Volume 30, Issue 3 (10-2021)                   JGUMS 2021, 30(3): 218-229 | Back to browse issues page

Research code: 960115137
Ethics code: IR.UMSHA.REC.1396.17


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1- Neurophysiology Research Center, Hamadan University of Medical Sciences, Hamadan, Iran.
2- Student Research Committee, School of Medicine, Guilan University of Medical Sciences, Rasht, Iran.
3- Cellular and Molecular Research Center, Guilan University of Medical Sciences, Rasht, Iran. , masoomeh_golipoor@yahoo.com
Abstract:   (1268 Views)
Background: Recently, researchers have considered extremely low-frequency electromagnetic fields (ELF-EMFs), as one of the non-invasive therapies, in the treatment of many severe neurological disorders, including Alzheimer Disease (AD). AD is a progressive neurodegenerative disease characterized by the deposition of amyloid plaques in the brain. However, the increase in microglial cells increases phagocytosis and the destruction of amyloid plaques. Therefore, the present study aimed to investigate the amount of β-amyloid precursor deposition and the number of microglia cells in the animal model of AD before and after exposure to ELF-EMFs. 
Objective: The aim of this study was to investigate the deposition of beta ameloid precursor and the number of microglial cells in the Alzheimer's animal model before and after exposure to magnetic waves.
Methods: Fifty male adult rats were randomly grouped into 5: The control group, the ELF-EMFs group, the AD group, the treatment group 1, and the treatment group 2. After the study period, the animals were killed for immunohistochemistry assessment to detect and compare the deposition of β-amyloid and the production of allograft inflammatory factor 1  (Iba1) protein.
Results: Exposure to ELF reduced the deposition of β-amyloid and increased microglia cells. However, these changes were not different between the control and ELF-EMFs groups (P<0.001).
Conclusion: ELF-EMF can reduce the formation of β-amyloid plaques and induce the proliferation of microglia cells. Therefore, they can be used to treat brain damage caused by Alzheimer disease. 
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Review Paper: Research | Subject: Special
Received: 2021/07/19 | Accepted: 2021/10/18 | Published: 2021/10/1

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