Current Neurology and Neuroscience Reports最新文献

{"title":"Mapping the Silent Onset of Parkinson's Disease: Monoamine Imaging in the Era of the Race for Preclinical Intervention.","authors":"Valentina Leta, Valtteri Kaasinen, Bénédicte Ballanger, Roberto Cilia","doi":"10.1007/s11910-026-01498-y","DOIUrl":"10.1007/s11910-026-01498-y","url":null,"abstract":"<p><strong>Purpose of the review: </strong>The main unmet need of Parkinson's disease (PD) is the lack of a therapy able to slow progression. The field is shifting from syndromic diagnosis toward biologically anchored definitions and staging, enabling PD identification before motor onset. In this context, imaging biomarkers provide in vivo measures to identify subtypes, enrich cohorts, and track changes in disease-modifying trials. This review focuses on the role of monoaminergic imaging for preclinical intervention.</p><p><strong>Recent findings: </strong>Monoaminergic imaging captures both the core substrate of motor phenoconversion and extranigral mechanisms underlying early non-motor symptoms. Presynaptic dopaminergic imaging remains the most robust marker of conversion risk in prodromal cohorts, while noradrenergic and serotonergic imaging delineate early brainstem and limbic involvement. Peripheral autonomic imaging further extends biomarker coverage, with cardiac sympathetic imaging detecting early extracerebral denervation in prodromal stages. Together, harmonised monoaminergic imaging provides a unifying framework for staging and clinical trial readiness.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"26 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148136942","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Astrocytopathy in Wernicke Encephalopathy and Neuromyelitis Optica Spectrum Disorder. Pathogenic Differences With Occasional Clinical and Neuroimaging Overlap. A Review.","authors":"Xiaojun Zhang, Jorge C Kattah","doi":"10.1007/s11910-026-01497-z","DOIUrl":"10.1007/s11910-026-01497-z","url":null,"abstract":"<p><p>PURPOSE OF THE REVIEW: There is an increasing number of single case reports describing patients with findings compatible with thiamine deficiency, in whom rapid replacement of thiamine fails to induce improvement. Further work-up identifies positive aquaporin-4 antibodies (AQP-4) leading to a final diagnosis of neuromyelitis optica spectrum disorder (NMOSD). Occasionally, NMOSD is the initial diagnosis, but it turns out that the patient has thiamine deficiency. Similarly, these two diagnoses may overlap, particularly with area postrema lesions and in other cases of protracted vomiting. RECENT FINDINGS: We reviewed the literature to attempt further clarification for this clinical overlap. The common denominator is the astrocyte, as cytotoxic edema due to impaired mitochondrial dysfunction and lactic acidosis in instances of thiamine deficiency causes downregulation of the AQP-4 receptor leading to vasogenic edema and breakdown of the blood-brain-barrier (BBB). Similar dysfunction of the AQP-4 receptor occurs because of IgG binding antibodies in NMOSD. Impaired glutamate transport in the astrocytic podocytes regardless of the AQP4 receptor etiologic mechanism causes excitotoxicity. Awareness of this clinical overlap is critical to initiate timely treatment in thiamine deficiency states and NMOSD</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"26 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13110201/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147764927","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Functional and Structural Brain Imaging Correlates of Treatment Response in Functional Movement Disorder.","authors":"Christian J Amlang, Alberto J Espay, David L Perez","doi":"10.1007/s11910-026-01496-0","DOIUrl":"10.1007/s11910-026-01496-0","url":null,"abstract":"<p><p>PURPOSE OF REVIEW: Functional movement disorder (FMD) is a biopsychosocially-complex condition with diverse neurologic, physical, and psychiatric manifestations. Converging neuroimaging evidence demonstrates abnormalities in networks supporting self-agency, attention, sensorimotor processing, multimodal integration, salience/threat detection, and interoception. This review summarizes recent work on the prognostic and therapeutic relevance of these findings. RECENT FINDINGS: Baseline functional neuroimaging predictors of outcome implicate cingulo-insular, frontolimbic, and subcortical circuits involved in attention, emotion regulation, and salience processing. Clinical improvement has been associated with activity changes in frontal premotor and regulatory regions, as well as in paralimbic areas. Preliminary studies of transcranial magnetic stimulation, transcranial direct-current stimulation, and neurofeedback suggest that targeted modulation of dysfunctional networks may alleviate symptoms. Neuroimaging features in FMD may inform outcome prediction, elucidate treatment-response mechanisms, and guide neuromodulation strategies. However, the field remains early in development, and larger, longitudinal studies are needed to translate these insights into routine clinical care.