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Cystatin C (γ-Trace) and β-Protein Coexist in the Cerebral Amyloid Angiopathy Causing Cerebral Hemorrhage and Consequential Vascular Dementia

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Part of the book series: Advances in Behavioral Biology ((ABBI,volume 38A))

Abstract

Cerebral amyloid angiopathy (CAA) is one of the important pathological changes of Alzheimer’s disease.1 CAA also causes unique cerebral hemorrhages. In typical cases, recurrent, multiple and lobar hemorrhages occur in normotensive elderly people and cause consequential dementia of the vascular type.2 As for the protein nature of the amyloid of CAA, there are at least two types of amyloid. One is β-protein (BP) and the other is variant cystatin C (CC). The former is found in CAA and in senile plaques of Alzheimer’s Disease(AD).3,4 CAA amyloid of normal elderly is also BP.5 On the other hand, variant CC is the main component of CAA amyloid of hereditary cerebral hemorrhage with amyloidosis (HCHWA) found in Iceland.6 Recently, we reported Japanese cases of CAA causin cerebral hemorrhage, of which amyloid shows the antigenicity of CC.7,8 Two of them had a family history of possible CAA and the others were sporadic.8 To characterize the Japanese cases of CAA with the deposition of CC and to compare them with Icelandic cases, we used the immunoperoxidase method in combination with anti-BP, conducted biochemical analyses, and studied the DNA of the CC gene.

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© 1990 Plenum Press, New York

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Fujihara, S. et al. (1990). Cystatin C (γ-Trace) and β-Protein Coexist in the Cerebral Amyloid Angiopathy Causing Cerebral Hemorrhage and Consequential Vascular Dementia. In: Nagatsu, T., Fisher, A., Yoshida, M. (eds) Basic, Clinical, and Therapeutic Aspects of Alzheimer’s and Parkinson’s Diseases. Advances in Behavioral Biology, vol 38A. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5844-2_23

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  • DOI: https://doi.org/10.1007/978-1-4684-5844-2_23

  • Publisher Name: Springer, Boston, MA

  • Print ISBN: 978-1-4684-5846-6

  • Online ISBN: 978-1-4684-5844-2

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