The Lancet Neurology

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Bepranemab in prodromal-to-mild Alzheimer’s disease did not meet the primary endpoint: CDR-SB change at week 80 was 2·15 (90 mg/kg) and 1·85 (45 mg/kg) vs 1·81 with placebo.

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Delpacibart zotadirsen (del-zota) in USA participants with DMD44 produced mean exon 44 skipping increases of 36·6% at 5 mg/kg and 43·4% at 10 mg/kg.

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Traumatic brain injury and spinal cord injury affect over 220 million people worldwide and are linked to cardiometabolic, endocrine, neurological, and psychiatric sequelae for years to decades after injury.

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Higher baseline plasma p-tau217 predicts cognitive impairment in a pooled multi-ethnic cohort, with APOE-ε4 carriers showing stronger risk and earlier timing per 1-SD increase.

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Antibody-mediated glial disorders targeting aquaporin-4 and myelin oligodendrocyte glycoprotein are distinct nosological entities with specific targets, mechanisms, syndromes, and treatment implications.

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Lecanemab infusions in early symptomatic Alzheimer’s disease patients are linked to significant, multidirectional changes in 34 of 130 plasma biomarkers, including partial normalization of p-tau217, MAPT, and GFAP.

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Multiple sclerosis genetics has identified hundreds of risk loci, but susceptibility findings have modest individual predictive value for disability accumulation, disease course, and treatment response.

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Multimodal diagnostics are enabling earlier detection of subtle spinal cord injury and subclinical neurodegeneration in degenerative cervical myelopathy, before overt clinical disability becomes apparent.

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Anti-amyloid monoclonal antibodies are clinically meaningful in symptomatic Alzheimer’s disease, and prevention trials are testing them in cognitively unimpaired people with biomarker evidence of AD neuropathological change (ADNC).

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Blood-based neurofilament light and phosphorylated tau 217 are being implemented in clinical practice for frontotemporal dementia, amyotrophic lateral sclerosis, and Alzheimer’s disease diagnosis.

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SAR443820, a CNS-penetrant oral RIPK1 inhibitor, did not improve ALSFRS-R over 24 weeks versus placebo in a phase 2 trial, with no significant difference.