In neurodegenerative disorders like Alzheimer’s disease (AD), synaptic communication within brain networks are impaired leading to significant memory deficits and dementia.
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Dundee
(Dundee City)
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Fulton Building, DD1 4HN
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This centre's achievements
2019
All courses are up to date
The average rating is higher than 3.7
More than 50 reviews in the last 12 months
This centre has featured on Emagister for 14 years
Subjects
Hormone
Increased
Contributory
Lifestyle
Risk
Imbalance
Clinical
Metabolic
Ad
Synaptic
Hippocampal
Amyloid
Course programme
Clinical studies indicate that diet and lifestyle are key risk factors for AD, with metabolic imbalance identified as an important contributory factor. Recent studies have linked the metabolic hormone leptin to an increased incidence of AD, which has fuelled the possibility that leptin-based therapies may be beneficial in AD. Indeed, our recent studies support this as we have identified not only a cognitive enhancing role for leptin (1), but treatment with leptin prevents hippocampal synaptic disruption and neuronal death in amyloid-based models of AD (2). Moreover, we have recently identified that the whole leptin molecule is not required for bioactivity, as a leptin fragment (leptin amino acids 116-130) mirrors the cognitive enhancing and neuroprotective actions of leptin. However our understanding of the neuroprotective actions of leptin in human AD pathology and in particular tau pathology is limited. Here we aim to use a range of model systems, including human induced pluripotent stem cell (iPSC) technologies, to mirror tau pathophysiology that occurs in human cases of AD, with a view to increasing our understanding of the neuroprotective and potential therapeutic actions of leptin and leptin fragments.
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University of Dundee Postgraduate Degrees
Investigations into the neuroprotective actions of leptin and leptin-based mimetics in models of tauopathy.
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