Current Opinion In Neurology[JOURNAL]
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200 papers
Movement disorders and Parkinson's disease: collaborative and interdisciplinary research to advance understanding of neural circuit dysfunction, pathophysiology, and care: new horizons in technology, neuroimaging, neurophysiology, and genetics toward personalized medicine.
Vidailhet M
Curr Opin Neurol · 2026 Aug · PMID 42388031 · Publisher ↗
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Editorial introduction.
Vidailhet M
Curr Opin Neurol · 2026 Aug · PMID 42388030 · Publisher ↗
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Multimodal mapping of balance dysfunction in Parkinson's disease: a consensus roadmap for research and intervention.
Shaikh AG, Antoniades C, Arshad Q … +20 more , Bhatia K, Bloem B, Bohnen N, Carpenter MG, D'Cruz N, Doumas M, Factor SA, Fasano A, Gulberti A, Hausdorf J, Kaski D, Mancini M, Pandey S, Paquette C, Rucker J, Seemungal B, Virmani T, Weerdesteyn V, Young W, Bronstein AM
Curr Opin Neurol · 2026 Aug · PMID 42307076 · Publisher ↗
PURPOSE OF REVIEW: Balance depends on accurate perception of self-motion and verticality and on multisensory integration for stance, and gait. In Parkinson's disease, balance is commonly impaired and variably affected by...
PURPOSE OF REVIEW: Balance depends on accurate perception of self-motion and verticality and on multisensory integration for stance, and gait. In Parkinson's disease, balance is commonly impaired and variably affected by treatment. Although vestibular and multisensory contributions are increasingly recognized, progress is limited by fragmented evidence, inconsistent methods, and artifact-prone measures. We provide a consensus roadmap across four domains - video-oculography/vHIT, VEMPs, posturography, and perceptual paradigms - to improve clinical translation of balance research in Parkinson's disease. RECENT FINDINGS: An interdisciplinary taskforce conducted a comprehensive literature review and a modified Delphi process (≥80% agreement), using virtual meetings, surveys, and an in-person consensus session. Oculography/vHIT shows largely preserved aVOR in Parkinson's disease but is vulnerable to Parkinson's disease specific artifacts, requiring standardization. VEMPs relate to brainstem and non-motor features but are limited by EMG-dependent confounds. Posturography reveals impaired multisensory integration with visual dependence and cholinergic contributions; reactive-capacity measures outperform sway alone. Perceptual paradigms show task-specific distortions and increased variability linked to axial/postural syndromes. SUMMARY: This consensus offers a practical roadmap, de-emphasize aVOR/vHIT as primary unsteadiness outcomes; use VEMPs as ancillary measures; prioritize posturography probing adaptability and reactive stepping; integrate wearables and neurochemical imaging; and adopt consortium-level minimum datasets to enable reproducible, phenotype-aware advances in Parkinson's disease balance research.
Tourette syndrome: brain neurophysiology, circuit dysfunction, and neuromodulation across invasive and noninvasive approaches.
Worbe Y, Courtin E
Curr Opin Neurol · 2026 Aug · PMID 42274162 · Publisher ↗
PURPOSE OF REVIEW: We review recent electrophysiological advances that have refined our understanding of tic generation in Tourette syndrome by characterizing dysfunction across cortico-striato-pallido-thalamo-cortical (...
