BACKGROUND: Cerebral amyloid angiopathy (CAA) is one of the main causes of intracerebral hemorrhage (ICH) in the elderly. OBJECTIVE: To analyze β-amyloid (Aβ) species in plasma in order to uncover biological markers that may contribute to improve the diagnosis of CAA in life. METHODS: We determined the level of Aβ(1-40), Aβ(N-40), Aβ(1-42) and Aβ(N-42) in plasma of CAA-related ICH patients (n = 29) and healthy controls (n = 21) using xMAP® technology. Hemorrhages were identified and classified using a CT scan and brain MRI. Patients were clinically classified as probable or possible CAA according to the Boston criteria. RESULTS: We found that plasma full-length Aβ(1-42) and truncated fragments Aβ(N-42) were higher in probable CAA patients than in controls (p < 0.001 and p = 0.046, respectively), and full-length Aβ(1-40) was selectively elevated in probable CAA compared to possible cases (p = 0.015) and controls (p = 0.005). In addition, plasma Aβ(N-42) levels were also higher in patients that presented multiple lobar macrohemorrhages compared to patients that had one symptomatic hemorrhagic event (p = 0.022), indicating that a certain degree of CAA severity is necessary to show increased Aβ fragments in peripheral circulation. CONCLUSION: Our results suggest that specific Aβ fragments in plasma might be considered as potential biomarkers for the diagnosis of CAA.
BACKGROUND:Cerebral amyloid angiopathy (CAA) is one of the main causes of intracerebral hemorrhage (ICH) in the elderly. OBJECTIVE: To analyze β-amyloid (Aβ) species in plasma in order to uncover biological markers that may contribute to improve the diagnosis of CAA in life. METHODS: We determined the level of Aβ(1-40), Aβ(N-40), Aβ(1-42) and Aβ(N-42) in plasma of CAA-related ICHpatients (n = 29) and healthy controls (n = 21) using xMAP® technology. Hemorrhages were identified and classified using a CT scan and brain MRI. Patients were clinically classified as probable or possible CAA according to the Boston criteria. RESULTS: We found that plasma full-length Aβ(1-42) and truncated fragments Aβ(N-42) were higher in probable CAA patients than in controls (p < 0.001 and p = 0.046, respectively), and full-length Aβ(1-40) was selectively elevated in probable CAA compared to possible cases (p = 0.015) and controls (p = 0.005). In addition, plasma Aβ(N-42) levels were also higher in patients that presented multiple lobar macrohemorrhages compared to patients that had one symptomatic hemorrhagic event (p = 0.022), indicating that a certain degree of CAA severity is necessary to show increased Aβ fragments in peripheral circulation. CONCLUSION: Our results suggest that specific Aβ fragments in plasma might be considered as potential biomarkers for the diagnosis of CAA.
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