Journal
JOURNAL OF ALZHEIMERS DISEASE
Volume 74, Issue 4, Pages 1189-1201Publisher
IOS PRESS
DOI: 10.3233/JAD-191254
Keywords
Alzheimer's disease; amyloid-beta; biomarkers; cerebral amyloid angiopathy; cerebrospinal fluid
Categories
Funding
- Rosetrees Trust
- NIHR
- Wolfson Foundation
- Weston Brain Institute
- National Institute for Health Research University College London Hospitals Biomedical Research Centre
- EPSRC [EP/J020990/1]
- MRC Dementias Platform UK [MR/L023784/1]
- ARUK [ARUK-Network 2012-6ICE, ARUK-PG2017-1946]
- Brain Research UK [UCC14191]
- Weston Brain Institute [UB170045]
- European Union [666992]
- UK Dementia Research Institute
- Stroke Association
- British Heart Foundation
- Department of Health's National Institute for Health Research (NIHR) Biomedical Research Centres funding scheme
- Swedish Research Council
- European Research Council
- UK Dementia Research Institute at UCL
- EPSRC [EP/J020990/1] Funding Source: UKRI
- MRC [UKDRI-1001, UKDRI-1003, MR/L023784/1] Funding Source: UKRI
- Engineering and Physical Sciences Research Council [EP/J020990/1] Funding Source: researchfish
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Background: There is limited data on cerebrospinal fluid (CSF) biomarkers in sporadic amyloid-beta (A beta) cerebral amyloid angiopathy (CAA). Objective: To determine the profile of biomarkers relevant to neurodegenerative disease in the CSF of patients with CAA. Methods: We performed a detailed comparison of CSF markers, comparing patients with CAA, Alzheimer's disease (AD), and control (CS) participants, recruited from the Biomarkers and Outcomes in CAA (BOCAA) study, and a Specialist Cognitive Disorders Service. Results: We included 10 CAA, 20 AD, and 10 CS participants (mean age 68.6, 62.5, and 62.2 years, respectively). In unadjusted analyses, CAA patients had a distinctive CSF biomarker profile, with significantly lower (p < 0.01) median concentrations of A beta(38), A beta(40), A beta(42), sA beta PP alpha, and sA beta PP beta. CAA patients had higher levels of neurofilament light (NFL) than the CS group (p < 0.01), but there were no significant differences in CSF total tau, phospho-tau, soluble TREM2 (sTREM2), or neurogranin concentrations. AD patients had higher total tau, phospho-tau and neurogranin than CS and CAA groups. In age-adjusted analyses, differences for the CAA group remained for A beta(38), A beta(40), A beta(42), and sA beta PP beta. Comparing CAA patients with amyloid-PET positive (n = 5) and negative (n = 5) scans, PET positive individuals had lower (p < 0.05) concentrations of CSF A beta(42), and higher total tau, phospho-tau, NFL, and neurogranin concentrations, consistent with an AD-like profile. Conclusion: CAA has a characteristic biomarker profile, suggestive of a global, rather than selective, accumulation of amyloid species; we also provide evidence of different phenotypes according to amyloid-PET positivity. Further replication and validation of these preliminary findings in larger cohorts is needed.
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