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.