Abstract: Methods and compositions are disclosed to treat neuropsychiatric disorders post-traumatic stress disorder (PTSD). In particular, described herein are angiotensin receptor blockers (ARBs), and in particular the combination of one or more ARB (such as telmisartan) and an agent that enhances the delivery of the ARB across the blood-brain barrier (such as minocycline). PTSD may be treated using a combination of telmisartan and minocycline at levels of each that are, by themselves, infective to treat PTSD. Also described herein are methods for treating PTSD by first identifying patents for whom the use of an ARB treatment would be effective, by determining that patient has a dysfunction in their angiotensin converting enzyme and/or other genes in the autonomic arousal axis.

Abstract: Described herein are assays, kits and methods for treating mood disorders by testing for one or more polymorphisms in a specific group of genes and for analyzing the results of polymorphism testing; the genes included may converge in one or more signaling pathways, and may be epigenetic. The genes are included based on the relationships of the proteins encoded by the genes in the context of particular signaling pathways and provide a diagnostically relevant nexus. Also described herein are methods of presenting the data collected by the screen, including methods of delivering interpretive comments and/or treatment guidance based on the results of the genetic screening either individually or based on the genetic composition of particular clusters of genes which may be related to each other. Importantly, drugs which modulate these genetic disturbances are described for targeted therapeutic use based upon companion diagnostic method.

Abstract: Methods and reports for presenting genetic information that is patient-specific and relevant to treatment of neuropsychiatric disorders, including treatment resistant psychiatric disorders, to aid in patient treatment in a phenotype, genotype or biomarker-specific manner. The methods and reports examine biomarkers for dysfunction of three axes relevant to treating neuropsychiatric disorders and provide interpretive comments to aid in treatment. Combining biomarker information from each of the three axes (the autonomic arousal axis, the emotional valence, attention, reward and executive brain function axis, and the long-term potentiation and long-term depression (LTP-LTD) function axis) provides an unexpectedly comprehensive and effective means for directing treatment of neuropsychiatric disorders, including particularly treatment resistant disorders (TRD).

Abstract: Methods and compositions are disclosed to treat neuropsychiatric disorders based upon a new framework of diagnosis. Axis I biomarkers include genes related to prefrontal dopamine synthesis and/or dopamine degradation. Axis II includes genes related to re uptake of dopamine, norepinephrine and serotonin and autonomic hyperactivity. Axis III includes genes relates to impairments in inflammatory pathways, glutamate neurotransmission and/or neurotrophic factors. Axis IV includes genes related to glutamate reuptake and predisposition to addictive behavior, and obsessive compulsions.

Abstract: Methods and reports for presenting genetic information that is patient-specific and relevant to treatment of neuropsychiatric disorders, including treatment resistant psychiatric disorders, to aid in patient treatment in a phenotype, genotype or biomarker-specific manner. The methods and reports examine biomarkers for dysfunction of three axes relevant to treating neuropsychiatric disorders and provide interpretive comments to aid in treatment. Combining biomarker information from each of the three axes (the autonomic arousal axis, the emotional valence, attention, reward and executive brain function axis, and the long-term potentiation and long-term depression (LTP-LTD) function axis) provides an unexpectedly comprehensive and effective means for directing treatment of neuropsychiatric disorders, including particularly treatment resistant disorders (TRD).

Abstract: Methods and reports for presenting genetic information that is patient-specific and relevant to treatment of neuropsychiatric disorders, including treatment resistant psychiatric disorders, to aid in patient treatment in a phenotype, genotype or biomarker-specific manner. The methods and reports examine biomarkers for dysfunction of three axes relevant to treating neuropsychiatric disorders and provide interpretive comments to aid in treatment. Combining biomarker information from each of the three axes (the autonomic arousal axis, the emotional valence, attention, reward and executive brain function axis, and the long-term potentiation and long-term depression (LTP-LTD) function axis) provides an unexpectedly comprehensive and effective means for directing treatment of neuropsychiatric disorders, including particularly treatment resistant disorders (TRD).

