|Sara Mokhtar won the CCS 3MT thesis heat |
in 2014. See video
Alzheimer’s disease (AD) is the most common form of dementia in the elderly. AD causes loss of memory, cognition, language and emotional stability and has currently no known cure. The aim of Sara's project was to find a novel target to stop the progression of the disease in order protect our aged population. It is well known that AD is caused by the accumulation of a normal protein in the brain called beta amyloid (Aβ).
Sara's project used brain samples from AD patients, along with a mouse model, to show that Aβ can alter the function of a protein called collapsin response mediator protein (CRMP2), which is responsible for the growth of neuronal projections, called axons. Altered CRMP2 prevents the elongation of those axons, which in turns inhibit communication between neurons and causes neuronal death. As part of her 2014 3MT presentation, Sara said, "We have demonstrated that Aβ can activate an enzyme called Rho kinase that then adds a phosphate ion to a specific site on CRMP2 protein, which in turn causes retraction of neuronal axons. Using stem cells, we have successfully blocked this particular site and preserved axonal growth. This could eventually be used to protect neuronal connections and reverse the effects of Aβ in AD."