Abstract
INTRODUCTION
Cerebral amyloid angiopathy (CAA) is characterized by the deposition of beta-amyloid (Aβ) in small vessels leading to hemorrhagic stroke and dementia. This study examined whether plasma Aβ42/40, phosphorylated-tau (p-tau), neurofilament light chain (NfL), and glial fibrillary acidic protein (GFAP) differ in CAA and their potential to discriminate Boston Criteria 2.0 probable CAA from healthy controls.
METHODS
Plasma Aβ42/40, p-tau-181, NfL, and GFAP were quantified using single molecule array (Simoa) and Aβ42/40 was also independently quantified using immunoprecipitation liquid chromatography mass-spectrometry (IPMS).
RESULTS
Forty-five participants with CAA and 47 healthy controls had available plasma. Aβ42/40 ratios were significantly lower in CAA than healthy controls. While p-tau-181 and NfL were elevated in CAA, GFAP was similar. A combination of Aβ42/40 (Simoa), p-tau-181, and NfL resulted in an area under the curve of 0.90 (95% confidence interval: 0.80, 0.95).
DISCUSSION
Plasma Aβ42/40, p-tau-181, and NfL differ in those with CAA and together can discriminate CAA from healthy controls.
Highlights
Participants with CAA had reduced plasma Aβ42/40 ratios compared to controls.
Plasma p-tau-181 and NfL concentrations are elevated in CAA compared to controls.
Plasma GFAP was similar in CAA and controls.
Together, plasma Aβ42/40, p-tau-181, and NfL had excellent discriminability for CAA.
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This post is Copyright: Ryan T. Muir,
Sophie Stukas,
Jennifer G. Cooper,
Andrew E. Beaudin,
Cheryl R. McCreary,
Myrlene Gee,
Krista Nelles,
Nikita Nukala,
Janina Valencia,
Kristopher M. Kirmess,
Sandra E. Black,
Michael D. Hill,
Richard Camicioli,
Cheryl L. Wellington,
Eric E. Smith | March 29, 2025