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1- Cellular and Molecular research center. School of Mediocine, Iran University of Medical Sciences, Tehran, Iran.
2- Department of Physiology, School of Medicine, Iran University of Medical Sciences, Tehran, Iran.
Purpose of study: Cognitive dysfunction is the most common problem of patients with Alzheimer’s disease (AD). The pathological mechanism of cognitive impairment in AD may contribute to neuronal loss as well as synaptic dysfunction and alteration in receptors of neurotransmitters. Mitochondrial synapses dysfunction due to the accumulation of amyloid beta, is among early pathological features of AD. The flavone Apigenin has been reported to play some protective role in AD through the anti-oxidative and anti-inflammatory properties. In this study, the effects of Apigenin on spatial working memory and neural protection by restoring mitochondrial dysfunction and inhibition of caspase 9 were investigated. 
Methods:  Intra-cerebroventricular (ICV) microinjection of amyloid beta 25-35 was used for AD modeling. Working memory was assessed twenty-one days later using Y maze test. Neuronal loss was detected in Hilus area of the hippocampus using Nissl and Fluoro-jade B staining, while immunohistochemistry was used to illustrate cytochrome c positive cells and caspase 9.
Results: The results revealed that Apigenin significantly ameliorated spatial working memory. It also significantly reduced the number of degenerative neurons in Hillus area. Apigenin almost completely blocked the release of cytochrome c and caspase 9 in Hilus.
Conclusion: Apigenin may improve the spatial working memory deficits and neuronal degeneration through amelioration of mitochondrial dysfunction.
Type of Study: Original | Subject: Cellular and molecular Neuroscience
Received: 2018/08/16 | Accepted: 2018/12/29

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