Sovateltide prevents beta‐amyloid plaque load and restores memory deficit in an APP/PS1 mouse model of Alzheimer's disease

Background Endothelin B (ETB) receptor agonist, sovateltide, is being investigated as a potential therapeutic agent for AD. However, its causative effects on decreasing beta‐amyloid (Aβ) plaque load and rescuing impaired memory in APP/PS1 mice remain unclear. In the present study, we have examined t...

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Bibliographic Details
Published in:Alzheimer's & dementia 2021-12, Vol.17 (S9), p.n/a
Main Authors: Briyal, Seema, Voshtina, Ralf, Gulati, Anil
Format: Article
Language:English
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Summary:Background Endothelin B (ETB) receptor agonist, sovateltide, is being investigated as a potential therapeutic agent for AD. However, its causative effects on decreasing beta‐amyloid (Aβ) plaque load and rescuing impaired memory in APP/PS1 mice remain unclear. In the present study, we have examined the effects of SOVA on Aβ plaques formation and functional recovery in transgenic AD mice and explored its mechanism(s) of action. Method APP/PS1 transgenic mice and C57BL/6 control mice were divided into two groups (vehicle and sovateltide). Sovateltide (5 μg/kg) was intravenously injected three times at 2‐hour intervals on days 1, 3, and 6 every month until study endpoints (3, 6, and 12 months age). Memory deficit was assessed using the Morris water maze test. Separate sets of mice were sacrificed at the end of 3, 6, and 12 months and Aβ plaque formation was examined in the brain. Mitochondrial dysfunction, neurogenesis, and synaptogenesis were assessed using western blot and immunofluorescence techniques. Result APP/PS1 transgenic mice showed significant (p
ISSN:1552-5260
1552-5279
DOI:10.1002/alz.057431