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Intra-Arterial Thrombolysis After Thrombectomy

Neurological disorders are the leading cause of disease burden worldwide. Stroke is the single largest contributor to that burden, and the second leading cause of global mortality. Approximately two-thirds of strokes are ischemic. Although 20% of ischemic strokes are large vessel occlusions, this subtype of stroke accounts for 60% to 90% of poststroke dependence or death, contributing disproportionately to societal burden. Acute stroke therapy is guided by the reperfusion hypothesis: when a cerebral artery is occluded, all downstream tissue is at risk of infarction and irreversible neuronal death. Recovery depends on rapid restoration of blood flow to the at-risk tissue (the ischemic penumbra); hence the term time is brain.

[Review] Blood and CSF biomarkers for multiple sclerosis: emerging clinical applications

Neurofilament light chain (NfL), glial fibrillary acidic protein (GFAP), chitinase-3-like protein 1 (CHI3L1), and other protein assays are being developed as diagnostic or prognostic biomarkers in multiple sclerosis. An increase in NfL concentrations reflects axonal damage resulting from the acute new inflammatory disease activity that occurs during a relapse. NfL concentrations can also reflect the occurrence of new MRI lesions. GFAP concentrations are increased in people with progressive forms of multiple sclerosis, and GFAP is an emerging biomarker of progression independent of relapses.

[Series] Diagnostic and other biomarkers of dementia with Lewy bodies: from research to clinical settings

Dementia with Lewy bodies is characterised clinically by visual hallucinations, fluctuating cognitive function, parkinsonism, and rapid eye movement sleep behaviour disorder, and can cause more frailty than other dementias. The disease is heterogeneous in presentation and progression, and misdiagnoses are common. In people with dementia with Lewy bodies, other brain copathologies are frequent, limiting the usefulness of some diagnostic biomarkers. This heterogeneity, together with the scarcity of diagnostic and prognostic biomarkers, has hindered the implementation of therapeutic trials.

[Series] The evolving therapeutic landscape of dementia with Lewy bodies

Dementia with Lewy bodies has a complex clinical presentation, with symptoms spanning cognitive, neuropsychiatric, motor, autonomic, and sleep domains. The disorder causes high morbidity, is associated with high caregiver burden, and can result in considerable health-care costs. Although symptomatic treatments remain scarce, emerging evidence supports a multipronged approach that integrates pharmacological and non-pharmacological interventions that target different signs and symptoms. Novel frameworks, such as the DIAMOND Lewy toolkit, provide structured management guidance.

[Series] Advances in the genetics and pathology of Lewy body dementia

Lewy body dementia is a heterogeneous disease that is underdiagnosed and poorly understood. Pathologically, Lewy body dementia is characterised by the accumulation of intraneuronal aggregates of misfolded α-synuclein, known as Lewy bodies and Lewy neurites. The genetic architecture of Lewy body dementia is complex, involving both common genetic variants with small risk effects and rare genetic variants with large effects. Alzheimer's disease pathology frequently coexists with Lewy body pathology and influences the clinical presentation.

[Articles] Lifetime and 10-year absolute risk of cognitive impairment in relation to amyloid PET severity: a retrospective, longitudinal cohort study

Lifetime and 10-year absolute risk for MCI and dementia among individuals who are currently cognitively unimpaired increase with increasing biological severity of Alzheimer's disease. This information should be important for risk–benefit evaluation of therapeutic interventions in the future. The high lifetime risk in participants with higher centiloid values addresses academic controversies concerning risk of future impairment associated with biomarkers of Alzheimer's disease among individuals who are cognitively unimpaired.

[In Context] I can't hear you singing

Stereocilia are specialised, non-motile cell projections on the surface of hair cells in the inner ear. They transform the mechanical energy of sound waves into electrical signals for the hair cells, which ultimately lead to an excitation of the auditory nerve, allowing hearing. These cell projetions can be damaged by exposure to loud noises and the ageing process, and genetic factors can also impair their function, leading to hearing loss. In a rather unique instance, stereocilia take the centre stage in a show, Ohio, currently at the Young Vic Theatre, in London, UK, in which hereditary hearing loss is the main theme.

