2021
DOI: 10.1161/strokeaha.120.033107
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Abstract: Cerebral amyloid angiopathy is a devastating cause of intracerebral hemorrhage for which there is no specific secondary stroke prevention treatment. Here we review the current literature regarding cerebral amyloid angiopathy pathophysiology and treatment, as well as what is known of the fibrinolytic pathway and its interaction with amyloid. We postulate that tranexamic acid is a potential secondary stroke prevention treatment agent in sporadic cerebral amyloid angiopathy, although further research is required.

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Cited by 10 publications
(7 citation statements)
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References 75 publications
(148 reference statements)
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“…One explanation for this finding is the interaction between CAA, the fibrinolytic system, and tranexamic acid, but current knowledge needs further exploration. 29 We urge caution in the interpretation of these results due to the limited sample size of the lobar CAA‐ICH group.…”
Section: Discussionmentioning
confidence: 93%
“…One explanation for this finding is the interaction between CAA, the fibrinolytic system, and tranexamic acid, but current knowledge needs further exploration. 29 We urge caution in the interpretation of these results due to the limited sample size of the lobar CAA‐ICH group.…”
Section: Discussionmentioning
confidence: 93%
“…Whereas the co‐localisation of uPA with Aβ in CAA patients and rTg‐DI models we describe here has not been described before, tPA, the tissue‐counterpart of uPA, has been found to co‐localise with Aβ in the cerebral vasculature of Tg2576 mice, an AD mouse model [34]. The co‐localisation of tPA and Aβ may be explained by the observations that both tPA and plasminogen bind to lysine‐rich structures, which are present both in fibrin and in Aβ [19].…”
Section: Discussionmentioning
confidence: 92%
“…A potential candidate biomarker for CAA is urokinase plasminogen activator (uPA), a serine-proteinase that cleaves plasminogen into plasmin in the fibrinolytic pathway. uPA and its tissue counterpart, tissue plasminogen activator (tPA), have been linked to (vascular) amyloidosis occurring in AD and CAA [16][17][18][19]. Also, fibrillar Aβ accumulation can induce (over)expression of uPA and tPA in vitro in cultured rat neurons [20].…”
Section: Introductionmentioning
confidence: 99%
“…Besides cSS and cerebral micro-and macro-bleeds, the mechanisms of cognitive decline in CAA also include ischemic injury to the white matter and disruption of structural and functional network integrity [92]. The CCA pathophysiology, treatment, and role of the fibrinolytic system have been recently extensively reviewed elsewhere [93].…”
Section: Mechanism Of Vcimentioning
confidence: 99%