Environmental Enrichment and Protection from Dementia
The clinical onset of AD may be affected not only by an increase in the progression of pathological changes in the brain, but also by an individual’s cognitive reserve. This is evidenced by studies demonstrating that there is a large discrepancy between the amount of AD pathology and the clinical manifestations of dementia. It is believed that cognitive reserve may be increased by social and intellectual interactions. This is supported by epidemiological studies suggesting that lifetime environmental factors such as education can reduce the risk of dementia. The Wicking Dementia Research and Education Centre is exploring the association between later life education and ageing related cognitve decline and dementia in a world first prospective longitudinal study, The Tasmanian Healthy Brain Project (THBP).
Cognitive reserve refers to an individual’s ability to utilize the brain networks that underlie cognitive function. However, the cellular correlates of cognitive reserve have not been fully defined. In this study we are using environmental enrichment in animal models to investigate the cellular correlates of cognitive reserve and the association between environmental enrichment, AD pathology and memory deficits. The focus of our study is to investigate how environmental enrichment affects neuronal circuitry, including synaptic alterations, changes in dendritic arbours, spine dynamics and myelination and how these factors relate to increased cognitive ability. We will also investigate how cognitive reserve is affected by the type of enrichment and how the enriched and non enriched brain responds to a novel stimulus. APP and WT mice in the intervention group (environmental enrichment) will me compared to APP and WT mice in standard housing. This study will aim to draw links between the THBP human study and environmental enrichment in APP and wild type mice.
| Objectives | These studies will determine the effect of environmental enrichment on AD-like pathology and cognitive performance in mouse models of AD. |
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