Key result
Intraperitoneal administration of the ACE2 activator diminazene aceturate (DIZE) restored associative recognition memory (p=0.0001) and reduced hippocampal insoluble Aβ42 and Aβ43 levels in symptomatic Tg2576 mice.
Why the study?
The regulatory renin-angiotensin system (rRAS) moderates classical RAS activity but is underactive in Alzheimer's disease, and the effect of enhancing the rRAS effector ACE2 on pathology and cognitive decline was investigated.
Does diminazene aceturate (DIZE) improve cognitive impairment and reduce amyloid pathology in the Tg2576 mouse model of Alzheimer's disease?
Population
Tg2576 mouse model of Alzheimer's disease
Comparison
Intraperitoneal diminazene aceturate (DIZE) administration vs not specified
Design
Preclinical animal model study
Authors
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ACE2 activation mitigated AD pathology in mice; leaves open translation to human prevention or therapy.
Does diminazene aceturate (DIZE) improve cognitive impairment and reduce amyloid pathology in the Tg2576 mouse model of Alzheimer's disease?
p-value: p=0.0001
Enhancement of brain ACE2 activity with DIZE protects against and reverses amyloid-related hippocampal pathology and cognitive impairment in a preclinical model of Alzheimer's disease.
Evans et al. (2020) studied Alzheimer's disease (Tg2576 mouse model) (n=182). Diminazene aceturate (DIZE) vs. Vehicle (saline) was evaluated on Associative recognition memory (Object-in-Place task discrimination ratio) (p=0.0001). Intraperitoneal administration of the ACE2 activator diminazene aceturate (DIZE) restored associative recognition memory (p=0.0001) and reduced hippocampal insoluble Aβ42 and Aβ43 levels in symptomatic Tg2576 mice.
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