The Homer Hack Research Grant Scheme
Announcing the 2024 successful research grantees
The Homer Hack is excited to announce the successful recipients of the 2024 competitive Research Round. The Scientific Advisory Committee undertook a comprehensive process to select two outstanding researchers who will assist us in increasing our robust research program.
Dr Jose Agustin Cota Coronado is the Leader of the human stem cell biology laboratory at the Translational Molecular Psychiatry (TMP) Group at Monash University. He will be conducting a project titled “Impact of in-utero exposure to infection on HOMER1 isoforms and the risk of autism”
This particular project will identify the functional consequences of cytokine exposure related to COVID- 19 infection in human neuronal cultures on distinct HOMER1 isoforms and neuronal and synaptic development. This will unveil whether HOMER1 is a central target after infection for biomarker or therapeutic development. The benefit of this project is that it will generate world-first knowledge on the neurodevelopmental consequences of HOMER1 dysregulation, the impact of which stands to benefit not only SARS-CoV-2 exposed infants but the millions of infants globally exposed to a range of infections or insults that alter HOMER1 expression. These planned experiments may enable the identification of HOMER1 and/or other related signalling molecules as biomarkers of adverse neurodevelopment, an outcome that would have a profound impact by enabling targeted early intervention of children at risk of neurodevelopmental disorders such as ASD
The second grantee, Dr.Muhammad Shahid Javaid PhD from the Department of Neuroscience, School of Translational Medicine, Monash University, The Alfred Centre will be completing a project titled “Patient-Specific Disease Models for Investigating Homer1 Gene Mutations: Implications for Neurological and Cardiovascular Conditions”.
The aim of this project is to gain a deeper understanding of and develop effective treatments for neurological and cardiovascular disorders linked to abnormal calcium signalling due to mutations in the Homer1 gene. To accurately reflect the pathophysiology of affected individuals, the project stresses the importance of using patient-specific neuronal disease models, with emphasis on astrocytes, another cell type of central nervous system, which is critical for synaptic plasticity and calcium signalling. Additionally, given that Homer1 has a potential role in modulating calcium signalling in the heart, it is crucial to investigate its impact on cardiac function and pathology. While Homer1 proteins are primarily known for their expression and function in the central nervous system, particularly in neurons and glial cells, research has indicated that certain members of the Homer family, including Homer1, may be expressed in cardiac tissue, although at lower levels compared to the central nervous system. This particular project will complement the 2023 research project "drug screening using Homer1 patient’s iPSCs-derived neurons for clinical trials of precision medicine."
We are thrilled to support these outstanding researchers and look forward to sharing their progress with you all in due course.
Our research program depends entirely on philanthropic collaboration and fundraising activities throughout the year. We extend a heartfelt thankyou to everyone who has been able to support and contribute in these ways.
Successful 2023 Grant Recipients
The Homer Hack announces two successful grant recipients as part of the 2023 Homer Hack Small Research Grant Scheme. Congratulations to Dr. Muhammad Javaid from the Department of Neuroscience Monash University Alfred Centre and Associate Professor Wah Chin Boon, BSc (Hons), from the The Florey Institute of Neuroscience and Mental Health as the inaugral successful grantees.
Dr Mahammad Javaid will be exploring "drug screening using Homer1 patient’s iPSCs-derived neurons for clinical trials of precision medicine."
The main objective of this project will be to develop effective treatments for neurological conditions linked to the abnormal function of HOMER1. The discovery of new effective medicines requires pathophysiological-matched disease models, ideally those based on affected individuals. Patient-specific stem cell-derived in vitro neuronal models can adequately recapitulate the pathophysiological and pharmaco-responsive properties of the ‘Homer-brain’. The drugs that are found to restore normal function in these models will also be used as targeted precision medicines to treat the neuronal complications associated with Homer variants. The proposed outcomes will reveal the drug targets that can not only be targeted to restore normal neuronal function in Homer1 patients but may also be used to treat other neurological diseases involving anomalous calcium signalling and mutant scaffolding proteins. Furthermore, an FDA-approved drug will be identified to treat Homer1 complications in the index patient for “n of 1” clinical trial.
Associate Professor Wah Chin Boon will be exploring the "Inhibitory effects of prenatal exposure of plastics on Homer genes and a potential therapeutic reversal".
This project aims to investigate whether (1) Homer 1 gene expression is reduced by prenatal DEHP exposure; (2) Homer 1 gene is hypermethylated by prenatal DEHP exposure; and (3) Homer 1 gene expression can be restored by 10HDA treatment, using a mouse model. It will explore the possible epigenetic effects of this exposure refering to long-term modifications of gene expression without altering the basic structure of DNA or DNA sequences.
It has been proposed that neurodevelopmental disorders (including autism spectrum disorder) caused by man- made chemicals operating on key genes have created a silent modern pandemic. Epidemiological data indicates likely prenatal epigenetic programming of neurodevelopmental genes such as Homer 1 genes and other scaffolding genes that a prospective association between prenatal phthalate exposure and adverse neurodevelopment may exist. This project will increase knowledge on HOMER gene function and related therapeutic approaches down- regulated HOMER gene function.