Statin therapy and the development of cerebral amyloid angiopathy

• Verfasst von: Reuter, Björn [VerfasserIn]
• Verfasst von: Grudzenski-Theis, Saskia [VerfasserIn]
• Verfasst von: Schad, Lothar R. [VerfasserIn]
• Verfasst von: Hennerici, Michael G. [VerfasserIn]
• Verfasst von: Fatar, Marc [VerfasserIn]
• Titel: Statin therapy and the development of cerebral amyloid angiopathy
• Titelzusatz: a rodent in vivo approach
• Verf.angabe: Björn Reuter, Alexander Venus, Saskia Grudzenski, Patrick Heiler, Lothar Schad, Matthias Staufenbiel, Michael G. Hennerici and Marc Fatar
• E-Jahr: 2016
• Jahr: 19 January 2016
• Umfang: 12 S.
• Fussnoten: Gesehen am 17.01.2019
• Titel Quelle: Enthalten in: International journal of molecular sciences
• Ort Quelle: Basel : Molecular Diversity Preservation International, 2000
• Jahr Quelle: 2016
• Band/Heft Quelle: 17(2016,1) Artikel-Nummer 126, 12 Seiten
• ISSN Quelle: 1422-0067
• ISSN Quelle: 1661-6596
• DOI: doi:10.3390/ijms17010126
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: amyloid
• Sach-SW: APP23
• Sach-SW: CAA
• Sach-SW: cerebral microbleeds
• Sach-SW: statins
• Sach-SW: transgenic mice
• K10plus-PPN: 1586321900

Abstract

Background: Cerebral amyloid angiopathy (CAA) is characterized by vascular deposition of amyloid β (Aβ) with a higher incidence of cerebral microbleeds (cMBs) and spontaneous hemorrhage. Since statins are known for their benefit in vascular disease we tested for the effect on CAA. Methods: APP23-transgenic mice received atorvastatin-supplemented food starting at the age of eight months (n = 13), 12 months (n = 7), and 16 months (n = 6), respectively. Controls (n = 16) received standard food only. At 24 months of age cMBs were determined with T2*-weighted 9.4T magnetic resonance imaging and graded by size. Results: Control mice displayed an average of 35 ± 18.5 cMBs (mean ± standard deviation), compared to 29.3 ± 9.8 in mice with eight months (p = 0.49), 24.9 ± 21.3 with 12 months (p = 0.26), and 27.8 ± 15.4 with 16 months of atorvastatin treatment (p = 0.27). In combined analysis treated mice showed lower absolute numbers (27.4 ± 15.6, p = 0.16) compared to controls and also after adjustment for cMB size (p = 0.13). Conclusion: Despite to a non-significant trend towards fewer cMBs our results failed to provide evidence for beneficial effects of long-term atorvastatin treatment in the APP23-transgenic mouse model of CAA. A higher risk for bleeding complications was not observed.