About the Project
Dementia describes a group of age-associated conditions of which cognitive decline is a major feature. Alzheimer’s disease (AD) is the most common cause of dementia and is characterised by the onset of a gradual cognitive decline. However, current treatments only offer short-term symptomatic relief and as yet there are no long-term treatments available to either stop or slow down the progression.
The biggest known risk factor for developing dementia is increasing age; however there are also a number of identified lifestyle risk factors associated with an increased risk of developing AD including diabetes, hypertension, low physical activity, obesity, smoking, and depression.
There is a well-established link between human obesity and a decline in cognitive performance. In support of this, high fat diet-induced obesity causes cognitive decline in animal models. There is also evidence that high fat diets can promote plaque and tangle pathology in a mouse model of Alzheimer’s disease.
The overarching aim of this project is to improve our understanding of the neurochemical alterations that occur in the brain under specific lifestyle regimes, namely exercise and high fat diet, and determine which biochemical changes occur that underlie alterations in cognitive performance. A greater understanding of how these lifestyle risk factors affect the brain and cognition is essential to identify novel drug targets for early intervention.
In addition to the pathological alterations seen in AD, neurochemical imbalances have also been reported in many neurotransmitter systems. More specifically, relating to cognition, reductions in dopamine, its metabolites and receptors have been found in AD.
Dopamine is one of the most important neurotransmitters for learning and memory and it has been shown that levels of dopamine decline by about 10% every ten years from early adulthood and this is associated with declines in cognitive and motor performance. A reduction of dopamine, dopamine metabolites, and dopamine receptors has been observed in AD. Furthermore, enhancement of dopaminergic transmission has been shown to improve cognitive impairment in AD.
Our recent data suggests that a lack of PFC dopamine, when required, may underlie the observed cognitive deficit in an animal model of cognitive dysfunction.
It is critical to determine the link between diet and exercise as risk factors for dementia with the cognition and the underpinning dopaminergic system.
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