PURPOSE OF REVIEW: We review recent electrophysiological advances that have refined our understanding of tic generation in Tourette syndrome by characterizing dysfunction across cortico-striato-pallido-thalamo-cortical (CSPTC) circuits and their time-resolved dynamics. We integrate evidence across spatial scales - from single-unit activity to large-scale network coupling - and examine how these findings provide a mechanistic framework for interpreting both invasive and noninvasive neuromodulation approaches. Finally, we discuss how electrophysiological signatures of tics and premonitory urges may serve as candidate biomarkers to guide future, dynamically informed interventions. RECENT FINDINGS: At the microscale, intraoperative recordings indicate that GPi neurons in Tourette syndrome exhibit a burst-pause firing pattern with phasic modulation preceding tic onset, consistent with transient pallidal disinhibition. At the mesoscale, LFP recordings from centromedian nucleus and aGPi show increased low-frequency (3-12 Hz) power and pallido-thalamic coherence during tics, accompanied by reduced phase synchrony, suggesting dysrhythmic rather than coordinated network activity. At the macroscale, combined intracranial and scalp EEG recordings demonstrate that thalamo-frontal alpha-band connectivity progressively declines in the ~1.3 s preceding tic onset, propagating from sensorimotor to prefrontal regions. Importantly, these pretic dynamics are captured by measures of inter-regional coupling rather than local power, highlighting the relevance of distributed network interactions. These findings are beginning to inform neuromodulation strategies across modalities. Deep brain stimulation (DBS) targeting thalamic or pallidal regions provides clinically meaningful tic reduction, while connectomic analyses emphasize the role of distributed fibre pathways over single anatomical targets. In parallel, noninvasive approaches show mixed results: cortical stimulation techniques such as rTMS and tDCS have yielded inconsistent effects, whereas peripheral rhythmic stimulation, such as 10 Hz median nerve stimulation, has demonstrated efficacy in controlled trials, potentially through modulation of sensorimotor network dynamics. SUMMARY: Electrophysiological evidence across spatial scales supports a model of Tourette syndrome as a disorder of dynamic CSPTC circuit dysfunction. At the cellular level, GPi neurons exhibit a sparse but high-intensity bursting regime, with activity changes preceding tic onset. At the population level, low-frequency oscillations in pallido-thalamic networks track tic severity and distinguish tics from voluntary movements. At the network level, thalamo-frontal alpha-band coupling appears to exert a stabilizing influence, whose progressive reduction precedes tic expression. Together, these findings suggest that tic generation arises from temporally evolving disruptions in distributed network coordination rather than from static abnormalities within isolated regions. This framework provides a common basis for understanding both invasive and noninvasive neuromodulation and supports the development of electrophysiological biomarkers for adaptive, closed-loop therapeutic strategies.
Dystonia: from phenotypes to genetics and therapeutic advances.
Chiang HL, Kuo YC, Lin CH
Curr Opin Neurol · 2026 Aug · PMID 42274155 · Publisher ↗
PURPOSE OF REVIEW: This review summarizes recent advances in the clinical classification, diagnostic approaches, genetic spectrum and therapeutic strategies for dystonia. RECENT FINDINGS: Dystonia is a heterogeneous move...
PURPOSE OF REVIEW: This review summarizes recent advances in the clinical classification, diagnostic approaches, genetic spectrum and therapeutic strategies for dystonia. RECENT FINDINGS: Dystonia is a heterogeneous movement disorder that may present as an isolated motor syndrome or as part of a broader neurological condition. Early recognition of its clinical features is essential for accurate diagnosis and timely treatment. Recent advances in genetics have identified multiple causative genes and provided insights into the molecular basis of dystonia; however, mechanism-based therapies remain limited. We highlight updated clinical classification systems and diagnostic algorithms, along with key clinical features that may indicate specific genetic forms of dystonia. Emerging insights into neuronal and circuit-level dysfunction are discussed, emphasizing underlying molecular mechanisms. In addition, we review current treatment strategies, including pharmacological therapies, botulinum toxin injections, and neuromodulation approaches such as deep brain stimulation. SUMMARY: Integrating clinical phenotyping with genetic and mechanistic insights provides a more precise diagnostic framework for dystonia. This approach facilitates improved patient stratification and lays the foundation for the development of mechanism-targeted therapies, ultimately advancing precision medicine in dystonia.
What can we learn from eye movements in movement disorders and Parkinson's disease?
Ravat P, Ghasia FF, Shaikh AG
Curr Opin Neurol · 2026 Aug · PMID 42274151 · Publisher ↗
PURPOSE: Studies of eye movements have evolved from clinical phenomenology to a probe of neural circuitry, cognition, and behavior offering a powerful, noninvasive window into nervous system function. In Parkinson's dise...