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"26 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-04-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147764937","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"When is the Radiologically Isolated Syndrome already Multiple Sclerosis According to the 2024 McDonald Criteria?","authors":"Lies Van Horebeek, Aysika Das, Jake Neufeld, Raphael Schneider","doi":"10.1007/s11910-026-01495-1","DOIUrl":"10.1007/s11910-026-01495-1","url":null,"abstract":"<p><p>PURPOSE OF REVIEW: The McDonald criteria assist neurologists in making accurate and timely diagnoses of multiple sclerosis (MS). The 2024 revision of these criteria aims to enable a more timely diagnosis by including additional biomarkers and alternative diagnostic approaches. They also extend to individuals with MRI findings typical of multiple sclerosis that lack classic MS symptoms, as they would previously have been classified as having radiologically isolated syndrome (RIS). This review examines the scientific foundation of the novel biomarkers used and how the revised criteria influence individuals undergoing diagnostic evaluation, clinical practice, and society. RECENT FINDINGS: Most research concentrates on the scientific foundation for the updates rather than their impact. Benefits and potential disadvantages of the revised criteria can be identified for individuals undergoing diagnostic evaluation, clinical practice, and society. Additional guidelines for real-life application to guide management decisions are advisable.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"26 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-04-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147764942","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessment and Management of Post-traumatic Headache.","authors":"Alex S Aguirre, Yasmine Elhefnawy, Alcy R Torres","doi":"10.1007/s11910-026-01494-2","DOIUrl":"10.1007/s11910-026-01494-2","url":null,"abstract":"<p><p>PURPOSE OF REVIEW: The goal of this narrative review is to provide a comprehensive analysis of Post-Traumatic Headache (PTH), addressing its epidemiology, pathophysiology, and multidisciplinary management. The paper seeks to explore the diagnostic controversies surrounding the timing of symptom onset and evaluates current assessment methods and treatment paradigms for this prevalent sequela of traumatic brain injury. RECENT FINDINGS: Recent research highlights that while current diagnostic criteria require headache onset within seven days of injury, delayed-onset symptoms are common, creating a significant diagnostic dilemma. Pathophysiologically, PTH is understood to be multifaceted, driven by neuroinflammation, neurometabolic cascades, and central sensitization. These processes result in clinical phenotypes that often mirror primary migraine or tension-type headaches. Additionally, while clinical history remains the gold standard for assessment, emerging blood biomarkers are showing promise as objective tools for evaluation. The review concludes that PTH management currently requires a multimodal approach, combining non-pharmacological interventions with pharmacological treatments adapted from primary headache protocols. A major takeaway is the lack of high-quality, PTH-specific randomized controlled trials, which currently forces a reliance on expert opinion rather than robust clinical evidence. To improve patient outcomes, future research must shift toward a more multi-disciplinary, patient-centered paradigm and focus on generating high-quality data to move beyond diagnostic controversies and empiric treatment.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"26 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-04-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147716396","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Redefining Stroke Care with Artificial Intelligence: Recent Advances.","authors":"Shivi Mendiratta, Mark Parsons, Carlos Garcia-Esperon, Amit Mehndiratta","doi":"10.1007/s11910-026-01493-3","DOIUrl":"10.1007/s11910-026-01493-3","url":null,"abstract":"<p><p>PURPOSE OF REVIEW: This review aims to provide an overview of how artificial intelligence (AI) is being integrated into stroke care across the full clinical spectrum with emphasis on its applications in diagnosis, management, and rehabilitation. The focus is on recent advances (2020–2025), addressing key questions on clinical utility and implementation challenges. RECENT FINDINGS: AI has shown promise in enhancing stroke diagnosis through imaging analysis, wearable sensors, and remote monitoring. In stroke management, it supports decision-making and therapy optimization. AI-enabled tools are also improving rehabilitation via robotics and computer vision, and aid prevention through risk prediction and community screening. However, challenges remain in model generalizability, acceptance by the community, and ethical concerns. AI is reshaping stroke care by enabling personalized, timely, and data-driven approaches which can significantly improve quality of life. Future progress will depend on transparent multimodal, globally validated models, supported by interdisciplinary collaboration.