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| Home > In process > Exploratory synergistic diagnostic value of CSF neurofilament light chain and topographic cortical atrophy in differentiating cerebral amyloid angiopathy from Alzheimer's disease - a pilot study |
| Home > In process > Exploratory synergistic diagnostic value of CSF neurofilament light chain and topographic cortical atrophy in differentiating cerebral amyloid angiopathy from Alzheimer's disease - a pilot study |
| Journal Article | DZNE-2026-01065 |
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2026
Elsevier Science
Amsterdam [u.a.]
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Please use a persistent id in citations: doi:10.1016/j.jns.2026.126200
Abstract: Background: Differentiating Cerebral Amyloid Angiopathy (CAA) from Alzheimer's disease (AD) in vivo is challenging due to overlapping amyloid pathology and limited availability sensitivity of hemorrhagic markers in memory clinic settings. We investigated whether integrating regional cortical atrophy with cerebrospinal fluid (CSF) neurofilament light chain (NfL), a marker of axonal injury, might have a diagnostic value. Methods: In this pilot study (n = 30, n = 12 CE and n = 18 probable CAA), cortical thickness was quantified via FreeSurfer MRI analysis and standardized into regional Z-scores. We applied a hypothesis-driven dual-region approach (entorhinal cortex vs. precuneus). Classification was performed using firth's penalized logistic regression because of sample size and validated via Leave-One-Out Cross-Validation (LOOCV). Results: AD exhibited widespread atrophy involving both medial temporal (entorhinal) and posterior parietal (precuneus) structures. In contrast, probable CAA presented with relative temporal preservation despite posterior involvement. CSF NfL was numerically higher in CAA (median 2830 pg/ml) than in AD (2105.5 pg/ml). A combined model (entorhinal, precuneus, and CSF NfL) achieved the highest in-sample discrimination (AUC = 0.86, 95% CI: 0.64–1.00), while LOOCV yielded an AUC of 0.61. Conclusion: The multimodal integration of temporal neurodegeneration and axonal injury captures the divergent pathophysiological signatures of AD and CAA, serving as an exploratory, hypothesis generating pathophysiological profile rather than a generalized diagnostic algorithm.
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