PURPOSE: Studies of eye movements have evolved from clinical phenomenology to a probe of neural circuitry, cognition, and behavior offering a powerful, noninvasive window into nervous system function. In Parkinson's disease (PD), ocular motor control has emerged as a uniquely informative model system, reflecting dysfunction across motor, cognitive, and executive domains. RECENT FINDINGS: Recent advances span four interconnected areas: executive behavior and cognition, gait and freezing of gait (FOG), neuromodulation, and machine learning. Antisaccades and related paradigms reveal early and progressive executive dysfunction in PD, linked to dopaminergic disruption of fronto-striatal and basal ganglia circuits. Naturalistic eye-tracking metrics further act as proxy markers of cognition, planning, and emotion processing. Oculomotor abnormalities also have direct functional consequences for visual search, walking, turning, and FOG, with shared neural substrates in frontal cortex, basal ganglia, and mesencephalic locomotor networks. Deep brain stimulation provides causal insight into these circuits, demonstrating target-, parameter-, and task-specific trade-offs between motor facilitation and inhibitory control. Finally, machine learning and emerging virtual reality (VR)- and mobile-based eye-tracking technologies enable high-dimensional analysis, early diagnosis, cognitive staging, and prognostic prediction, including identification of prodromal FOG. SUMMARY: Collectively the research has offered scalable biomarkers and mechanistic insight that bridge cognition, movement, and neuromodulation.
Functional movement disorders: diagnosis, pathophysiology, and treatment.
Maillard A, Mhanna E, Faiz H … +1 more , Garcin B
Curr Opin Neurol · 2026 Aug · PMID 42266072 · Publisher ↗
PURPOSE OF REVIEW: Functional movement disorders (FMD) are common and potentially reversible causes of movement disorders, yet they remain under-recognized and frequently misdiagnosed. RECENT FINDINGS: Diagnosis has shif...
PURPOSE OF REVIEW: Functional movement disorders (FMD) are common and potentially reversible causes of movement disorders, yet they remain under-recognized and frequently misdiagnosed. RECENT FINDINGS: Diagnosis has shifted from an exclusion-based model to a positive rule-in approach grounded in positive clinical signs such as inconsistency (distractibility and variability), with electrophysiology providing useful support in selected cases. Current pathophysiological models suggest that FMD arise from interacting abnormalities in predictive coding, sensorimotor integration, altered sense of agency, maladaptive attentional focus, and disrupted limbic-motor network connectivity. These mechanisms may contribute both to symptom generation and maintenance. Prognosis is variable and often guarded, highlighting the importance of early diagnosis and timely intervention. Management should rely on a clear and validating explanation of the diagnosis, individualized rehabilitation focused on movement retraining, and tailored psychotherapy addressing perpetuating cognitive, behavioral, and emotional factors. Pharmacological treatment has a mainly an adjunctive role, particularly for comorbid psychiatric symptoms, pain, and sleep disturbances. SUMMARY: FMD require an integrated, multidisciplinary, and patient-centered approach to optimize functional recovery and long-term outcomes.
Galectins in the brain: advances in neuroinflammation, neuroprotection and therapeutic opportunities: Erratum.
Curr Opin Neurol · 2026 Jun · PMID 42051238 · Publisher ↗
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Progress in the mechanism of neuronal surface P antigen modulating hippocampal function and implications for autoimmune brain disease: Erratum.
Curr Opin Neurol · 2026 Jun · PMID 42051237 · Publisher ↗
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Investigational approaches to multiple sclerosis therapy.
Boeckers JM, Pawlitzki M, Hartung HP … +2 more , Ruck T, Meuth SG
Curr Opin Neurol · 2026 Jun · PMID 42051236 · Publisher ↗
PURPOSE OF REVIEW: Multiple sclerosis (MS) research is entering a new therapeutic era. Beyond relapse rate reduction, the prevention of disability progression and, ideally, even the avoidance of disease development are n...
PURPOSE OF REVIEW: Multiple sclerosis (MS) research is entering a new therapeutic era. Beyond relapse rate reduction, the prevention of disability progression and, ideally, even the avoidance of disease development are now being formulated as new therapeutic goals. This review summarizes emerging treatment strategies spanning next-generation immunomodulation, Epstein-Barr virus (EBV) targeted interventions, remyelination agents, and cell-based therapies. RECENT FINDINGS: Central nervous system (CNS) penetrant Bruton's tyrosine kinase (BTK) inhibitors show early indications of slowing progression by targeting compartmentalized inflammation. Fc-silent CD40L blockade offers a non-depleting alternative and suppresses magnetic resonance imaging (MRI) activity in a phase 2 trial. EBV-directed strategies, including adoptive T-cell therapy and prophylactic or therapeutic vaccines, represent initial attempts to modify a likely causal driver of MS. Remyelination candidates including clemastine, selective M1 muscarinic receptor antagonists and other emerging agents, demonstrate biological activity but limited clinical benefit. Cell-based approaches, such as mesenchymal stem cell derived neural progenitors (MSC-NPs) and CD19 or B-cell maturation antigen (BCMA) targeted chimeric antigen receptor T-cell (CAR-T) constructs, remain early phase but show initial biological signals. SUMMARY: These advances mark a shift toward precision immunomodulation, causal targeting, and CNS repair, with BTK inhibitors and CD40L blockade advancing as promising candidates to address progression in MS.
