Uncovering How Gene Regulators Protect Neurons Against Alzheimer's
Principal Investigator
Raffaella Nativio, PhD
Imperial College of Science, Technology and Medicine
London, United Kingdom
About the Research Project
Program
Award Type
Standard
Award Amount
$299,943
Active Dates
July 01, 2024 - June 30, 2027
Grant ID
A2024018S
Goals
This study will focus on understanding how epigenetic factors, especially transcriptional repressors, influence gene expression in neurons and contribute to Alzheimer’s disease. The research aims to identify how these transcriptional repressors protect neurons from Alzheimer’s-related stress, potentially leading to new treatments for enhancing brain resilience against Alzheimer’s.
Summary
This study will focus on understanding how epigenetic factors, especially transcriptional repressors, influence gene expression in neurons and contribute to Alzheimer’s disease. The research aims to identify how these transcriptional repressors protect neurons from Alzheimer’s-related stress, potentially leading to new treatments for enhancing brain resilience against Alzheimer’s.
Unique and Innovative
Our study will be the first to systematically and unbiasedly define the landscape of Transcriptional Repressors (TRs) in neurons affected by Alzheimer’s disease (AD) using advanced epigenomic methods, including 3D genome conformation. This study will not only identify key epigenetic regulators but also underscores the potential for developing epigenetic drugs to enhance neuronal resilience. Given the reversible nature of epigenetic modifications, the identification of TRs could pave the way for new therapeutic strategies that could alter the progression of AD.
Foreseeable Benefits
Upon completing the study, we expect to significantly advance the understanding of Alzheimer’s disease from an epigenetic perspective. By identifying specific transcriptional repressors and their pathways, our research may lead to targeted therapies that boost neuronal resilience and potentially delay or prevent Alzheimer’s. This work could open new therapeutic avenues for AD and provide valuable insights into cell-specific epigenetic mechanisms in neurodegenerative research.
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