The Natoli Group

 

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Researcher's projects

1. MicroRNA as regulators of inflammation and the inflammasome

The most common cause of blindness in Australia is Age-Related Macular Degeneration (AMD), costing the Australian economy ~5 billion dollars annually and ~350 billion dollars globally. The study of miRNAs will provide a new avenue for drug discovery for diseases such as AMD, and have applications for other neurodegenerative diseases. MiRNA are small non-coding RNA molecules that post transcriptionally regulate gene expression and are considered the ‘master regulators’ of gene transcription. We are looking at using miRNA as therapeutics to reduce inflammation and inflammasome activation in retinal degenerations.

2. Molecular and epigenetic regulation by recruited and resident monocytes in retinal degeneration

Dysregulation of microglia/macrophages is a key pathogenic mechanism underlying many age-related neurodegenerative diseases, highlighting the importance of understanding how these cells respond to ageing and stress. We are deciphering the molecular profile of the resident microglia and recruited macrophages in the retina, to further understand their role in disease progression and to explore the possibility of reprogramming ageing cells to a quiescent state in order to preserve retinal function.

3. Novel therapeutics for reducing the progression of Age-Related Macular Degeneration

Current projections indicate that by 2030, 1.7 million people in Australia will suffer vision loss due to Age-Related Macular Degeneration (AMD), with a major contribution being the current lack of treatment options available for the more prevalent atrophic or ‘dry’ form of the disease. We are exploring a number of therapeutic options, including gene-based therapies, non-invasive therapeutics and novel compounds. We are actively engaging with commercial partners to help develop strategies to reduce inflammation and cell death in all forms of AMD.

4. The role of complement in retinal degeneration

Dysregulation of complement is strongly associated with Age-related Macular Degeneration (AMD). However, the events that lead to complement activation are poorly understood, and how complement causes photoreceptor cell loss is not known. We have developed a unique mouse model of photo-oxidative retinal damage, which mimics facets of the more prevalent form of AMD, ‘dry’ AMD, for which there are no current treatments. Using this model and human tissue we have found that retinal microglia are responsible for depositing complement, and are exploring if inhibition of this pathway is protective against progressive retinal cell death.

Available student projects

We are always looking out for fantastic students to be involved with our group. Projects will focus on aspects of the current projects indicated above including:

1. MicroRNA as regulators of inflammation and the inflammasome

2. Molecular and epigenetic regulation by recruited and resident monocytes in retinal degeneration

3. Novel therapeutics for reducing the progression of Age-Related Macular Degeneration

4. The role of complement in retinal degeneration

We enjoy meeting and discussing projects with potential students to tailor projects to the individual. If you are interested in being involved in our research please don't hesitate to contact me at any time.

Current student projects

1. MicroRNA as regulators of inflammation and the inflammasome

-Joshua Chu-Tan and Riemke Aggio-Bruce

2. Molecular and epigenetic regulation by recruited and resident monocytes in retinal degeneration

- Riemke Aggio-Bruce

3. Novel therapeutics for reducing the progression of Age-Related Macular Degeneration

- Nilisha Fernando and Yen-Zhen Lu

4. The role of complement in retinal degeneration

- Nilisha Fernando,Helen Jiao and Tanja Racic

Past student projects

The role of complement in retinal degeneration

- Dr Matt Rutar (University of Melbourne)

Members

Leader

Publications

Selected Publications

Updated:  24 October 2017/Responsible Officer:  Director, JCSMR/Page Contact:  Web Manager