News in autoimmune myelitis in the oncological context.
Collongues N
Curr Opin Neurol · 2026 Jun · PMID 42046908 · Publisher ↗
PURPOSE OF REVIEW: Autoimmune myelitis represents a heterogeneous group of disorders whose classification has evolved substantially over the past decade. Advances in antibody diagnostics and the widespread use of immune...
PURPOSE OF REVIEW: Autoimmune myelitis represents a heterogeneous group of disorders whose classification has evolved substantially over the past decade. Advances in antibody diagnostics and the widespread use of immune checkpoint inhibitors (ICIs) in oncology have reshaped current concepts, revealing mechanistic and clinical overlaps between antibody-mediated, paraneoplastic, and treatment-induced myelopathies. RECENT FINDINGS: Antibody-associated myelitis, including myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD), aquaporin-4 (AQP4)-immunoglobulin G (IgG)-positive NMOSD and glial fibrillary acidic protein (GFAP) astrocytopathies, accounts for many cases previously labeled idiopathic. Paraneoplastic myelitis is rare but severe, possibly overlapping with NMOSD or GFAP astrocytopathies. In parallel, ICIs have emerged as a novel trigger of immune-mediated myelitis, capable of inducing de novo inflammatory spinal cord syndromes or unmasking latent autoimmune diseases, including AQP4-IgG-positive NMOSD and GFAP astrocytopathies but not MOGAD. SUMMARY: Autoimmune myelitis is best conceptualized within an etiological and context-dependent framework integrating antibody status, oncological evaluation, and exposure to immunotherapies. The expanding interface between astrocytopathies, paraneoplastic syndromes, and ICI-associated myelitis has important diagnostic and therapeutic implications, underscoring the need for systematic antibody testing and cancer screening in patients with inflammatory myelopathy.
Genetic role in autoimmune encephalitis and paraneoplastic neurological syndromes.
Binks SNM, Yip J, Knight JC
Curr Opin Neurol · 2026 Jun · PMID 42007814 · Full text
PURPOSE OF REVIEW: To synthesize evidence and recent advances concerning genetic contributors to autoimmune encephalitis (AE) and paraneoplastic neurological syndromes (PNS), relating these to disease processes and clini...
PURPOSE OF REVIEW: To synthesize evidence and recent advances concerning genetic contributors to autoimmune encephalitis (AE) and paraneoplastic neurological syndromes (PNS), relating these to disease processes and clinical management. RECENT FINDINGS: The known immunogenetic role of the human leucocyte antigen (HLA) region - critical to immune and infection response - was refined. A multiethnic IgLON5 study revealed DQ associations, surpassing those previously demonstrated with DR , and arguing for T cell involvement. In PNS with anti-Hu antibodies, a DQB1*02:01 ~ DRB1*03:01 haplotype was preferentially linked to a sensory neuropathy phenotype.Outside the HLA, there were genome-wide association studies (GWAS) in the two commonest AEs. The first AE GWAS with discovery and validation cohorts took place in leucine-rich glioma-inactivated 1-antibody encephalitis (LGI1-Ab-E). This identified a risk locus in PTPRD , a protein tyrosine phosphatase with dual immune and brain activity, and a polygenic risk score (PRS). In N -methyl- d -aspartate receptor-antibody encephalitis (NMDAR-Ab-E), a discovery-only cohort implicated the type 1 interferon pathway gene IFIH1. SUMMARY: Genetic status can perform as a biomarker or prioritize targets for drug development. The paucity of familial cases, the allele frequency of risk HLAs in healthy individuals, and the applicability of PRS, support a multihit model combining genetic and environmental risks.
