, roughly 50 % of these individuals will still experience HIV-1-associated neurocognitive disorders (HAND). Additionally, the gastrointestinal microbiome has been reported to be dysbiotic in HIV-1 infected individuals, regardless of adherence to cART. Current research has pointed to the gut-brain-microbiota axis as a potential target to treat both cognitive deficits and microbial changes. The present study investigated S-Equol (SE) as a potential therapeutic for HAND by modulating the gastrointestinal microbiome.</p><p><strong>Methods: </strong>The study included 21 HIV-1 Tg rats and 21 F344 control animals to test the effect 0.2 mg SE has on cocaine-maintained responding on a PR schedule of reinforcement.</p><p><strong>Results: </strong>Gastrointestinal microbiome alterations between genotypes were found at the phylum and genus level, regardless of treatment group, and SE treatment had both main effects and interactions with genotype. <i>Prevotella_UCG_001</i> was significantly associated with lever presses for drug, suggesting an effect on motivation for cocaine. <i>Alloprevotella</i> was found to significantly differentiate between genotype by treatment effects, indicating that SE differently affects genotypes.</p><p><strong>Conclusions: </strong>SE may provide a novel adjuvant treatment in addition to cART for HIV-1-associated dysbiosis and associated neurocognitive dysfunction.</p>","PeriodicalId":74278,"journal":{"name":"NeuroImmune pharmacology and therapeutics","volume":"4 4","pages":"325-337"},"PeriodicalIF":0.0,"publicationDate":"2025-12-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12755389/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145890720","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":"Extracellular vesicle-based therapies for neurodegenerative diseases.","authors":"Guoku Hu, Christina Gogzheyan, Sudipta Panja, Susmita Sil, Howard E Gendelman","doi":"10.1515/nipt-2025-0016","DOIUrl":"10.1515/nipt-2025-0016","url":null,"abstract":"<p><p>Extracellular vesicles (EVs) are mediators of neurodegeneration and emerging therapeutic tools for central nervous system disorders. On the one hand, they help spread beta amyloid, tau, <i>α</i>-synuclein, TDP-43, and mutant SOD1, contributing to the signs and symptoms of Alzheimer's, Parkinson's, Amyotrophic lateral sclerosis, and Huntington's Diseases. By activating glial cells, they promote chronic neuroinflammation through carrying cytokines, inflammasomes, and chemokines. On the other hand, EVs' ability to transport neuroregulatory products and cross the blood-brain barrier makes them ideal vehicles for drug delivery. Their function can be surface-modified to deliver targeted therapies, including anti-inflammatory and neuroprotective regulatory RNAs, proteins, and lipids, as well as factors that help maintain neural homeostasis. Notably, we suggest that colostrum-derived EVs, enriched with growth factors and immune-regulatory microRNAs, offer a natural, scalable, and biocompatible source for neuroprotective treatment. Although EVs can act as \"Janus-faced\" entities - serving both as disease initiators and versatile therapeutic vehicles - controlling their activity can enable immune-based therapeutics for neurodegenerative diseases.</p>","PeriodicalId":74278,"journal":{"name":"NeuroImmune pharmacology and therapeutics","volume":"4 4","pages":"377-390"},"PeriodicalIF":0.0,"publicationDate":"2025-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12755078/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145890784","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":"Maternal opioid use is associated with altered placental bacterial DNA and activation of immune-apoptotic pathways.","authors":"Yaa F Abu, Junyi Tao, Arumugam Jayakumar, Hussain Hussain, Michel Paidas, Sabita Roy","doi":"10.1515/nipt-2025-0011","DOIUrl":"10.1515/nipt-2025-0011","url":null,"abstract":"<p><strong>Objectives: </strong>Opioid use during pregnancy is associated with adverse perinatal outcomes, but its effects on placental biology are not well understood. Because the placenta plays a vital role in fetal development and immune regulation, we examined how maternal opioid exposure influences microbial DNA signatures and immune gene expression in the placenta.</p><p><strong>Methods: </strong>Placentas from opioid-exposed and control C57 BL/6 female mice were analyzed through 16S rRNA gene sequencing, bulk RNA sequencing and pathway enrichment analysis.</p><p><strong>Results: </strong>Opioid-exposed placentas showed altered microbial DNA profiles, including increased α-diversity and enrichment of <i>Staphylococcus</i> spp. Transcriptomic analysis revealed 357 differentially expressed genes, emphasizing immune pathways, including dendritic cell-NK cell crosstalk, immunogenic cell death, and cytokine storm signaling. STAT3 signaling and heparan sulfate biosynthesis were downregulated. Pathways related to apoptosis, cytotoxicity, and neonatal death were upregulated.