Provided herein are methods for preventing or treating post-traumatic stress disorder (PTSD) in a subject, the methods including: administering an agent which inhibits formation of a glucocorticoid receptor (GR)-FK506 Binding Protein 51 (FKBP51) complex (GR-FKBP51 complex), or which disrupts already formed GR-FKBP51 complex, to the subject; thereby reducing a level of GR-FKBP51 complex in the subject and preventing or treating the PTSD. Also provided are methods for diagnosing a subject as having, or being at risk of developing, a PTSD, the methods including steps of: measuring a level of a GR-FKBP51 complex in the subject; comparing the measured level to a reference level of a non-PTSD condition; and identifying the subject as having, or being at risk of developing, PTSD where the measured level is elevated relative to the reference level. Agents, compositions, and/or kits for the diagnosis and/or treatment of PTSD are also described.

Trigeminal nerves are stimulated based upon pulse counting and chronobiology. A cutaneous electrode assembly is applied to the forehead to stimulate the ophthalmic nerves. A method may include determining a number of pulses to be administered to a patient based upon the disorder being treated, and pulsing current through an electrode assembly to stimulate the patient's supraorbital and supratrochlear nerves with the determined number of pulses. Another method may include determining a pulse repetition frequency for pulses to be administered to a patient based upon the disorder being treated, and pulsing current through an electrode assembly to stimulate the patient's supraorbital and supratrochlear nerves at the pulse repetition frequency.

Provided herein are methods for diagnosing a psychotic disorder, such as schizophrenia, schizoaffective disorder or psychosis, predicated on a determination of a methylation phenotype of the subject based in part on the identity of a specific polymorphism in the MTHFR gene and the analysis of a suite of biomarkers and other functional measures and indices. Also provided herein are methods for predicting prognosis and functional outcomes for subjects having a psychotic disorder, and for treating subjects having a psychotic disorder.

A method of measuring and identifying LSD and its major metabolite O-H-LSD, by obtaining a sample from an individual, and measuring, identifying, and quantifying LSD and O-H-LSD in the sample by performing a LC-MS/MS analysis. A method of treating and monitoring individuals taking LSD, by administering a microdose of LSD, a prodrug of LSD, or an analog of LSD to the individual, monitoring the individual by obtaining a sample from an individual and measuring and identifying the analytes in the sample by performing a LC-MS/MS analysis, and adjusting the microdose based on the amount of LSD quantified in the LC-MS/MS analysis. A method of adjusting dosing of LSD, by administering a microdose of LSD, a prodrug of LSD, or an analog of LSD to the individual, and adjusting the microdose based on blood concentration analytics.

The present disclosure relates to exosomal complement mediators, cytokines, and mitochondrial electron transport biomarkers and diagnostic and prognostic methods for depression, psychosis and schizophrenia. The disclosure also provides compositions for detecting exosomal complement mediators, cytokines, and mitochondrial electron transport biomarkers in biological samples as well as compositions and methods useful for treating depression, psychosis and schizophrenia.

A method of dosing and treating patients with a psychedelic, by administering a psychedelic at a dose of a microdose, minidose, psychedelic dose, good effect dose, ego-dissolution dose, or cardiovascular safe dose, and producing maximum positive subjective acute effects that are known to be associated with more positive long-term outcomes and minimizing negative acute effects. A method of determining a dose of a psychedelic for an individual, by administering a dose of a psychedelic to the individual of a microdose, minidose, psychedelic dose, good effect dose, ego-dissolution dose, or cardiovascular safe dose, determining positive acute effects and negative acute effects in the individual, and adjusting the dose to provide more positive acute effects than negative acute effects in the individual. Methods of treating psychiatric conditions or providing therapy. A method of defining therapeutic doses of a psychedelic in clinical trials. A method of monitoring individuals for depression after treatment with LSD.

The present invention relates to a method for preventing or treating pathological conditions associated with intense stress such as Post-Traumatic Stress Disorder (PTSD) by targeting the endogenous PAI-1 (Type 1 Plasminogen Activator Inhibitor). In the present invention, inventors demonstrate that there is a shift in the balance between the expression of tPA and PAI-1 proteins in a hippocampal region of a preclinical model of Post-Traumatic Stress (PTSD), is responsible for the transition between moderate stress which increases memory and facilitates adaptation and intense stress intense stress which induce pathological memories. In conditions of moderate stress, glucocorticoid hormones (GC) increase the expression of the tPA protein in the hippocampal brain region which by triggering the Erk1/2.sup.MAPK cascade strengthens memory. When stress is particularly intense, very high levels of GC then increase the production of PAI-1 protein, which by blocking the activity of tPA induces PTSD-like memories. Accordingly, inhibition of PAI-1 activity represent a new therapeutic approach to this debilitating condition and PAI-1 body fluid level in patient after trauma could be a predictive biomarker of the subsequent appearance of PTSD.

The present application relates to psilocin derivatives of Formula (1), to processes for their preparation, to compositions comprising them and to their use in activation of a serotonin receptor in a cell, as well as to treating diseases, disorders or conditions by activation of a serotonin receptor in a cell.

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Biomarkers for assessing the efficacy of prophylactic treatments of stress-induced affective disorders are provided.

Disclosed are means and methods of identifying risk of suicide and/or suicidal ideation by assessment of immunologically related cytokines and cells. In one embodiment, a score, termed the “Campbell Score” is devised based on assessment of serum cytokines, ability of immune cells to make cytokines when stimulated ex vivo, and ability of immune cells to produce neurotransmitters when stimulated ex-vivo. In on embodiment the concentration of interleukin-6 is utilized as a means of assessing suicidal propensity along, and/or in combination with metabolites of the enzyme indolamine 2,3 deoxygenase.