Cytoplasmic HDAC4 recovers synaptic function in the 3×Tg mouse model of Alzheimer's disease.
Claudia ColussiGiuseppe AcetoCristian RipoliAlessia BertozziDomenica Donatella Li PumaElena PaccosiMarcello D'AscenzoClaudio GrassiPublished in: Neuropathology and applied neurobiology (2022)
These results highlight a new role of cytoplasmic HDAC4 in providing a structural and enzymatic regulation of postsynaptic proteins. Our findings suggest that controlling HDAC4 localisation may represent a promising strategy to rescue synaptic function in AD, potentially leading to memory improvement.