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ABSTRACT: Introduction
Growing evidence suggests a role for neuroinflammation in Alzheimer's disease (AD). We investigated complement pathway activity in AD patient cerebrospinal fluid (CSF) and evaluated its modulation by the anti-tau antibody semorinemab.Methods
Immunoassays were applied to measure CSF complement proteins C4, factor B (FB), C3 and their cleavage fragments C4a, C3a, and factor Bb (Bb) in AD patients and a separate cognitively unimpaired (CU) cohort.Results
All measured CSF complement proteins were increased in AD versus CU subjects, with C4a displaying the most robust increase. Finally, semorinemab did not have a significant pharmacodynamic effect on CSF complement proteins.Discussion
Elevated levels of CSF C4a, C4, C3a, C3, Bb, and FB are consistent
SUBMITTER: Sandoval C
PROVIDER: S-EPMC11567840 | biostudies-literature | 2024 Nov
REPOSITORIES: biostudies-literature