Abstract: Described is a method for treating a social memory deficit in a subject with a neuropsychiatric disease is treated by administering a peptide encoded by 2510002D24Rik or Atp23 genes, a vector expressing such peptide, or an agent capable of increasing the level or activity of such peptide. The method may be used to treat schizophrenia or autism. The peptide, vector or agent can be administered directly to the hippocampus, such as by transcranial surgical injection.

Abstract: The invention is directed to methods and compositions for treating a disease associated with ventricular enlargement such as 22q11 deletion syndrome (22q11 DS) and schizophrenia (SCZ) by replenishment of decreased levels of miR-382-3p and/or miR-674-3p or inhibition of dopamine receptor Drd1 in ependymal cells.

Abstract: The invention is directed to a method for improving learning and/or memory (e.g., auditory, visual, somatosensory or motor) in adults and children of an age which is beyond the early critical period for learning, said method comprising inhibiting (i) ecto-5?-nucleotidase (Nt5e, aka CD73) or (ii) A1 adenosine receptor (A1R, aka Adora1) expression or function in the brain. The invention is also directed to a method for treating learning and memory defects and neurological diseases associated with an abnormal auditory, visual, or somatosensory perception by inhibiting Nt5e or A1R expression or function in the brain.

Abstract: The invention is directed to a method for treating the 22q11 deletion syndrome (22q11 DS) and schizophrenia (SCZ) by replenishment of decreased levels of miR-338-3p in thalamic neurons.

Abstract: The invention is directed to a method for treating the 22q11 deletion syndrome (22q11 DS) and schizophrenia (SCZ) by replenishment of decreased levels of miR-338-3p in thalamic neurons.

Abstract: The present invention embraces methods for the diagnosis and treatment of learning or mental disorders such as schizophrenia using miR-25, miR-98, or miR-185.

Abstract: The invention is directed to a method for treating the 22q11 deletion syndrome (22q11 DS) and schizophrenia (SCZ) by replenishment of decreased levels of miR-338-3p in thalamic neurons.

Abstract: The invention is directed to a method for improving learning and/or memory (e.g., auditory, visual, somatosensory or motor) in adults and children of an age which is beyond the early critical period for learning, said method comprising inhibiting (i) ecto-5?-nucleotidase (Nt5e, aka CD73) or (ii) A1 adenosine receptor (A1R, aka Adora1) expression or function in the brain. The invention is also directed to a method for treating learning and memory defects and neurological diseases associated with an abnormal auditory, visual, or somatosensory perception by inhibiting Nt5e or A1R expression or function in the brain.

Abstract: The present invention embraces methods for the diagnosis and treatment of learning or mental disorders such as schizophrenia using miR-25, miR-98, or miR-185.

Abstract: The present invention embraces methods for the diagnosis and treatment of learning or mental disorders such as schizophrenia using miR-25, miR-98, or miR-185.

Abstract: The present invention embraces methods for the diagnosis and treatment of learning or mental disorders such as schizophrenia using miR-25, miR-98, or miR-185.

Abstract: The present invention embraces methods for the diagnosis and treatment of learning or mental disorders, as well as the identification of agents useful in the treatment of such disorders based upon the identified involvement of Sarcoplasmic Ca2+-ATPase type 2 Protein in synaptic plasticity and neurotransmitter release in 22q11 deletion/DiGeorge Syndrome.

Abstract: The present invention embraces methods for the diagnosis and treatment of learning or mental disorders, as well as the identification of agents useful in the treatment of such disorders based upon the identified involvement of Sarcoplasmic Ca2+-ATPase type 2 Protein in synaptic plasticity and neurotransmitter release in 22q11 deletion/DiGeorge Syndrome.