T cells in antibody-associated CNS autoimmunity: a mechanistic approach across autoimmune encephalitis and paraneoplastic disorders.
Leypoldt F, Scheffold A, Saggau C
Curr Opin Neurol · 2026 Jun · PMID 41982079 · Publisher ↗
PURPOSE OF REVIEW: Autoimmune encephalitis (AE), paraneoplastic neurological syndromes (PNS), and glial antibody-mediated disorders (for example, AQP4-NMOSD) are traditionally classified based on the target antigens of t...
PURPOSE OF REVIEW: Autoimmune encephalitis (AE), paraneoplastic neurological syndromes (PNS), and glial antibody-mediated disorders (for example, AQP4-NMOSD) are traditionally classified based on the target antigens of their respective autoantibodies. However, recent insights from immunogenomics, single-cell sequencing, and neuropathology indicate that T cell programs substantially influence disease initiation, localization, and chronicity. This review highlights three emerging dimensions of T-cell involvement - circulating exhausted-like helper T-cell memory, intrathecal T-B cooperation, and parenchymal tissue-resident cytotoxicity - that offer new perspectives on clinical and pathological features across these disorders. RECENT FINDINGS: In AQP4-NMOSD, circulating exhausted-like CD4 + T cells may constitute a durable autoreactive memory reservoir capable of re-initiating plasmablast responses. In LGI1- and CASPR2-associated encephalitis, systemic and intrathecal CD4 + differentiation appears to support systemic antibody maturation and local plasmablast expansion, with emerging hints of some accompanying CD8 + -mediated tissue injury. In contrast, in PNS and intracellular antigen-associated AE, CD8 + T cell-mediated cytotoxicity dominates and is characterized by parenchymal CD8 + tissue-resident memory (TRM) signatures. SUMMARY: These T-cell dimensions may provide a useful framework for understanding clinical paradoxes - such as relapse despite B-cell depletion, persistent memory dysfunction in IgG4-AE, and therapeutic inefficacy in PNS - and suggest opportunities for therapeutic strategies targeting exhausted T-cell memory, intrathecal cooperation, or TRM stability.
Mechanisms of paraneoplastic neurological syndromes.
Kunchok A, Vogrig A, Graus F
Curr Opin Neurol · 2026 Jun · PMID 41979003 · Full text
PURPOSE OF REVIEW: This review describes the mechanisms of paraneoplastic neurological syndromes (PNS) and the recent advances underlying these. RECENT FINDINGS: This review covers advances in the understanding of the im...
PURPOSE OF REVIEW: This review describes the mechanisms of paraneoplastic neurological syndromes (PNS) and the recent advances underlying these. RECENT FINDINGS: This review covers advances in the understanding of the immunobiology of PNS. Specifically, evidence that PNS associated with antibodies against intracellular antigens are T-cell mediated processes, of interferon-γ signaling, major histocompatibility complex (MHC) class I upregulation, and granzyme mediated neuronal death. In contrast, PNS with antibodies against neuronal surface antigens are antibody-mediated and cause reversible neuronal dysfunction. Further, the perennial question of why only few patients develop these disorders is emerging from studies of tumor genomics and host HLA associations. Finally, immune checkpoint inhibitors have demonstrated the role of immune tolerance breakdown in the development of these disorders. SUMMARY: These advancements in understanding of mechanisms of PNS have several implications for clinical practice and research. For clinical practice, these findings may lead to prognostication of risk of PNS in cancer patients and potential novel therapeutic approaches. For research, these findings have important implications for understanding tumor immunology, and immune tolerance.
Cognition in multiple sclerosis.
De Meo E, Portaccio E, Amato MP
Curr Opin Neurol · 2026 Jun · PMID 41960777 · Full text
PURPOSE OF REVIEW: Cognitive dysfunction in multiple sclerosis (MS) has gained increasing attention over recent decades, reflecting its substantial effects on day-to-day functioning and the limited availability of target...
