Resmi Menon
Alzheimer’s Disease Research
‘Determining the intracellular trafficking pathways of tachykinin-copper(II)-receptor complexes and elucidation of the fate of copper’
Western Sydney University, NSW
Awarded 2018
Co-funded by David Holz and Rotary Club of Holroyd
“Neurodegenerative diseases are complex and highly challenging to treat. Many, including Alzheimer’s disease, have no truly disease-modifying interventions and current medications tend to focus on symptom relief. ”
Researcher Profile
Resmi Menon have completed undergraduate degrees in Bachelor of Zoology and Bachelor of Education followed by a Master of Science (MSc) and Master of Philosophy in ‘Stress Physiology and Endocrinology’ from University of Kerala, India. For her MPhil research, Resmi studied the adaptability of aquatic organisms to metal toxicity which has a strong link with her current PhD study.
After graduation Ms Menon taught biological science to high school and undergraduate students for almost 5 years. After moving firstly to Switzerland and then to Australia Resmi began a PhD at Western Sydney University in the winter of 2017.
Project Summary
During the normal brain function, neurotransmitters flow from one neuron to a neighbouring cell where they bind at sites called receptors. The binding ‘switches on’ the receptor allowing signals to flow within the cell. Disruption to the function of these molecules contributes to the symptoms seen in Alzheimer’s patients like memory loss and cognition difficulties. An important neurotransmitter family are the neurokinins which have broad roles in cognition, emotion and inflammation and have been widely implication in Alzheimer’s disease. Another important element in the brain is copper. It helps many enzymes and antioxidants work, and outside the cell it can bind to receptors and modify signalling behaviour.
This makes maintenance of copper levels inside and outside cells critical for normal brain function.
Intriguingly, in Alzheimer’s Disease the plaques are full of copper which has many neurological consequences including reduced signalling ability and metal deficiency in brain cells. Further, it is thought that copper directly contributes to radical induced oxidative stress observed in Alzheimer’s disease. We know that some neurokinin molecules can bind copper and we now predict that neurokinins can help brain cells maintain normal copper levels. A potential consequence of plaque formation is that this activity is modified. The overall aim of this project is to determine how neurokinins contribute to the maintenance of correct copper levels in the brain.
Supervisors: Dr Christopher Edward Jones, Dr Mark Jones and Dr Jo-Anne Chuck.