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Complement Activation in Capillary Cerebral Amyloid Angiopathy.
Matsuo, Ko; Shindo, Akihiro; Niwa, Atsushi; Tabei, Ken-Ichi; Akatsu, Hiroyasu; Hashizume, Yoshio; Akiyama, Haruhiko; Ayaki, Takashi; Maki, Takakuni; Sawamoto, Nobukatsu; Takahashi, Ryosuke; Oikawa, Shinji; Tomimoto, Hidekazu.
Afiliação
  • Matsuo K; Department of Neurology, Mie University Graduate School of Medicine, Tsu, Japan.
  • Shindo A; Department of Neurology, Mie University Graduate School of Medicine, Tsu, Japan.
  • Niwa A; Department of Neurology, Mie University Graduate School of Medicine, Tsu, Japan.
  • Tabei KI; Department of Dementia Prevention and Therapeutics, Mie University Graduate School of Medicine, Tsu, Japan.
  • Akatsu H; Choju Medical Institute, Fukushimura Hospital, Toyohashi, Japan.
  • Hashizume Y; Choju Medical Institute, Fukushimura Hospital, Toyohashi, Japan.
  • Akiyama H; Department of Clinical Research, Yokohama Brain and Spine Center, Yokohama, Japan.
  • Ayaki T; Department of Neurology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
  • Maki T; Department of Neurology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
  • Sawamoto N; Department of Neurology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
  • Takahashi R; Department of Neurology, Kyoto University Graduate School of Medicine, Kyoto, Japan.
  • Oikawa S; Department of Environmental and Molecular Medicine, Mie University Graduate School of Medicine, Tsu, Japan.
  • Tomimoto H; Department of Neurology, Mie University Graduate School of Medicine, Tsu, Japan.
Dement Geriatr Cogn Disord ; 44(5-6): 343-353, 2017.
Article em En | MEDLINE | ID: mdl-29421784
BACKGROUND: Cerebral amyloid angiopathy (CAA) is classified as type 1 with capillary amyloid ß (Aß) or type 2 without capillary Aß. While it is known that CAA activates complement, an inflammatory mediator, there is no information on the relationship between capillary Aß and complement activation. METHODS: We evaluated 34 autopsy brains, including 22 with CAA and 12 with other neurodegenerative diseases. We assessed the vascular density of CAA by analyzing the expression of complement (C1q, C3d, C6, C5b-9), macrophage scavenger receptor (MSR), and apolipoprotein E (ApoE). RESULTS: Capillary immunostaining for C1q, C3d, MSR, and ApoE was identified almost exclusively in CAA-type1 brains. There was intense expression of C1q, C3d, MSR, and ApoE, as well as weaker expression of C5b-9 and C6 in the arteries/ arterioles of both CAA subtypes, but not in control brains. C5b-9 and C6 were preferentially expressed in arteries/arterioles with subcortical hemorrhage or cortical superficial siderosis. Triple immunofluorescence revealed that C1q, C3d, and ApoE were colocalized with Aß in CAA brain capillaries. CONCLUSION: Complement, MSR, and ApoE were only coexpressed in the presence of Aß accumulation in capillaries, suggesting a role for complement activation in the propagation of Aß. Additionally, C5b-9 expression may be associated with hemorrhagic brain injury in CAA.
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Texto completo: 1 Coleções: 01-internacional Contexto em Saúde: 6_ODS3_enfermedades_notrasmisibles Base de dados: MEDLINE Assunto principal: Capilares / Angiopatia Amiloide Cerebral / Ativação do Complemento Limite: Aged / Aged80 / Female / Humans / Male / Middle aged Idioma: En Revista: Dement Geriatr Cogn Disord Ano de publicação: 2017 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Contexto em Saúde: 6_ODS3_enfermedades_notrasmisibles Base de dados: MEDLINE Assunto principal: Capilares / Angiopatia Amiloide Cerebral / Ativação do Complemento Limite: Aged / Aged80 / Female / Humans / Male / Middle aged Idioma: En Revista: Dement Geriatr Cogn Disord Ano de publicação: 2017 Tipo de documento: Article