Stem cell therapies for brain disorders
May 2015 "Red Lab Coat Day". L-R standing: Dr Steven Petratos (group leader). Dr Beatriz Garcillan (Research Fellow associated with Immunology BAFF lab), Mrs Maha Bakhuraysah (PhD student), Mr Jae Young Lee (PhD student), Ms Kylie Magee (Laboratory Manager), Dr Christopher Siatskas (Research Fellow), Mrs Pei Mun Aui (Research Assistant). L-R seated: Mrs Amani Alrehaili (PhD student), Miss Melissa Biemond (Honours student), Miss Erica Kim (MBiomedSc student)
i. Multiple Sclerosis
Multiple sclerosis (MS) is commonly induced by the specific destruction of the protective sheath of nerve fibres, known as myelin, by immune cells, which mistakenly attack this structure. However, it has been shown that MS does not only consist of this disease pattern but is a multifactorial disease with continual destruction of the nerve fibres even without large numbers of immune cells invading the brain and the spinal cord. Importantly, the molecules which may contribute or initiate such damage in MS are becoming known and by targeting these molecules during MS it may be possible to limit the destruction which occurs to nerve fibres in the brain and spinal cord, promoting a better clinical outcome for individuals suffering with MS. We intend to look at how damage occurs in nerve fibres with progressive clinical symptoms in the experimental animal model of MS and attempt to block the molecules that propagate the nerve fibre degeneration using novel strategies to deliver agents to the brain and spinal cord.
Alzheimer's disease (AD) is one of the most prevalent severe neurological disorders afflicting our aged population. Cognitive decline, a major symptom exhibited by AD patients, is associated with neuritic dystrophy, a degenerative growth state of neurites. The molecular mechanisms governing neuritic dystrophy remain unclear. Mounting evidence indicates that the AD-causative agent, β-amyloid protein (Aβ), induces neuritic dystrophy. Our group is investigating potential molecular pathways, which may be modulated subsequent to Aβ-dependent interactions with the neuronal membrane as a consequence of increasing amyloid burden in the brain.
Projects and Opportunities
None currently available. For other current student research projects please visit the CCS 2015 Honours project index.
See more publications at Dr Steven Petratos's ROPES profile
Alsanie, W.F., Niclis, J.C., Petratos, S., 2013, Human embryonic stem cell-derived oligodendrocytes: protocols and perspectives, Stem Cells and Development [P], vol 22, issue 18, Mary Ann Liebert Inc Publishers, USA, pp. 2459-2476.
Lee, J.Y., Petratos, S., 2013, Multiple sclerosis: does Nogo play a role?, The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry [P], vol 19, issue 4, Sage Publications Inc, USA, pp. 394-408.
Litwak, S.A., Payne, N.L., Campanale, N.V., Ozturk, E., Lee, J.Y., Petratos, S., Siatskas, C., Bakhuraysah, M., Bernard, C.C.A., 2013, Nogo-receptor 1 deficiency has no influence on immune cell repertoire or function during experimental autoimmune encephalomyelitis, PLoS ONE [P], vol 8, issue 12 (Art. No.: 0082101), Public Library of Science, United States, pp. 1-13.
Petratos, S., Lee, J.Y., 2013, Stop CRMPing my style: A new competitive model of CRMP oligomerization, Journal Of Neurochemistry [P], vol 125, issue 6, Wiley-Blackwell Publishing Ltd, United Kingdom, pp. 800-802.
Mokhtar, S., Bakhuraysah, M., Cram, D.S., Petratos, S., 2013, The beta-amyloid protein of alzheimer's disease: communication breakdown by modifying the neuronal cytoskeleton, International Journal of Alzheimer's Disease [E], vol 2013, issue Art. No.: 910502, Hindawi Publishing Corporation, United States, pp. 1-15.