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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.
Highlights
In the last decades the relevance of cerebral amyloid angiopathy (CAA) as a substantial human neurovascular and neurodegenerative disease was increasingly recognized
We investigated the long-term effects of atorvastatin administration in the APP23 transgenic mouse model by use of magnetic resonance imaging (MRI) and Prussian blue (PB)/Thioflavin S staining
Treatment with atorvastatin had no significant influence on the mortality rate with 12/29 controls dying within the study period (41%) compared to 4/17 mice treated for 16 months (24%, p = 0.21), 4/11 mice treated for 12 months (36%, p = 0.78), and 5/11 mice treated for eight months (46%, p = 0.82)
Summary
In the last decades the relevance of cerebral amyloid angiopathy (CAA) as a substantial human neurovascular and neurodegenerative disease was increasingly recognized. Histopathological studies in Alzheimer’s disease (AD) research in the 1970s and 1980s demonstrated accompanying vascular amyloid β (Aβ) deposits, in particular the implementation of magnetic resonance imaging (MRI) and development of transgenic mouse models made an important contribution to our CAA knowledge and led to a burst of scientific interest and research in this field [2,3,4]. Cerebral amyloid angiopathy (CAA) is characterized by vascular deposition of amyloid β (Aβ) with a higher incidence of cerebral microbleeds (cMBs) and spontaneous hemorrhage. 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.
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