</p><p><strong>Conclusions: </strong>Maternal opioid exposure may disrupt placental microbial and immune environments, potentially leading to structural compromise through immune-mediated cellular apoptosis.</p>","PeriodicalId":74278,"journal":{"name":"NeuroImmune pharmacology and therapeutics","volume":"4 4","pages":"353-362"},"PeriodicalIF":0.0,"publicationDate":"2025-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12755123/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145890787","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":"HIV-associated sensory neuropathy: current progress and future challenges.","authors":"Isaac J Gamez, Ajay Pal, Connor Haines, Subo Yuan","doi":"10.1515/nipt-2025-0010","DOIUrl":"10.1515/nipt-2025-0010","url":null,"abstract":"<p><p>Currently, no US Food and Drug Administration-approved treatments exist to manage HIV-associated sensory neuropathy (HIV-SN) and management is largely confined to adjusting antiretroviral therapy (ART) doses and medications. Thus, this urgent health crisis requires strong research commitment to identify a cure or palliative treatment. This review explores the current state-of-the-art related to HIV-SN. It first explores recent developments in the understanding of HIV-SN, emphasizing the importance of developments in the HIV-SN mouse model and non-myelination intra epidermal never fiber denervation. Next, the neurotoxic side effects of ART are summarized. Finally, we explore the interactions and synergy between HIV-SN and ART in the pathogenesis of peripheral neuropathy. While the overall mortality related to HIV has decreased significantly in recent decades, further elucidation of the exact mechanisms of HIV-SN is needed to better treat patients living with HIV as a chronic condition.</p>","PeriodicalId":74278,"journal":{"name":"NeuroImmune pharmacology and therapeutics","volume":"4 4","pages":"363-375"},"PeriodicalIF":0.0,"publicationDate":"2025-12-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12755124/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145890723","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":"Structural Brain Abnormalities and Neuropsychiatric Symptoms in Post-COVID Condition.","authors":"Meghann Ryan, Jared Thomas, Jeremy Wang, Huajun Liang, Eric Cunningham, Thomas Ernst, Linda Chang","doi":"10.1515/nipt-2025-0012","DOIUrl":"10.1515/nipt-2025-0012","url":null,"abstract":"<p><strong>Objectives: </strong>We aimed to cross-sectionally and longitudinally compare brain morphometry and neuropsychiatric symptoms, and evaluate their relationship, in participants with Post-Coronavirus Disease Condition (PCC) and healthy Controls.</p><p><strong>Methods: </strong>At Baseline, 29 PCC (19 female; average age=42.4±12.2 years; 242±156 days since infection) and 25 Controls (14 female; 44.1±12.3 years) completed the NIH Toolbox Emotion, Motor and Cognition Batteries; Patient Reported Outcomes Measurement Information System (PROMIS); and structural brain MRI (thickness, areas, volumes). We compared neurobehavioral performance on the NIH Toolbox and PROMIS and structural brain morphometry for 34 cortical regions and 8 subcortical volumes, between PCC and matched Controls at Baseline (~8 months post-infection) and 11 PCC and 7 Controls at a Follow-Up Visit (~3 years post-infection).</p><p><strong>Results: </strong>At Baseline, PCC had significantly larger putamen and amygdala (FDR-corrected <i>p</i>=0.04; +5.3 and 5.9%) and a trend for larger hippocampus and accumbens (uncorrected-<i>p</i>=0.012 and 0.027, +5.1 and 12.9%) than Controls. PCC also tended to have 4 thicker cortices (<i>p</i>=0.010-0.049; +3.6-6.5%), 6 larger surface areas (<i>p</i>=0.009-0.023; +5.9-8.6%), and 9 larger cortical volumes (<i>p</i>=0.003-0.008; +4.2-10.7%). These abnormal measures were associated with more anxiety, depression, and pain (<i>r</i>=0.5-0.75; <i>p</i>=0.005-0.04). At Follow-Up, PCC had more sadness, fear, pain, and fatigue compared to Controls. However, group differences in morphometry diminished and PCC neurobehavioral performance tended to improve.</p><p><strong>Conclusions: </strong>Structural abnormalities in PCC suggest compensatory processes such as enhanced myelination or neurogenesis, rather than neuroinflammation, which in turn may contribute to persistent neurobehavioral symptoms. However, these alterations and symptoms may improve three years after infection.</p>","PeriodicalId":74278,"journal":{"name":"NeuroImmune pharmacology and therapeutics","volume":" ","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12674627/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145679588","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}