We studied longitudinal changes of the levels of anti-
amyloid β (anti-Aβ) antibody,
amyloid β (Aβ)
protein, and
interleukin 8 (IL-8) in cerebrospinal fluid (CSF) of a patient with
cerebral amyloid angiopathy-related
inflammation (CAA-ri) in whom
steroid treatment resulted in clinical improvement. The diagnosis of CAA-ri was established with brain biopsy. Levels of anti-Aβ 42 antibody, Aβ 40, Aβ 42 and
IL-8 in CSF were measured in the CAA-ri patient at 23 time points in the 8-month
clinical course. These CSF samples were divided into 2 groups: those obtained before (n = 12) and those after (n = 11) oral
corticosteroid therapy was started. We compared these levels between CSF samples obtained before and after
therapy. The mean levels of anti-Aβ 42 antibody and
IL-8 were significantly higher in CSF samples of the CAA-ri patient before oral
corticosteroid therapy than those after
therapy. A positive correlation was noted between levels of anti-Aβ 42
antibodies and
IL-8 in CSF of this patient. There were no significant differences of mean levels of Aβ 40 and Aβ 42 between CSF samples obtained before and after oral
corticosteroid therapy. It was possible that the autoinflammatory process with anti-Aβ 42
antibodies and
IL-8 may have been involved in the pathogenesis of CAA-ri, and that
corticosteroid therapy directly affected levels of anti-Aβ 42 antibody and
IL-8. In summary, CAA-ri
encephalopathy is a relapsing or progressive disorder and may be treatable by adequate immunosuppressive therapy. The anti-Aβ 42 antibody in CSF is a useful
biological marker for therapeutic monitoring of CAA-ri.