Alexander Sekita, Maximilian I Sprügel, Stefanie Balk, David Haupenthal, Tobias Engelhorn, Manuel Alexander Schmidt, Arnd Doerfler, Timo Jan Oberstein, Juan Manuel Maler, Johannes Kornhuber, Piotr Lewczuk, Veit Rothhammer, Stefan Schwab, Joji B Kuramatsu, Jochen A Sembill
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引用次数: 0
Abstract
Introduction: Reduced cerebrospinal fluid (CSF) amyloid beta (Aβ) 40 has been reported in cerebral amyloid angiopathy (CAA) diagnosed by hemorrhagic magnetic resonance imaging (MRI) markers. Whether similar alterations occur when fulfilling Boston Criteria 2.0 solely through non-hemorrhagic markers remains unclear.
Methods: We analyzed 358 memory clinic patients undergoing MRI and CSF assessment. CAA was categorized by hemorrhagic markers (CAA 1.5 H) or exclusively non-hemorrhagic markers (CAA 2.0 NH) per Boston Criteria 1.5 and 2.0, respectively. Primary comparison of CSF-Aβ40 between CAA groups was complemented by secondary (Aβ42, phosphorylated tau [p-tau181], total tau [t-tau]) and exploratory analyses including Alzheimer's disease (AD), mild cognitive impairment (MCI), and healthy controls, adjusted for age, sex, MRI characteristics, and assay type.
Results: Sixty-five patients were reclassified as CAA 2.0 NH. Aβ40 was higher in CAA 2.0 NH than CAA 1.5 H (15,808 vs. 13,792 pg/ml, p = 0.033) and did not differ from AD, MCI, or controls. p-tau181 reached significance after adjustment (p = 0.010), likely reflecting AD co-pathology. However, within CAA-2.0-NH, patients with AD CSF profile showed Aβ40 comparable to hemorrhagic CAA.
Discussion: Non-hemorrhagic imaging markers alone were not associated with characteristic CAA-related CSF alterations, suggesting biological heterogeneity, limited specificity, or lesion type-dependent variability.
期刊介绍：
Alzheimer''s & Dementia: Diagnosis, Assessment & Disease Monitoring (DADM) is an open access, peer-reviewed, journal from the Alzheimer''s Association® that will publish new research that reports the discovery, development and validation of instruments, technologies, algorithms, and innovative processes. Papers will cover a range of topics interested in the early and accurate detection of individuals with memory complaints and/or among asymptomatic individuals at elevated risk for various forms of memory disorders. The expectation for published papers will be to translate fundamental knowledge about the neurobiology of the disease into practical reports that describe both the conceptual and methodological aspects of the submitted scientific inquiry. Published topics will explore the development of biomarkers, surrogate markers, and conceptual/methodological challenges. Publication priority will be given to papers that 1) describe putative surrogate markers that accurately track disease progression, 2) biomarkers that fulfill international regulatory requirements, 3) reports from large, well-characterized population-based cohorts that comprise the heterogeneity and diversity of asymptomatic individuals and 4) algorithmic development that considers multi-marker arrays (e.g., integrated-omics, genetics, biofluids, imaging, etc.) and advanced computational analytics and technologies.
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