I currently teach introductory biochemistry, with a focus on cellular metabolism, to second year undergraduate Science students, and Molecular Neuroscience to 3rd and 4th year undergraduate Science students. An outline of my courses and all courses taught by staff in the Department of Biochemistry are available in UCC's Book of Modules.

• Identification of molecular cell signalling pathways that cause Alzheimer’s disease and related neurodegenerative disorders;
• Molecular signals that control cell survival and cell death in the ageing adult brain;
• Elucidation of novel molecular targets for the treatment of age-related neurodegenerative disorders, in particular Alzheimer’s disease.

Alzheimer’s disease is the most common form of dementia in old age and affects an ever-increasing number of our population. The dementia of Alzheimer’s disease is caused by a progressive destruction of neurons in specific regions of the brain associated with memory, higher mental function and personality. This neuronal cell loss is associated with the progressive build up of two pathological insoluble lesions, ß-amyloid plaques, composed of the 39-42 amino acid ß-amyloid peptide, and neurofibrillary tangles, which are predominantly composed of hyper-phosphorylated tau protein. Despite considerable research work, the biological mechanisms underlying the build up of these pathologies and the relationship of these pathologies to neurodegeneration in Alzheimer’s are still unknown, and unfortunately no treatment exists that can effectively treat Alzheimer’s disease.

One of the major aims of research in our lab is to define the critical molecular signal transduction events that go awry in the human brain with ageing to cause neurodegeneration in Alzheimer’s disease. This is important both in understanding the disease, but also in developing novel and effective treatment strategies for the disease. Our work also focuses in part, on signal transduction in other related age-related neurodegenerative disorders, such as the taupopathies, Parkinson’s disease and Huntington’s disease, as similar neuronal signaling pathways are emerging to be affected in Alzheimer’s disease and these related disorders.

At present we use several experimental approaches to investigate and characterise the relationship between key neuronal signal transduction pathways and Alzheimer’s disease pathology. These approaches use cell and molecular technologies to examine signal transduction in brains of individuals who have had Alzheimer’s disease, in transgenic animal models of Alzheimer’s disease, and in cell systems which express mutant genes that can cause Alzheimer’s disease. Presently this work is focused primarily upon:

• Akt/ PTEN signal transduction in brain development, brain ageing and age-related neurodegenerative disorders;
• Integrity of the Insulin and insulin-like growth factor receptor signaling in adult brain function, and in Alzheimer’s disease and related disorders;
• Characterisation of the role and regulation of the ß- site APP cleaving enzyme (BACE), and its relationship to amyloid-ß production in Alzheimer’s disease;
• The role of calcium signal transduction in Alzheimer’s disease.