Document Type : Original research articles
Authors
1
Department of Medical Physiology, Faculty of Medicine, South Valley University, Qena 83523, Egypt.
2
Department of Medical Physiology, Faculty of Medicine, Assiut University, Assiut, Egypt.
3
Department of Human Anatomy & Emberyology, Faculty of Medicine, South Valley University, Qena 83523, Egypt.
4
Department of Cell and Tissues, Faculty of Vet. Medicine, Assiut University, Assiut, Egypt.
Abstract
Background: Alzheimer’s disease (AD) represents the most prevalent type of dementia, characterized by neurodegenerative and neurobehavioral changes, memory loss and cognitive difficulties. Previous studies have indicated that ketogenic diet (KD) has neuroprotective effects. However, the impact of KD on AD – associated pathology and its protective mechanism remains unclear.
Objectives: The present study aims to investigate the efficacy of KD in improving cognitive dysfunction and neurodegenerative pathology of AD, as well as the possible underlying mechanisms.
Materials and methods: This study was an experimental randomized control trial, 30 male albino Sprague Dowely rats were included; rats were divided into three groups; sham control, AD model rats and AD-KD fed group. AD was induced by intraperitoneal injection of aluminum chloride (AlCl3) for 60 days in AD model rats and AD-KD fed group then AD-KD fed group continue on KD with a fat to carbohydrate and protein ratio of 3.1:1 for another 8 weeks. We investigated the effect of KD on cognitive dysfunction associated with AD. For this study, T-maze test, acetylcholinesterase (AChE) enzyme, malondialdehyde (MDA), and superoxide dismutase (SOD) enzyme assessment using ELISA, and histological assessment of the hippocampus using H&E and toluidine blue staining were performed.
Results: Compared with sham control group, results showed significantly decreased alteration score percentage in forced alteration T-maze test (p<0,001), increased levels of AChE enzyme (p<0,001) and oxidative stress biomarkers indicated by increased level of MDA (p<0,001) and decreased level of SOD enzyme (p<0,001), with declined neuronal survival in the hippocampus of AD model rats. Feeding on KD for eight weeks ameliorate AD- associated cognitive impairments by decreasing oxidative stress, increasing neuronal survival and reducing neural apoptosis in the hippocampus.
Conclusion: The resulting data have the potential to provide ketogenic diet as a new type of non- pharmacological therapy for AD.
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