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Effects of Chronic Hypoxia on the Expression of Seladin-1/Tuj1 and the Number of Dark Neurons of Hippocampus Publisher Pubmed



Mahakizadeh S1 ; Mokhtari T2, 3 ; Navaee F4 ; Poorhassan M4 ; Tajik A5 ; Hassanzadeh G6
Authors
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Authors Affiliations
  1. 1. Department of Anatomy, School of Medicine, Alborz University of Medical Sciences, Karaj, Iran
  2. 2. CAS Key Laboratory of Mental Health, Institute of Psychology, Beijing, China
  3. 3. Department of Psychology, University of Chinese Academy of Sciences, Beijing, China
  4. 4. Department of Anatomy, School of Medicine, Shahidbeheshti University of Medical Sciences, Tehran, Iran
  5. 5. Student Research Committee, Alborz University of Medical Sciences, Karaj, Iran
  6. 6. Department of Anatomy, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran

Source: Journal of Chemical Neuroanatomy Published:2020


Abstract

Background: There are evidences showing the relation between chronic hypoxia and Alzheimer's disease (AD) as a metabolic neurodegenerative disease. This study was designed to evaluate the effects of chronic hypoxia on factors which characterized in AD to introduce a new model of AD-dementia. Methods and materials: Twenty-four male rats were randomly divided in three groups: Control group (Co), Sham group (Sh), Hypoxia induction group (Hx, exposed to hypoxic chamber [oxygen 8% and nitrogen 92%] for 30 days, 4 h/day). Spatial learning and memory were analyzed using the Morris water maze task. At day 30 after hypoxia period, animals were sacrificed and serum was gathered for pro-inflammatory cytokines (interleukin-1β and tumor necrosis factor) measurements and brains were used for molecular and histopathological investigations. Results: According to behavioral studies, a significant impairment was seen in Hx group (P < 0.05). TNF-α and IL-1β showed a significant enhanced in Hx group comparing with Co group and Sh group (P < 0.05). As well, the gene expression of seladin-1, Tuj1 and the number of seladin-1+, Tuj1+neurons significantly decreased and also the mean number of dark neurons significantly increased in CA1 and CA3 regions of hippocampus. Conclusions: In this study, a new model of AD was developed which showed the underlying mechanisms of AD and its relations with chronic hypoxia. Hypoxia for 30 days decreased seladin-1, Tuj1 expression, increased the number of dark neurons, and also induced memory impairment. These results indicated that chronic hypoxia mediated the dementia underlying AD and AD-related pathogenesis in rat. © 2020 Elsevier B.V.
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