Immunohistochemical study of leptin receptors in hippocampus of rats with hypoperfusion-induced neurodegeneration /
Longer life expectancy leads to shifting in age-related diseases such as dementia and Alzheimer's disease (AD). The main area affected in AD is the hippocampus, where memory and cognitive processing occurs. Persistent moderate disturbance in cerebral blood flow contributes to dementia and AD. T...
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| Main Author: | |
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| Format: | Thesis |
| Language: | English |
| Published: |
Kuantan, Pahang :
Kulliyyah of Medicine, International Islamic University Malaysia,
2018
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| Subjects: | |
| Online Access: | Click here to view 1st 24 pages of the thesis. Members can view fulltext at the specified PCs in the library. |
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| Summary: | Longer life expectancy leads to shifting in age-related diseases such as dementia and Alzheimer's disease (AD). The main area affected in AD is the hippocampus, where memory and cognitive processing occurs. Persistent moderate disturbance in cerebral blood flow contributes to dementia and AD. The model involved to induce cerebral hypoperfusion is known as chronic bilateral common carotid arteries ligation, which is also known as 2-vessel occlusion (2VO). Leptin is known to aid memory processing. The main aim in this study was to investigate leptin receptor in hippocampus of rats with hypoperfusion-induced neurodegeneration by using immunohistochemistry, and to study the serum leptin level in animals with the same procedure using enzyme-linked immunosorbent assay (ELISA). The rats were divided into 3 groups: 4 weeks, 6 weeks, and 8 weeks post-2VO. There was no change in serum leptin levels post 2VO procedure. However, there was significant reduction in leptin receptor-immunoreactivity in CA1 of hippocampus after 2VO in time-dependent manner. The reduction in leptin receptor could explain the loss of neuroprotective effect on neurons as well as impairment of the activation of the memory pathway in the hippocampus. |
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| Physical Description: | xiv, 81 leaves : colour illustrations ; 30cm. |
| Bibliography: | Includes bibliographical references (leaves 68-74). |