This project aims to chemically synthesise compounds that destabilise and deconstruct the β-amyloid oligomer molecular-environment that facilitates β-amyloid gain in neurotoxic function.
This project aims to chemically synthesise compounds that destabilise and deconstruct the β-amyloid oligomer molecular-environment that facilitates β-amyloid gain in neurotoxic function.
This project aims to chemically synthesise compounds that destabilise and deconstruct the β-amyloid oligomer molecular-environment that facilitates β-amyloid gain in neurotoxic function.
Project dates: This chemical-medicinal synthesis project commenced 2013 and is ongoing.
Grants and funding: ARC DP Grant submitted; miscellaneous research funds.
Every four seconds there is a new case of dementia in the world. There are 7.7 million new cases of dementia each year and the global cost of Alzheimer's Disease (AD) and dementia is estimated to be $604 billion. The alarmingly increasing incidence of AD worldwide is paralleled by the search for compounds with neuroprotective activity, a search that has intensified in recent years.
AD is a multifactorial disease, correlated with neuronal damage in different brain areas and is still incurable. Because of this, protection of neuronal cells by anti-amyloidogenic substances or the retardation of amyloid fibril formation is of high priority and an actively pursued therapeutic concept.
This project is driven by the efforts and enthusiasm of RMIT scientists and postgraduate students who realise there can be no health without mental health. It is their objective to synthesise green tea inspired compounds against AD as a cost effective and accessible therapy option.
Generation of scaffolds to prevent brain β-amyloid misfolding and aggregation.
Natural green tea product epigallocatechingallate [EGCG] inspired analogues/scaffolds can be produced from intermediates utilised in total synthesis that are not easily accessed from green tea biosynthesis.
Natural products such as EGCG target proteins with a high number of protein-protein functional interactions (high biological network connectivity) and that these protein targets have higher network connectivity than disease genes. This suggests that modified EGCG or novel small molecules will be required to discover drugs targeting the root causes of dementia disease in the future.
Acknowledgement of Country
RMIT University acknowledges the people of the Woi wurrung and Boon wurrung language groups of the eastern Kulin Nation on whose unceded lands we conduct the business of the University. RMIT University respectfully acknowledges their Ancestors and Elders, past and present. RMIT also acknowledges the Traditional Custodians and their Ancestors of the lands and waters across Australia where we conduct our business - Artwork 'Sentient' by Hollie Johnson, Gunaikurnai and Monero Ngarigo.
Acknowledgement of Country
RMIT University acknowledges the people of the Woi wurrung and Boon wurrung language groups of the eastern Kulin Nation on whose unceded lands we conduct the business of the University. RMIT University respectfully acknowledges their Ancestors and Elders, past and present. RMIT also acknowledges the Traditional Custodians and their Ancestors of the lands and waters across Australia where we conduct our business.