Reversal of blood-brain barrier dysfunction for the treatment of Alzheimer's disease
Alzheimer’ disease (AD) is the leading cause of dementia with up to 1 diagnosis being predicted every 30 seconds by 2050. Despite this, a cure for this disorder is currently unavailable. It is suggested that aberrant brain parenchymal accumulation of the extracellular protein β-amyloid (Aβ) mediates the neuronal toxicity associated with AD, and this accumulation has been more recently demonstrated to be due to faulty clearance of Aβ from the brain parenchyma into the bloodstream across the blood-brain barrier (BBB).
Our laboratory focusses on the mechanisms responsible for the faulty BBB clearance of Aβ, the transporters which are responsible for this faulty clearance, and approaches that can be exploited to enhance BBB transporter function assessed by in vitro and in vivo methods.