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Abstract

Background & Aims Cerebral amyloid angiopathy (CAA) is associated with lobar intracerebral haemorrhage, but there are no good outcome markers known for early disease. CSF biomarkers hold promise as dynamic and potentially reversible measures, with potential for use in therapeutic trials. Methods We performed a detailed comparison of CSF markers, comparing patients with CAA, Alzheimer’s disease (AD) and control subjects (HV), recruited from the Biomarkers and Outcomes in CAA (BOCAA) study, and a Specialist Cognitive Disorders Service. Results: We included 10 CAA patients, 20 AD patients and 10 HV (mean age ± SD 68.6±3.0, 62.5±4.1 and 62.2±5.4 years, respectively). Patients with CAA had a distinctive CSF biomarker profile compared with AD and HV groups, with significantly lower (p<0.01) median concentrations of all amyloid components measured, including Aβ38, Aβ40, Aβ42, sAPPα and sAPPβ. CAA patients had higher levels of CSF NFL than the HV group, but there were no differences in CSF total tau, phospho-tau, sTREM2 or neurogranin concentrations. AD patients had higher total tau, phospho-tau and neurogranin than HV and CAA groups. Comparing CAA patients with amyloid-PET positive and negative scans, PET positive individuals had lower concentrations of CSF Aβ42, and higher total tau, phopho-tau, NFL and neurogranin concentrations consistent with an “AD-like” profile. Conclusions: Our findings suggest that CAA has a characteristic biomarker profile suggesting a global, rather than selective, accumulation of all amyloid species measured, consistent with the protein elimination failure hypothesis. We also provide evidence of different phenotypes according to amyloid-PET positivity.

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© Copyright 2019 Morressier GmbH. All rights reserved.

© Copyright 2019 Morressier GmbH.
All rights reserved.