Executive Summary : | Alzheimer's disease (AD) is a neurodegenerative disorder characterized by synaptic loss in the hippocampus due to Aβ aggregation. Sleep deprivation is a new risk factor identified, with decreased sleep increasing β-amyloid protein in the brain and higher incidence of memory impairment in individuals with sleep deprivation. The role of lack of sleep as a risk factor for AD is not well studied, especially REM sleep, which is crucial for memory consolidation. Regular exercise is a non-pharmacological approach that can improve memory impairment and cognitive function, acting as a preventive strategy against dementia. The neuroprotective effects of exercise may involve new angiogenesis, neurogenesis, and synaptic plasticity. Physical exercise can improve cognitive ability and is associated with a boost in hippocampal volume. Studies suggest that regular exercise positively influences cognition and memory in elderly patients, but the mechanism behind this is still not well understood.
This study aims to correlate the effect of exercise on Aβ aggregation severity and other morphological and functional neuronal alterations in AD. The objective is to develop exercise as a preventive targeted therapy and understand the molecular mechanism between sleep deprivation and synaptic abnormality in AD so that target molecules can be identified for drug therapy for AD treatment. The study will involve 64 rats divided into eight groups: control, Sham, AD, SD, AD+SD, control+exercise, SD+exercise, AD+Exercise, and AD+SD+exercise. |