PURPOSE OF REVIEW: Cognitive dysfunction in multiple sclerosis (MS) has gained increasing attention over recent decades, reflecting its substantial effects on day-to-day functioning and the limited availability of targeted therapies. This review addresses contemporary advances in the role of cognition to detect disease progression, examines biological and MRI correlates of cognitive dysfunction, and summarizes the evidence for treatment effects. RECENT FINDINGS: Cognitive changes can capture both acute relapse-related drops (including isolated cognitive relapses) and gradual decline consistent with progression independent of relapse activity (PIRA). Among fluid markers, serum neurofilament light chains relates to cognition mostly in relapsing disease, whereas glial fibrillary acidic protein seems to track global progression more than cognitive changes. Cerebrospinal fluid (CSF) candidate markers (CHI3L1, parvalbumin) and synaptic proteins (SNAP-25, neurogranin, β-synuclein) may help identifying patients at higher risk of cognitive decline. MRI demonstrates that grey-matter pathology best explains long-term cognitive trajectories while newer readouts (radiomics, quantitative susceptibility mapping of deep-grey nuclei, structural-functional disconnection and multiplex network indices, and choroid-plexus/glymphatic measures) add mechanistic and prognostic specificity beyond lesion burden and bulk atrophy. Data-driven cognitive phenotyping yields reproducible, biologically anchored profiles that outperform dichotomous impaired/preserved labels. Therapeutically, higher-efficacy disease-modifying therapies show the clearest association with preserved processing speed; cognitive rehabilitation, augmented in some settings by transcranial direct-current stimulation, produces additional gains. SUMMARY: Routine assessment and monitoring of cognitive functions should be embedded in MS care to detect relapse-related changes and progressive decline. Identifying fluid and MRI biomarkers of cognitive dysfunction may help individuate novel targets and specific treatments.
Medical management of refractory trigeminal neuralgia.
Stern JI, Chiang CC, Robertson CE
Curr Opin Neurol · 2026 Jun · PMID 41952523 · Publisher ↗
PURPOSE OF REVIEW: First- and second-line medical and surgical therapies for trigeminal neuralgia (TN) may have limited efficacy or tolerability in some individuals. In addition, even when these therapies are initially s...
PURPOSE OF REVIEW: First- and second-line medical and surgical therapies for trigeminal neuralgia (TN) may have limited efficacy or tolerability in some individuals. In addition, even when these therapies are initially successful, efficacy frequently wanes over time. This narrative review presents medication options for intractable trigeminal neuralgia with a focus on new and upcoming therapies. RECENT FINDINGS: Lacosamide, eslicarbazepine, and botulinum toxin are increasingly used for intractable TN, with recent studies demonstrating efficacy. Basimglurant and vixotrigine (BIIB074) are investigational agents currently or recently studied for treatment of TN. Intravenous (i.v.) sodium channel blockers, i.v. magnesium, multiple formulations of lidocaine, and sumatriptan can be used for acute treatment of intractable TN. SUMMARY: Multiple medical therapies exist for treatment of intractable TN, with newer options demonstrating efficacy in recent studies. Investigational agents are currently being studied as potential future options for management of intractable TN.
Focus on migraine prodrome: what should clinicians know?
Ngo M, Ehsani-Nia MI, Ailani J
Curr Opin Neurol · 2026 Jun · PMID 41952417 · Publisher ↗
PURPOSE OF REVIEW: The prodromal phase of migraine is highly prevalent and can be very disabling. In this review, we seek to understand the clinical features of prodrome and its underlying pathophysiology. Our aim is to...
PURPOSE OF REVIEW: The prodromal phase of migraine is highly prevalent and can be very disabling. In this review, we seek to understand the clinical features of prodrome and its underlying pathophysiology. Our aim is to assess the impact of early treatment of migraine during the prodromal phase. RECENT FINDINGS: A recent phase 3 trial showed ubrogepant is effective at preventing migraine during the prodromal phase. Further studies have shown it is effective in reducing disabling symptoms of the prodrome itself and positive patient reported outcomes. SUMMARY: The prodromal phase of migraine presents the earliest opportunity to treat migraine and prevent disability. Studies have shown that the use of medications during this phase of migraine to be effective with recent studies showing ubrogepant is effective when used during prodrome.
Oxidative and nitrosative damage in multiple sclerosis.
Prozorovski T, Meuth SG, Hartung HP … +1 more , Berndt C
Curr Opin Neurol · 2026 Jun · PMID 41952414 · Full text
PURPOSE OF REVIEW: It is increasingly recognized that reactive oxygen and nitrogen species (ROS and RNS) are not only damaging molecules, but also essential signaling molecules regulating functions on organellar, cellula...
