A non-transitory computer-readable medium stores a program that, when executed, causes a computer to (i) cause a biomarker-measuring apparatus to measure concentrations of biomarkers, including a concentration of 3-hydroxybutyrate, in a blood sample collected from a subject to be tested, (ii) acquire the concentrations of the biomarkers measured by the biomarker-measuring apparatus, (iii) calculate a discriminant value based on the concentrations of the biomarkers, (iv) evaluate severity of depression of the subject or predict a symptom of depression of the subject based on the discriminant value, and (v) output results obtained from evaluating the severity of depression of the subject or from predicting the symptom of depression of the subject.

In light of a discovery that astroglial Kir4.1 in lateral habenula drives neuronal bursts in depression, the present disclosure provides a pharmaceutical agent and a method of use thereof for treating depression. The pharmaceutical agent can inhibit an activity of an astroglial potassium channel, and especially suppress expression or functionality of Kir4.1, in astrocytes in the lateral habenula of a subject so that bursting activity of neurons in the lateral habenula of the subject can be suppressed. The pharmaceutical agent can include a vector expressing a target nucleotide sequence in the astrocytes in the lateral habenula, whose expression is configured to suppress Kir4.1 expression by RNA interference, or to block Kir4.1 functionality by a dominant negative effect of a mutant Kir4.1 protein. The pharmaceutical agent can alternatively comprise a small molecule compound, or an active macromolecule such as an anti-Kir4.1 antibody, configured to directly inhibit the astroglial potassium channel activity.

The present invention provides combinations of biomarkers that can be used in the diagnosis and differentiation of bipolar disorder and schizophrenia. The present invention therefore provides methods of differentiating, diagnosing and treating bipolar disorder and schizophrenia, by examining relevant proteins and RNA in a patient sample.

A method treats patient with treatment resistant depression, adjunct to standard antidepressant treatment or as monotherapy. These patients will be identified by non-response to at least one pharmacological antidepressant treatment with a sufficient dose and over a sufficient period of time. Further, one embodiment of the method includes a procedure to identify patients who would benefit from a combination of standard antidepressants with the described compounds from the start of the treatment in order to maximize the likelihood of response. Another embodiment of the method combines the described compounds with forms of Magnesium salts in order to overcome longer term tolerability issues with the compounds. An important downstream mechanism of the described interventions is the property to reduce the production and or increase the absorption of cerebrospinal fluid to treat a variety of symptoms, including cognitive dysfunction, memory loss, apathy, sleep disturbances, pain disorders, and somatoform pain and headache.

The present disclosure relates to a method for diagnosing mood disorder such as mania, depression and mania mixed using a circadian rhythm. According to the diagnostic method of the present disclosure, the condition of mood disorder can be diagnosed objectively and clearly based on the advance or delay of the circadian rhythm. That is to say, hypomania, mania, depression, mixed mania, etc. may be determined quickly and adequately so that appropriate therapeutic intervention can be made. In addition, according to the diagnostic method of the present disclosure, schizophrenia which is frequently confused with severe depression or bipolar disorder can be distinguished clearly. In addition, the selection of a therapeutic drug can be benefited greatly through this.

Disclosed are a protein and a gene each of which is a factor involved in latent infection with a herpesvirus. An antibody against the factor was detected in approximately 50% of patients suffering from mental disorders, whereas the antibody was hardly detected in healthy persons. Further, a mouse having SITH-1 introduced therein developed a mental disorder such as a manic-depressive illness or depression-like disorder. Based on these findings, it is possible to provide a method for objectively determining a mental disorder and an animal model of a mental disorder.

A method for treating a subject with depression characterized by having an increased burst firing in neurons of a lateral habenula in the subject is provided. The method includes a step of administering to the subject a pharmaceutical composition capable of inhibiting the burst firing in the lateral habenula of the subject. The pharmaceutical composition includes one or more active pharmaceutical agents, which can suppress the burst firing in the lateral habenula of the subject and can include at least one of an N-methyl-D-aspartate receptor (NMDAR) inhibitor or a T-type calcium channel inhibitor. The pharmaceutical composition can be in a formulation allowing for local administration to the lateral habenula of the subject, or can be in a formulation configured for systemic administration to the subject. A method for testing a test substance for an antidepressive effect is also provided.

The application of PDCD4 as a drug treatment target for anti-depression and/or anti-anxiety disorders has been proved by experimental research that the increase of PDCD4 is an important factor leading to depression in the process of stress; PDCD4 as a target to inhibit its expression or function can play a good antidepressant role, and has no effect on normal physiological state. Therefore, PDCD4 can be used as a target in the preparation and screening of antidepressant and/or anxiolytic drugs, which has a broad application prospect.

The present invention relates to the use of the editing profile of PDE8A pre-mRNA as a specific bio marker of ADARs activities in evolved primate, particularly in Human tissues. The present invention also relates to an in vitro method for predicting in Human an alteration of the mechanism of the ADARs catalysed pre-mRNA editing of target genes, by analysing the PDE8A pre-mRNA editing profile in a peripheral tissue sample containing cells expressing said PDE8A pre-mRNA, such as blood sample. The present invention is also directed to an in vitro method for the screening of potential therapeutic compound and to predict and assess therapeutic efficacy and/or efficiency or to diagnose potential severe brain or peripheral drug side effects implementing said PDE8A pre-mRNA editing profile as specific biomarker. The present invention is further directed to a method for determining the PDE8A pre-mRNA editing profile in Human, particularly by capillary electrophoresis single-strand conformation polymorphism (CE-SSCP) method after amplification by a nested PCR. Finally the invention relates to particular nucleic acid primers implemented in said nested PCR and kit comprising such sets of primers and human cells capable of expressing PDE8A and ADARs.

Disclosed are a protein and a gene each of which is a factor involved in latent infection with a herpesvirus. An antibody against the factor was detected in approximately 50% of patients suffering from mental disorders, whereas the antibody was hardly detected in healthy persons. Further, a mouse having SITH-1 introduced therein developed a mental disorder such as a manic-depressive illness or depression-like disorder. Based on these findings, it is possible to provide a method for objectively determining a mental disorder and an animal model of a mental disorder.