ACVR1C and Alzheimer disease: Therefore, our ability to enable learning and enhance synaptic plasticity in aging and 5xFAD mice through Acvr1c wildtype over-expression also raises the possibility of a self-regulating mechanism where regulation downstream of ACVR1C (SMAD-dependent signaling) becomes impaired with age and AD and is maintained through self-directed aberrant epigenetic/SMAD repressor complex regulation which may repress Acvr1c expression.