PURPOSE OF REVIEW: It is increasingly recognized that reactive oxygen and nitrogen species (ROS and RNS) are not only damaging molecules, but also essential signaling molecules regulating functions on organellar, cellular, organ, and organism levels. Nevertheless, damaging capacity of different ROS and RNS are connected to almost all diseases, including (neuro-)inflammation. One of the most frequent neuroinflammatory diseases is multiple sclerosis (MS). In this opinion article, we discuss recent advances in knowledge about oxidative and nitrosative damage, redox regulation, and the related ferroptotic cell death mechanism in initiation and progression of MS. RECENT FINDINGS: Specific improvement of supportive or inhibition of harmful redox processes in either brain or immune cells showed great impact on disease severity in MS models. Moreover, (circulating) markers of oxidative damage may hold promise as a supplementary diagnostic tool to differentiate different subtypes of MS. SUMMARY: Oxidative damage is well established as driver of MS. Nevertheless, molecular redox mechanisms underlying initiation and progression of MS are not well known. This existing research gaps impedes the establishment of successful antioxidative therapies.
PET imaging of microglial pathology in multiple sclerosis.
Hartiala O, Tuomaala J, Airas L
Curr Opin Neurol · 2026 Jun · PMID 41947663 · Full text
PURPOSE OF REVIEW: This review evaluates recent advances in the development of translocator protein (TSPO) - and purinergic receptor-binding PET tracers and highlights the capacity of TSPO-PET-imaging to capture microgli...
PURPOSE OF REVIEW: This review evaluates recent advances in the development of translocator protein (TSPO) - and purinergic receptor-binding PET tracers and highlights the capacity of TSPO-PET-imaging to capture microglial activation across multiple regions of interest in multiple sclerosis brain. We discuss the added value of integrating PET-derived measures with fluid and metabolic biomarkers, as well as their successful application in recent clinical trials. RECENT FINDINGS: Recent research highlights PET as a robust molecular imaging tool for detecting microglial activation and implicates dysregulated microglial activity as a key driver of smouldering multiple sclerosis pathology. PET-detectable microglial activation appears not merely as a secondary response to neuroaxonal injury but is increasingly recognized as an integral inflammatory component of ongoing pathological processes that lead to future brain atrophy and clinical deterioration. SUMMARY: Recent advances establish PET as an essential research tool for evaluating the presence of smouldering inflammation in MS brain not detectable using MRI. Furthermore, PET-based methods have proven suitable for measuring glial responses to potentially neuroprotective therapies currently under development.
Assessing treatment response in multiple sclerosis.
Föttinger F, Krajnc N, Bsteh G
Curr Opin Neurol · 2026 Jun · PMID 41947653 · Full text
PURPOSE OF THE REVIEW: The evaluation of treatment response in multiple sclerosis (MS) has become increasingly nuanced as the field shifts from a primarily relapse-oriented perspective toward a more comprehensive underst...
PURPOSE OF THE REVIEW: The evaluation of treatment response in multiple sclerosis (MS) has become increasingly nuanced as the field shifts from a primarily relapse-oriented perspective toward a more comprehensive understanding of the continuous interaction between inflammatory and neurodegenerative mechanisms. RECENT FINDINGS: Traditional clinical measures, while indispensable, capture only a fraction of the disease process and are insufficient to detect the insidious progression that accounts for a substantial proportion of long-term disability. Enhanced functional assessments provide greater sensitivity to subtle clinical deterioration, and MRI remains the principal modality for identifying subclinical focal inflammatory activity. In parallel, biomarkers of neurodegeneration, including inner retinal layer thinning measured by optical coherence tomography (OCT) and fluid biomarkers such as serum neurofilament light chain (sNfL) and glial fibrillary acidic protein (GFAP), offer complementary insights into diffuse pathological processes that elude conventional monitoring. SUMMARY: A personalized monitoring strategy that integrates clinical assessment, imaging and fluid biomarkers holds the greatest promise for improving the detection of subclinical disease activity, refining risk stratification, and enabling more informed and individualized treatment decisions in contemporary MS care.
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