Abstract: Methods and compositions are provided for reducing the effects of amyloid beta (A?) oligomers on a cell. Aspects of the methods generally include providing an agent that prevents A? oligomer activation of PirB/LILRB2 protein on cells, or providing a PirB/LILRB2 polypeptide composition to cells to prevent the A? oligomer activation of cells mediated by non-PirB/LILRB2 receptors. These methods find many uses, for example, in treating the decline in CNS function in individuals suffering from an A?-associated disease or disorder, and for screening candidate agents to identify new therapeutics that interfere with these toxic effects of A? in individuals having an A?-associated disease or disorder.

Abstract: Targeting and disrupting paired-immunoglobulin-like receptor B (PirB) function increases synaptic connectivity and plasticity even after the critical period, and can enable significant structural and functional recovery from amblyopia. Provided are compositions comprising PirB, or LILRB2 (leukocyte immunoglobulin-like receptor 2) polypeptides for disrupting PirB/LILRB2 signaling, and methods of using the compositions for treating disorders associated with reduced synaptic plasticity including amblyopia.

Abstract: Methods and compositions are provided for reducing the effects of amyloid beta (A?) oligomers on a cell. Aspects of the methods generally include providing an agent that prevents A? oligomer activation of PirB/LILRB2 protein on cells, or providing a PirB/LILRB2 polypeptide composition to cells to prevent the A? oligomer activation of cells mediated by non-PirB/LILRB2 receptors. These methods find many uses, for example, in treating the decline in CNS function in individuals suffering from an A?-associated disease or disorder, and for screening candidate agents to identify new therapeutics that interfere with these toxic effects of A? in individuals having an A?-associated disease or disorder.

Abstract: Class I major histocompatibility complex, is required in the activity-dependent refinement and plasticity of connections in the developing and adult central nervous system, demonstrating that molecules can perform critical roles in both systems. Similarities in the cellular signaling mechanisms of the immune and nervous systems provide for development of therapeutic and diagnostic agents in abnormal neuronal cellular function.

Abstract: Class I major histocompatibility complex, is required in the activity-dependent refinement and plasticity of connections in the developing and adult central nervous system, demonstrating that molecules can perform critical roles in both systems. Similarities in the cellular signaling mechanisms of the immune and nervous systems provide for development of therapeutic and diagnostic agents in abnormal neuronal cellular function.