Gerhard Schratt received the FreeNovation Grant 2025 over 220.000 CHF from the Novartis Foundation. The CRISPR gene-editing technology will be used to block the access of inhibitory microRNAs to gene copies, thereby boosting the expression of the corresponding protein. This could represent a novel therapeutic strategy to restore normal protein expression in haploinsufficiencies, genetic disorders where one functional copy of a gene is not enough to compensate for the other non-functional copy.
In our new study published in the Proceedings of the National Academy of Science (PNAS), we describe a microRNA-based mechanism that coordinates the scaling of inhibitory and excitatory synapses during homeostatic plasticity, with possible implications for sleep regulation. Colameo et al., PNAS 2025 Apr 8;122(14):e2500880122. doi: 10.1073/pnas.2500880122.
Circular RNAs are a recently discovered class of non-coding RNAs and are highly expressed in mammalian neurons. In a new study published in Nature Communications, Kelly et al. identified a circular RNA which controls the formation of silent synapses, dormant neural connections that can be activated for memory formation. These findings increase our understanding of the molecular mechanisms underlying synaptic plasticity and memory.
Unipolar and bipolar depression are often misdiagnosed, hampering medical treatment. In a recent paper published in EMBO Reports, we describe a microRNA signature in human peripheral blood which distinguishes bipolar from unipolar depression patients. Studies in mice further revealed an important function of these microRNAs in the brain. Our results could pave the way towards the translation of microRNA biomarkers to clinical practice in psychiatry.
Gerhard Schratt received a grant over 93'900 CHF from the Dr. Wilhelm Hurka Stiftung for projects on Parkinson’s Disease and related Neurodegenerative Disorders. This project will explore the potential of antisense oligonucleotides targeting microRNAs to prevent synapse loss, mitochondrial dysfunction and cell death in a human neuron culture model of Parkinson’s Disease. This represents a first step towards the development of antisense oligonucleotide therapies for Parkinson’s Disease.