These actions are thought to be largely attributable to the dephosphorylation by synj1 of phosphoinositol 4,5-bisphosphate (PIP2) to inositol 4-monophosphate (PIP1).25 Synj1 expression is increased in the brains of humans and mouse ApoE4 carriers of mild cognitive impairment and early AD associated with reduced levels of PIP2 in tissue homogenates and synaptosomes, and the genetic reduction of synj1 rescued AD-related cognitive impairments in ApoE4 mice.23 Whether Synj1 could modulate recovery after SCI is not known. The gene discussed is APOE; the disease is Alzheimer disease.