To clarify pathomechanisms of cerebral amyloid angiopathy‐related inflammation/vasculitis (CAA‐ri).
We collected cerebrospinal fluid (CSF) samples of nine patients with CAA‐ri of before (acute CAA‐ri group) and after treatment (post‐treatment CAA‐ri group) and nine patients with CAA (CAA without inflammation group). We examined anti‐amyloid β protein (Aβ) antibody titer by ELISA, and measured 27 Cytokines, nine matrix metalloproteinases (MMPs), and four tissue inhibitors of MMPs (TIMPs) by multiplexed fluorescent bead‐based immunoassay.
We demonstrated TIMP‐2 (median) in CSF of the acute CAA‐ri group (30,994.49 pg/ml, p = 0.007) and the post‐treatment CAA‐ri group (36,430.97 pg/ml, p = 0.001) was significantly elevated compared to that of the CAA without inflammation group (22,013.58 pg/ml). TIMP‐1 was also higher in the post‐treatment CAA‐ri group than that in the CAA without inflammation group (58,167.75 pg/ml vs. 45,770.03 pg/ml, p = 0.005). There was a significant positive correlation between TIMP‐1 and anti‐Aβ antibodies in CAA‐ri (r
s = 0.900, p = 0.037). Median MMP‐2 tended to be higher in the acute and post‐treatment CAA‐ri groups (10,619.82 pg/ml and 8396.98 pg/ml, respectively) than in the CAA without inflammation group (4436.34 pg/ml). Platelet‐derived growth factor (PDGF)‐BB levels before treatment were higher than those after treatment (median, 12.66 pg/ml vs. 6.39 pg/ml; p = 0.011) and correlated with the titer of anti‐Aβ antibodies (r
s =0.900, p = 0.037).
Elevated levels of MMP‐2, TIMP‐1, and TIMP‐2 might be related to the development of CAA‐ri. Elevation of PDGF‐BB could be a useful marker for clinical diagnosis of CAA‐ri.