Sir Richard Lewis Maxwell Faull
ONZM BMedSc MBChB PhD DSc FRSNZ
Research | Current
- Human neurodegenerative diseases
- Alzheimer's disease
- Huntington's disease
- Parkinson's disease
We have a broadly-based, multidisciplinary HRC Research Programme on "Neurodegeneration in the Human Brain - Mechanisms and Therapeutic Targets" in collaboration with Dr Henry Waldvogel and Dr Maurice Curtis (Department of Anatomy with Radiology), Professor Mike Dragunow and Dr Michelle Glass in the Department of Pharmacology, and Dr Lynette Tippett (Department of Psychology) , which uses the human tissue stored in our Human Brain Bank and the molecular, cellular biological and imaging resources in the Centre for Brain Research. Research in the group is focused on the following major project areas:
- Molecular biological and anatomical studies on the chemical changes in the following major neurodegenerative diseases of the human brain – Huntington’s disease, Alzheimer’s disease, schizophrenia, Parkinson’s disease, epilepsy and Motor Neuron disease.
- Correlation of the clinical profile with the chemical anatomical pathology and genotype in Huntington’s disease, in order to determine whether variations in clinical symptomatology are reflected by variations in the chemical pathology and HD gene.
- The establishment of a transgenic sheep model of Huntington's disease in collaboration with Dr Russell Snell (School of Biological Sciences), Dr Simon Bawden (South Australian Research Development Institute), and Dr Marcy Macdonald and Professor Jim Gusella (Harvard University). This will be the first large animal model of a human brain disease in the world and will provide for studies on the pathogenesis and molecular mechanisms of Huntington's disease and, most importantly, will provide an animal model (whose brain is very similar to the human brain) for the development of novel therapeutic strategies for treating this tragic inherited human brain disease. This project has receceived major funding from The Freemasons of New Zealand.
- Molecular mechanisms and patterns of nerve cell death and repair in these neurodegenerative diseases focusing on the role of transcription factors and growth factors, and using in vitro cell culture models, and transgenic animal models.
- Investigations on the potential of various novel methods to treat neurodegenerative diseases including gene therapy techniques (decoy DNA, antisense DNA, peptide nucleic acids), and neurotrophins to prevent neuronal death in neurodegenerative diseases.
- In collaboration with Dr Bronwen Connor and Professor Mike Dragunow in Pharmacology, and Dr Maurice Curtis (University of Goteborg, Sweden) we are also studying neurogenesis in the human brain. The specific areas of interest are: (i) whether stem cells in the adult human brain and spinal cord have the ability to proliferate and form new neurons in response to brain injury and disease (Huntington's disease, Parkinson's Disease, Epilepsy, Alzheimer's disease, Motor Neuron Disease, Stroke); (ii) the pathways of neurogenesis in the human brain; (iii) the mechanisms involved in the induction of neurogenesis in the injured or diseased adult brain; and (iii) do stem cells have the potential to ‘repair’ the injured or diseased adult brain and spinal cord.
Selected publications and creative works (Research Outputs)
- Subarmaniam, N. S., Bawden, C. S., Rudiger, S. R., Yazbeck, R., Faull, R. L. M., Snell, R. G., & Howarth, G. S. (2019). Development of a novel C-13-labelled methionine breath test protocol for potential assessment of hepatic mitochondrial function in sheep using isotope-ratio mass spectrometry. INTERNATIONAL JOURNAL OF MASS SPECTROMETRY, 442, 102-108. 10.1016/j.ijms.2019.05.011
Other University of Auckland co-authors: Russell Snell
- Patassini, S., Begley, P., Xu, J., Church, S. J., Kureishy, N., Reid, S. J., ... Unwin, R. D. (2019). Cerebral Vitamin B5 (D-Pantothenic Acid) Deficiency as a Potential Cause of Metabolic Perturbation and Neurodegeneration in Huntington's Disease. Metabolites, 9 (6).10.3390/metabo9060113
Other University of Auckland co-authors: Suzanne Reid, Henry Waldvogel, Russell Snell
- Govindpani, K., McNamara, L. G., Smith, N. R., Vinnakota, C., Waldvogel, H. J., Faull, R. L., & Kwakowsky, A. (2019). Vascular Dysfunction in Alzheimer's Disease: A Prelude to the Pathological Process or a Consequence of It?. Journal of clinical medicine, 8 (5).10.3390/jcm8050651
Other University of Auckland co-authors: Henry Waldvogel, Andrea Kwakowsky, Karan Govindpani, Chitra Vinnakota
- Waldvogel, H. J., Biggins, F. M., Singh, A., Arasaratnam, C. J., & Faull, R. L. M. (2019). Variable colocalisation of GABAA receptor subunits and glycine receptors on neurons in the human hypoglossal nucleus. Journal of chemical neuroanatomy, 97, 99-111. 10.1016/j.jchemneu.2019.02.005
Other University of Auckland co-authors: Henry Waldvogel
- Murray, S. J., Black, B. L., Reid, S. J., Rudiger, S. R., Simon Bawden, C., Snell, R. G., ... Faull, R. L. M. (2019). Chemical neuroanatomy of the substantia nigra in the ovine brain. Journal of chemical neuroanatomy, 97, 43-56. 10.1016/j.jchemneu.2019.01.007
Other University of Auckland co-authors: Suzanne Reid, Russell Snell, Henry Waldvogel
- Singh-Bains, M. K., Mehrabi, N. F., Sehji, T., Austria, M. D. R., Tan, A. Y. S., Tippett, L. J., ... Faull, R. L. M. (2019). Cerebellar degeneration correlates with motor symptoms in Huntington disease. Annals of neurology, 85 (3), 396-405. 10.1002/ana.25413
Other University of Auckland co-authors: Malvindar Singh-Bains, Nasim Mehrabi, Micah Daniel Austria, Lynette Tippett, Henry Waldvogel, Adelie Tan
- Xu, J., Patassini, S., Rustogi, N., Riba-Garcia, I., Hale, B. D., Phillips, A. M., ... Stevens, A. (2019). Regional protein expression in human Alzheimer's brain correlates with disease severity. COMMUNICATIONS BIOLOGY, 210.1038/s42003-018-0254-9
Other University of Auckland co-authors: Henry Waldvogel
- Merienne, N., Meunier, C., Schneider, A., Seguin, J., Nair, S. S., Rocher, A. B., ... Pellerin, L. (2019). Cell-Type-Specific Gene Expression Profiling in Adult Mouse Brain Reveals Normal and Disease-State Signatures. Cell reports, 26 (9), 2477-2493.e9. 10.1016/j.celrep.2019.02.003