ACE2/Ang-(1-7)/MasR axis in AD
| Type of evidence (clinical or experimental) | Main finding | References |
|---|---|---|
| Human (postmortem human brain tissue from AD patients) | - ACE2 activity was decreased by about 50%- ACE2 reduction strongly associated to increased Aβ and phosphorylated tau levels | Kehoe et al., 2016 [140] |
| Human (cerebrospinal fluid from AD patients) | - ACE2 increased in association with aging in the control group but not in AD- ACE2 enzyme activity correlated positively with albumin, a marker of blood-brain barrier integrity | Kehoe et al., 2019 [141] |
| Human (postmortem human brain tissue from AD patients) | - Increased Ang II/Ang-(1-7) ratio in AD in comparison to age-matched controls | Kehoe et al., 2016 [140] |
| Human (plasma from AD patients) | - Decreased Ang-(1-7) plasma levels in AD compared with matched controls- Ang-(1-7) plasma levels were positively correlated to cognitive performance | Jiang et al., 2016 [143] |
| Animal (mouse model of sporadic AD) | - Reduced Ang-(1-7) levels in cerebral cortex and hippocampus during disease progression- Ang-(1-7) levels had a negative correlation with hyperphosphorylated tau | Jiang et al., 2016 [144] |
| Animal (established transgenic APP mouse model, Tg2576 mice) | - Enhancement of brain ACE2 activity lowered hippocampal Aβ and improved cognition- ACE2 enhancement restored hippocampal MasR levels | Evans et al., 2019 [142] |