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"26 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147644377","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Effects of Adenosine A1/A3 Receptors Agonist on Improving the Outcomes of TBI and Stroke: Focus on AST-004.","authors":"Andrea Howard, Mario Di Napoli, Ahmed S Raihane, Michael Ortiz, Giorgio Bacchin, Sean Maez, Nikita Jaiswal, Eder Cáceres, Alibay Jafarli, Afshin A Divani","doi":"10.1007/s11910-026-01492-4","DOIUrl":"10.1007/s11910-026-01492-4","url":null,"abstract":"<p><p>PURPOSE OF REVIEW: This review explores the therapeutic potential of dual adenosine A1 and A3 receptor (A1R/A3R) agonism as a neuroprotective treatment for acute ischemic stroke (AIS) and traumatic brain injury (TBI). Current AIS treatments, tissue plasminogen activator and mechanical thrombectomy, are limited by narrow therapeutic windows and strict eligibility criteria. In contrast, TBI management remains primarily supportive, with no Food and Drug Administration-approved therapies targeting the underlying molecular pathology. Dual A1R/A3R agonists offer a new approach by modulating injury pathways at the cellular level, potentially serving as an adjunct or alternative to existing therapeutic options. RECENT FINDINGS: A1R and A3R are G protein-coupled receptors that control neuroinflammation, excitotoxicity, and metabolic balance. Preclinical studies using rodent and non-human primate models of AIS and TBI have shown that dual A1R/A3R agonists reduce infarct size, slow lesion growth, preserve penumbral tissue, and enhance neurological recovery. These effects are mediated through astrocyte activation, support of mitochondrial function, and suppression of pro-inflammatory cytokines. The neuroprotective effects follow a U‑shaped dose–response pattern, where only intermediate doses provide benefit, whereas lower and higher doses are less effective. Compared to monotherapies, A1R/A3R agonists activate multiple overlapping pathways, including neurotransmitter regulation, apoptosis control, and blood-brain barrier function. Dual A1R/A3R agonists are a promising and adaptable neuroprotective strategy for both AIS and TBI. Their wide-ranging mechanism offers benefits beyond current revascularization options, especially for patients ineligible for tPA or thrombectomy. Early-phase data indicate strong translational potential, and ongoing trials will determine whether these results translate into improved clinical outcomes. Given the urgent need for effective neuroprotectants, A1R/A3R agonists could become an essential component of neurocritical care. AST-004 has recently advanced into a Phase II clinical evaluation, with ongoing assessments of its safety and effectiveness in humans.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"26 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-03-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147572846","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Preclinical Models of Traumatic Brain Injury: Advances in In Vitro Models.","authors":"Delin Zeng, Barclay Morrison","doi":"10.1007/s11910-026-01491-5","DOIUrl":"10.1007/s11910-026-01491-5","url":null,"abstract":"<p><p>PURPOSE OF REVIEW: In vitro traumatic brain injury (TBI) models are invaluable tools for elucidating cellular injury mechanisms and enabling preclinical drug screening. This review discusses recent advances in two main areas: neural culture systems and mechanical injury models. RECENT FINDINGS: The adoption of human induced pluripotent stem cell (iPSC)-derived neural cells in 3D cultures, including cerebral organoids and scaffold-based constructs, has substantially improved species and structural relevance of in vitro TBI models. However, future development of functional vascularization and mature synaptic circuitry remains necessary. Mechanical injury models, including stretch, compression, and blast, are well established. Tissue tolerance thresholds (i.e. tissue strain and strain rate) for injury outcomes (i.e. cell death and electrophysiological deficits) have been extensively characterized in rodent studies, but comparable benchmarks for human neural cultures are lacking. With the growing use of human iPSC-derived neural cells, a critical next step is to recalibrate established mechanical injury models for human neural cultures to define human-specific tolerance thresholds, thereby enabling more mechanistically grounded preclinical therapeutic testing.