[In Context] Everything is connected: sparks will fly in coproduction spaces

Art and science are not poles apart. That discussion is over—move aside for the evolving role of coproduction in scientific research. Including participants with lived experience is now a must have. Such inclusion might push some people out of their comfort zone by breaking down hierarchical structures historically established in medical settings, but with a level-playing field, everyone is teacher and student. Could this approach create anarchy? Perhaps a little, but that is part of the process, and is where the magic happens, as demonstrated at this year's University College London's (UCL) Trellis Arbor project, a knowledge-exchange programme for staff and researchers of the Queen Square Institute of Neurology and artists and communities.

[In Context] Si je ne me trompe pas: Charcot's neurological legacy in the 21st century

2025 marks the bicentenary of the birth of Jean-Martin Charcot (1825-1893), the first major international clinical neurologist. In this celebration year, symposia, exhibitions, and congresses have highlighted Charcot's seminal contributions: his descriptions of Parkinson's disease and amyotrophic lateral sclerosis; his anatomical studies linking clinical signs to specific lesions; his teaching methods that drew colleagues from around the world. Yet, beyond this historical perspective, it is fitting to examine Charcot in the context of the 21st century.

[In Context] Krithi Irmady

Krithi Irmady is an Assistant Professor at Rockefeller University, New York, NY, USA. She studied medicine in Mysore, India, and completed her doctorate at the University of Heidelberg in Germany. She trained in Adult Neurology at Yale University (New Haven, CT), and Movement Disorders at Columbia University (New York, NY, USA). Her research focuses on RNA dysregulation in Parkinson's disease, with the goal of developing novel therapies and peripheral biomarkers.

[In Context] Aseptic meningitis

In 1932, the Guy's Hospital (London, UK) physician John Ryle lectured on meningitis and meningism. By meningitis he meant the pathological state that involved inflammation, usually infective, of the meninges; and by meningism, he meant a clinical condition comprising Kernig's sign and neck rigidity but lacking final proof of bacteria in the CSF. Ryle argued that meningism was always indicative of irritation of the meninges or a mild meningitis, even if it was aseptic, giving as examples the aseptic meningitis of subarachnoid haemorrhage and the meningism seen in cases of pneumonia and otitis media, which he speculated was due to the “chemical products of fever or contiguous infection”.

[In Context] Ian McKeith: pioneer, collaborator, runner

Ian McKeith has always liked running. When I spoke to him, he had just completed the Great North Run, the world's most populous half-marathon, which takes place annually in northeast England. The first time he ran it was in 1982. Now, just into his seventies, he says: “it took me twice as long as it did when I was 28 years old. But I'm lucky still to be able to do it.” McKeith, Emeritus Professor of Old Age Psychiatry at Newcastle University (Newcastle upon Tyne, UK) ran to raise funds for the Lewy Body Society, a charity he helped establish 20 years ago.

[Corrections] Correction to Lancet Neurol 2025; 24: 969–75

Blauwendraat C, Morris HR, Keuren-Jensen KV, Noyce AJ, Singleton AB. The temporal order of genetic, environmental, and pathological risk factors in Parkinson's disease: paving the way to prevention. Lancet Neurol 2025; 24: 969–75—In this Personal View, figures 1 and 2 were transposed. This correction has been made to the online version as of Nov 12, 2025.

[Corrections] Correction to Lancet Neurol 2025; 24: 512–23

Manley GT, Dams-O’Connor K, Alosco ML, et al. A new characterisation of acute traumatic brain injury: the NIH-NINDS TBI Classification and Nomenclature Initiative. Lancet Neurology 2025; 24: 512–23—In this Policy Review, Rachel Sayko Adam's name was listed incorrectly in the appendix. This correction has been made to the online version as of Nov 12, 2025.

[Corrections] Correction to Lancet Neurol 2020; 19: 391–401

Zhang C, Zhang M, Qui W, et al. Safety and efficacy of tocilizumab versus azathioprine in highly relapsing neuromyelitis optica spectrum disorder (TANGO): an open-label, multicentre, randomised, phase 2 trial. Lancet Neurol 2020; 19: 391–401—In the Declaration of interest section of this Article, statements have been corrected for Fu-Dong-Shi. These corrections have been made to the online version as of Nov 12, 2025.