Protective role of Apelin-13 on amyloid β25–35-induced memory deficit; Involvement of autophagy and apoptosis process

Publication date: Available online 5 October 2018Source: Progress in Neuro-Psychopharmacology and Biological PsychiatryAuthor(s): Samaneh Aminyavari, Maryam Zahmatkesh, Maryam Farahmandfar, Fariba Khodagholi, Leila Dargahi, Mohammad-Reza ZarrindastAbstractAlzheimer's disease (AD) by progressive neurodegenerative pattern is associated with autophagy stress which is suggested as a potential cause of amyloid β (Aβ) aggregation and neural loss. Apelin-13, a neuropeptide with modulatory effect on autophagy, has been shown the beneficial effects on neural cell injuries. We investigated the effect of Apelin-13 on Aβ-induced memory deficit as well as autophagy and apoptosis processes. We performed bilateral intra-CA1 injection of Aβ25–35 alone or in combination with Apelin-13. Spatial reference and working memory was evaluated using the Morris water maze (MWM) and Y-maze tests. Hippocampus was harvested on 2, 5, 10 and 21 days after Aβ injection. The light chain 3 (LC3II/I) ratio, histone deacetylase 6 (HDAC6) level, Caspase-3 cleavage, and mTOR phosphorylation were assessed using western blot technique. Intra-CA1 injection of Aβ caused impairment of working and spatial memory. We observed higher LC3II/I ratio, cleaved caspase-3 and lower HDAC6, and p-mTOR/mTOR ratio in Aβ-treated animals. Apelin-13 provided significant protection against the destructive effects of Aβ on working and spatial memory. Apelin-13 prevented the increase of LC3II/I ratio and cleaved caspase-3 on...
Source: Progress in Neuro Psychopharmacology and Biological Psychiatry - Category: Psychiatry Source Type: research
More News: Brain | Neurology | Psychiatry