Targeting MEF2A for the treatment of neurodegenerative disease
Dendritic remodeling may have application to neurodegenerative disease, neurodevelopment disorders, brain trauma, and psychiatric disorders. It is anticipated that MEF2A (myocyte enhancer factor 2A), mechanisms will also lead to new diagnostic tools for the study of synaptic development and function, spanning both CNS drug discovery and neurodevelopmental research.
Innovations and Advantages
Post-synaptic differentiation of dendrites is an essential step in synapse formation and is intrinsic to neural reprogramming following CNS trauma or neurodegenerative disease. Investigators from Harvard Medical School have discovered an important molecular switch of the transcription factor known as MEF2A, which is able to modulate dendritic plasticity in CNS granule neurons. Functional analysis has pinpointed this switch to lysine-403, where sumoylation enhances morphogenesis of dendritic claws, while acetylation inhibits it. Moreover, the decision for either sumoylation or acetylation is traced to the phosphorylation status of a neighboring serine residue. This highly specific mechanism of post-synaptic plasticity underscores promising opportunities for modulating MEF2A through a variety of small molecule drugs.
Intellectual Property Status: Patent(s) pending
For further information, please contact:
Michal Preminger, Director of Business Development
Reference Harvard Case #2627