DEVELOPMENT OF ANIMAL MODEL OF DEMENTIA INDUCED BY INTRACEREBROVENTRICULAR ALLOXAN IN SWISS WEBSTER MICE

Dementia is a neurodegenerative condition that is mainly experienced by the elderly population. The most prominent clinical manifestation of dementia is cognitive decline, especially memory. Worldwide, 35.6 million people are affected by dementia, with 58% living in low- and middle-income countri...

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Bibliographic Details
Main Author: Zahra Amatullah, Anita
Format: Final Project
Language:Indonesia
Online Access:https://digilib.itb.ac.id/gdl/view/62168
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Institution: Institut Teknologi Bandung
Language: Indonesia
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Summary:Dementia is a neurodegenerative condition that is mainly experienced by the elderly population. The most prominent clinical manifestation of dementia is cognitive decline, especially memory. Worldwide, 35.6 million people are affected by dementia, with 58% living in low- and middle-income countries. In drug development, testing in animal models is a prerequisite for further drug evaluation in human. This study was aimed to develop a model of dementia in male Swiss Webster mice induced by alloxan intracerebroventricularly. In this study, mice were divided into control group that receiving artifical cerebrospinal fluid (ACSF) and alloxan-induced dementia group that treated with alloxan at 1, 3.2, 5.6 or 10 mg/kg bw intracerebroventricularly. Tests for memory performance were carried out using water maze apparatus with escape latency time (ELT) as parameter. ELT is the time that mice needed to climb the hidden platform in the water maze. This test performed on days 1, 2, 3, 5 and 7 of treatment. At the end of the experiment representative mice from each group were sacrificed for brain histological examination. Data obtained were processed using one-way ANOVA and post hoc LSD analysis. Results showed that baseline ELT was 13.45+4.9 sec. ELT values of control group given ACSF were not different from baseline (p>0.05). Meanwhile, ELT in groups treated with 1 and 3.2 mg/kg alloxan were significantly different from baseline (p<0.05), on the other hand, the group treated with 5.6 mg/kg alloxan did not show significant different in ELT compared to baseline. When daily ELT were compared between treatment group, significant difference was observed between group receiving 3.2 mg/kg alloxan and control on day 5 (p<0.05), and between 5.6 mg/kg alloxan-treated group and control on day 7 (p<0.05). While on test day 1, 2, and 3 showed no significant difference (p>0.05) between all treatment group compared to control. Brain histology revealed larger number of necrotic neuroglia and pyramid cells in alloxan-treated group compared to control. Taken together, results of the present study suggest that alloxan can be utilized as dementia-inducing agent in mice.