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Cerebrospinal fluid cytokines and metalloproteinases in cerebral amyloid angiopathy‐related inflammation
Author(s) -
Sakai Kenji,
NoguchiShinohara Moeko,
Ikeda Tokuhei,
Hamaguchi Tsuyoshi,
Ono Kenjiro,
Yamada Masahito
Publication year - 2021
Publication title -
acta neurologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.967
H-Index - 95
eISSN - 1600-0404
pISSN - 0001-6314
DOI - 10.1111/ane.13382
Subject(s) - cerebral amyloid angiopathy , inflammation , cerebrospinal fluid , matrix metalloproteinase , medicine , angiopathy , antibody , gastroenterology , pathology , immunology , endocrinology , diabetes mellitus , disease , dementia
Objectives To clarify pathomechanisms of cerebral amyloid angiopathy‐related inflammation/vasculitis (CAA‐ri). Methods 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. Results 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). Conclusions 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.