2026-10-07 11:03 |
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2026-10-07 10:50 |
[FZJ-2026-04883]
Journal Article
Werner, J.-M. ; Gödel, P. ; Galldiks, N. ; et al
Non‐ICANS neurotoxicity after BCMA‐directed CAR‐T therapy: Clinical spectrum, outcomes, and a framework for neurology–oncology co‐management
Ciltacabtagene autoleucel (cilta-cel), a B-cell maturation antigen (BCMA)–directed chimeric antigen receptor T-cell (CAR-T) therapy, has demonstrated deep and durable responses in patients with relapsed or refractory multiple myeloma and is rapidly moving into routine clinical practice worldwide.1, 2 While cytokine release syndrome (CRS) and immune-effector cell-associated neurotoxicity syndrome (ICANS) are well described, increasing attention is directed toward rarer but potentially severe neurotoxicity outside the ICANS spectrum.3, 4 Non-ICANS immune-effector cell-associated (IEC) toxicities reported after BCMA-directed CAR-T therapies include movement/neurocognitive treatment-emergent events with Parkinsonism-like features (IEC-PKS), cranial nerve palsies (IEC-NP), Guillain–Barré-syndrome-like presentations (IEC-GBS), and myelopathy.5 Phenotypes can overlap and evolve over weeks, complicating recognition and therapeutic decision-making.The biological basis of delayed non-ICANS neurotoxicity after BCMA-directed CAR-T therapy is an active area of investigation. Early reports have detected CAR-T in the cerebrospinal fluid (CSF) during neurotoxicity and, in individual cases, have described neuropathologic evidence of lymphocytic infiltration in affected brain regions, findings compatible with central nervous system (CNS) trafficking and the persistence of CAR-T, together with local inflammatory tissue injury.4 These observations have raised the possibility of an on-target/off-tumor mechanism in susceptible neural tissues, although causality has not been established.4, 6 At the cohort level, delayed non-ICANS neurotoxicity has been linked to pronounced CAR-T expansion and persistence and to heightened immune activation, often in patients with clinically relevant CRS and/or ICANS, suggesting that both cellular kinetics and inflammatory activation may contribute.3, 5-8 Despite these signals in clinical trials and real-world settings, non-ICANS neurotoxicity remains insufficiently characterized, and data from large in-label cohorts are limited. [...]
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2026-10-07 10:45 |
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2026-10-07 10:42 |
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2026-10-07 10:38 |
[FZJ-2026-04880]
Journal Article
Ballasch, I. ; Faßbender, R. ; Oezguer, O. A. ; et al
Development of a picture‐based tool for subjective deficits in cognition and ADLs
Traditional instruments assessing activities of daily living (ADLs) and cognitive complaints are language based and insufficiently capture technology‐based ADLs, limiting use among individuals with limited language proficiency or language impairments. We developed the picture‐based assessment of subjective deficits in cognition and ADL (Pic‐ADL) to address this gap and reflect contemporary everyday functioning.METHODSThe Pic‐ADL is a picture‐based self‐report questionnaire covering cognitive and ADL complaints, including novel items on digital media [...]
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2026-10-07 10:32 |
[FZJ-2026-04879]
Journal Article
Olschewski, D. N. ; Koenig, A. M. ; Nerone, H. M. ; et al
Microglia derived from human induced pluripotent stem cells are regulated by osteopontin, an endogenous extracellular matrix protein maintaining immune homeostasis
Introduction: Microglia are brain-resident immune cells responsible for maintaining homeostasis, coordinating responses to injury and disease, and mediating regeneration. Upon activation, they undergo dynamic changes in morphology, gene expression, and function, reflecting the nature and context of the stimuli encountered. [...]
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2026-10-07 10:27 |
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2026-10-07 10:13 |
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2026-10-07 10:03 |
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2026-10-07 09:58 |
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