Targeting MEF-2 for the Treatment of Neurodegenerative Disease

Summary 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 Mef-2 (myocyte enhancer factor 2A), 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 Mef-2 through a variety of small molecule drugs.

Applications Dendritic remodeling may have application to neurodegenerative disease, neurodevelopment disorders, brain trauma, and psychiatric disorders. It is anticipated that Mef-2 mechanisms will also lead to new diagnostic tools for the study of synaptic development and function, spanning both CNS drug discovery and neurodevelopmental research. For Further Information Please Contact the Director of Business Development Michal Preminger Email: [email protected] Telephone: (617) 432-0920

Inventor(s): Bonni, Azad

Type of Offer: Licensing



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