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"26 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-03-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147572854","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Amyloid and Tau Co-pathology in Parkinson Disease and Atypical Parkinsonism.","authors":"Maria Jose Angel Pinto, Indira García Cordero, Guido Dorman, Gabriel Mizraji, Chloe Anastassiadis, Oscar Gershanik, Blas Couto","doi":"10.1007/s11910-026-01488-0","DOIUrl":"10.1007/s11910-026-01488-0","url":null,"abstract":"<p><strong>Purpose of review: </strong>We performed a narrative review of the literature of amyloid and tau co-pathology in Parkinson Disease and atypical parkinsonism in Pubmed database, including articles published between January 2020 to July 2025.</p><p><strong>Recent findings: </strong>In the last decade, different multicenter research efforts have worked to improve the accuracy of clinical-pathological diagnosis in neurogenerative disease. In this search, growing evidence from neuropathology, neuroimaging and fluid biomarkers have highlighted the role of Alzheimer's disease (AD) co-pathology in Parkinson's disease (PD) and atypical parkinsonism (AP) disorders potentially affecting progression, motor phenotype and cognitive status. Regarding studies of structural and functional imaging evidencing the presence of Amyloid-β (Aβ), tau, as co-pathologies contribute to α-synuclein-related profile of cortical atrophy, network disruption, as well as clinical heterogeneity in PD and AP disorders. In AP fluid biomarkers have shown limited diagnostic accuracy. Neuropathological evidence from systematic post-mortem surveys confirmed that diffuse and neuritic Aβ plaques are uncommon in non-demented PD (10%), intermediate in PD-dementia (30-40%), and frequent in Dementia with Lewy Bodies (60-80%). The evidence in PD and DLB showed that Aß fluid biomarkers may predict clinical trajectory and cognitive decline, while Aβ-imaging would help stratifying patients and directing therapeutic pipeline designs. In AP disorders, including progressive supranuclear palsy and corticobasal degeneration, a combined multimodal assessment of molecular imaging, structural and functional magnetic resonance with fluid biomarkers shall guarantee future differential diagnosis and prediction of clinical outcomes. Although there are no currently accepted biomarkers for PD or AP, the recent design of plasma tau biomarkers and seed-amplification assays are promising approaches which are also reviewed here.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"26 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-03-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147509992","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Recent Advances in Targeted Therapies for Adult Gliomas.","authors":"Aleksandra B Lasica, Alice R Tang, Arooba Iqbal, Vihang Nakhate, Patrick Y Wen","doi":"10.1007/s11910-026-01484-4","DOIUrl":"10.1007/s11910-026-01484-4","url":null,"abstract":"<p><p>PURPOSE OF REVIEW: Incorporation of molecular diagnostics has transformed the classification and risk stratification of adult gliomas, revealing a spectrum of therapeutically actionable targets. This review evaluates Food and Drug Administration (FDA)-approved and investigational targeted therapies and discusses the major challenges and future directions facing the field. RECENT FINDINGS: Landmark FDA approvals, such as vorasidenib for isocitrate dehydrogenase (IDH)-mutant gliomas, dabrafenib and trametinib for BRAF V600E-mutated gliomas, neurotrophic tyrosine receptor kinase (NTRK) inhibitors for NTRK fusion-positive tumors and dordaviprone for H3K27M-mutant diffuse midline gliomas, underscore a new era of targeted therapies in neuro-oncology. These molecularly-driven therapies deliver tangible clinical benefit to select subsets of patients with molecularly defined tumors. However, they are not curative, and tumors with these targetable alterations constitute a minority of adult gliomas. Novel agents targeting DNA repair and metabolic dependencies, and leveraging immune-based and advanced strategies of drug delivery, are under investigation. Targeted therapies have begun to transform the management of molecularly defined subsets of adult glioma, though their clinical benefits remain limited to date.</p>","PeriodicalId":10831,"journal":{"name":"Current Neurology and Neuroscience Reports","volume":"26 1","pages":""},"PeriodicalIF":7.4,"publicationDate":"2026-03-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13013171/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147510014","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}