What is the clinical evidence from this study?

Study design: Other. Population: Cerebral amyloid angiopathy. Intervention: Telmisartan or lisinopril vs. untreated Tg-SwDI mice and wild-type controls. Primary outcome: AT1R levels in 13 brain regions.

May 21, 2025Open Access

Chronic Treatment of a Mouse Model of Cerebral Amyloid Angiopathy and Brain AT 1 Receptor Expression

Key Result

Treatment with sub-depressor doses of telmisartan or lisinopril caused no significant alterations in brain AT1 receptor levels in a mouse model of cerebral amyloid angiopathy.

Structured PICO

Does telmisartan or lisinopril alter brain AT1 receptor levels in a mouse model of cerebral amyloid angiopathy?

Population

Tg-SwDI mice, a model of cerebral amyloid angiopathy, treated from 3 to 8 months of age.

Intervention

Sub-depressor doses of either telmisartan or lisinopril from 3-8 months of age

Comparator

Untreated Tg-SwDI mice and wild-type controls

Outcome

Levels of AT1R in 13 brain regions determined by receptor autoradiography postmortemsurrogate

Chronic treatment with sub-depressor doses of telmisartan or lisinopril did not significantly alter brain AT1 receptor levels in a mouse model of cerebral amyloid angiopathy.

Abstract

Abstract Introduction The renin-angiotensin-aldosterone system (RAAS) has been shown to be dysregulated in dementia, with elevated levels of angiotensin-converting enzyme (ACE), angiotensin (Ang) II, and Ang II type 1 receptors (AT 1 Rs). Cerebral amyloid angiopathy (CAA), a common cerebrovascular disease, currently has no treatment or cure available. We aimed to determine if a mouse model with CAA (Tg-SwDI) also exhibits elevated levels of AT 1 Rs and whether RAAS-targeting drugs (telmisartan and lisinopril) mitigate these effects. Materials and Methods Tg-SwDI mice were treated with sub-depressor doses of either telmisartan or lisinopril from 3-8 months of age, with blood pressure being monitored 2 and 4 months after the start of treatment. Postmortem, receptor autoradiography was performed to determine levels of AT 1 R in 13 brain regions in untreated and treated Tg-SwDI mice compared to wild-type controls (C57Bl/6J). Results No statistically significant differences among groups were observed in any of the 13 regions analyzed. However, trends with medium to large effect sizes were observed. Conclusions CAA did not significantly dysregulate AT 1 R levels in the brains of Tg-SwDI mice compared to wild-type mice. Drug treatment caused no significant brain AT 1 R alterations. Further studies are required to determine if the trends observed are pathophysiological and pharmacologically significant.

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