Abstract: Described herein are compounds (including medical foods, pharmaceutical compositions, methods of compounding them), methods and systems for the diagnosis and/or treatment of prodromal schizophrenia. For example, described herein are methods of treating a developmentally-based neuropsychiatric disorder (schizophrenia) that includes first determining if a subject is at risk for such a disorder by examining phenotypical, serological immune markers and genotypical biomarkers. The biomarkers may be used to tailor the dose to be delivered by the medial food or pharmaceutical composition. Also described are compounds for treating prodromal (rather than full-blown) schizophrenia.

Abstract: Methods and reports for presenting genetic information that is patient-specific and relevant to treatment of neuropsychiatric disorders, including treatment resistant psychiatric disorders, to aid in patient treatment in a phenotype, genotype or biomarker-specific manner. The methods and reports examine biomarkers for dysfunction of three axes relevant to treating neuropsychiatric disorders and provide interpretive comments to aid in treatment. Combining biomarker information from each of the three axes (the autonomic arousal axis, the emotional valence, attention, reward and executive brain function axis, and the long-term potentiation and long-term depression (LTP-LTD) function axis) provides an unexpectedly comprehensive and effective means for directing treatment of neuropsychiatric disorders, including particularly treatment resistant disorders (TRD).

Abstract: Methods and reports for presenting genetic information that is patient-specific and relevant to treatment of neuropsychiatric disorders, including treatment resistant depression. The methods and reports described include genotype information for each of six specific genetic loci and allow patient-specific therapy for the effective treatment of treatment resistant disorders (TRD).

Abstract: Describe herein are medical foods, pharmaceutical compositions, methods of compounding them, and method of using them for the treatment of developmentally-based neuropsychiatric disorders including particularly autism, ADHD, and persistent developmental disorders. The medical foods and pharmaceutical compositions typically include a methylglycine compound or precursor compound and an acetylcysteine compound or precursor compound. These methylglycine and acetylcysteine compounds may be prepared for sustained release or delivery. In some variations, a method of treating a developmentally-based neuropsychiatric disorder includes first determining if a patient is at risk for such a disorder by examining either or both phenotypical and genotypical biomarkers. The biomarkers may be used to tailor the dose to be delivered by the medial food or pharmaceutical composition.

Abstract: Methods, kits, screens, assays, treatments and treatment regimes for treating a patient at risk for or suffering from dementia, and particularly Alzheimer's dementia which are based upon identification of enhanced risk by genotyping APOE and APOJ. In particular, described herein are methods for the prophylactic treatment of dementia based upon results of said genotyping. The systems and methods herein described may be used both to detect and to target the primary genetically mediated pathways associated with amyloid burden. For example, a system for deciding treatment based on previously identified genetic polymorphisms (e.g., APOE4, polymorphism in APOJ) that affect amyloid clearance is described herein; such patients may respond to treatments that modulate glial based GLT-1 (e.g., Tianeptine) and/or enhance HSP expression/activity (e.g., GGA).

Abstract: Described herein are assays, kits and methods for treating mood disorders by testing for one or more polymorphisms in a specific group of genes and for analyzing the results of polymorphism testing; the genes included may converge in one or more signaling pathways, and may be epigenetic. The genes are included based on the relationships of the proteins encoded by the genes in the context of particular signaling pathways and provide a diagnostically relevant nexus. Also described herein are methods of presenting the data collected by the screen, including methods of delivering interpretive comments and/or treatment guidance based on the results of the genetic screening either individually or based on the genetic composition of particular clusters of genes which may be related to each other. Importantly, drugs which modulate these genetic disturbances are described for targeted therapeutic use based upon companion diagnostic method.

Abstract: Described herein are assays, kits and methods for treating depression, including the diagnosis and treatment of depression based on the determination of genetic predispositions towards inhibition or enhancement of Ca2+/calmodulin-dependent protein kinase II (CaMKII). For example, described herein are methods and kits (including assays) for determining if one or more gene in an excitatory or inhibitory pathway for modulating CaMKII activity or expression is likely to be inhibited or enhanced by an SNP. Also described are methods and kits (including assays) for prescribing treatment based on the identification of SNPs that may modulate CaMKII.