The present invention relates to expression constructs and viral and other vectors for the treatment and/or prevention of chronic pain.

Provided is a biomarker for bipolar disorder, comprising Syt7 gene and/or an expression product thereof. Also provided is use of the Syt7 gene and/or the expression product thereof in the preparing a medicament for treating bipolar disorder. By monitoring the Syt7 gene and/or the expression product thereof, medicaments for treating bipolar disorder can be screened, thus providing support for diagnosis and treatment targeting Syt7 molecules.

Provided is an obsessive-compulsive disorder animal model and a production method thereof, in which a neuronal circuit connecting the basolateral amygdala (BLA) and the dorsomedial striatum (DMS) is activated. In the present disclosure, it was confirmed that the BLA and DMS are connected to each other, and that when the BLA-DMS neuronal circuit is activated, there is a large increase in checking, repeating, cleaning, and collecting, which are compulsive behaviors representative of obsessive-compulsive disorder, and a decrease in cognitive flexibility. Therefore, animals in which the BLA-DMS neuronal circuit is activated may be useful as animal models for studying obsessive-compulsive disorder. In particular, the obsessive-compulsive disorder animal model can reproduce all of the compulsive behaviors and thus may become the first animal model to provide an understanding of the interactions between anxiety behaviors and compulsive behaviors, which existing animal models have not been able to provide.

It is shown that ventral hippocampal kindling results in functional reorganization of the ventral hippocampal excitatory circuits. Most pronounced is the connectivity to the medial prefrontal cortex, with increased volume of activation on fMRI and increased amplitude of activation on electrophysiology. There is evidence of increased anxiety following kindling Methods are provided for simultaneous LFP-fMRI to image single seizures Imaging the spatiotemporal dynamics of individual seizures enables characterization of propagation patterns of focal and secondary-generalized seizures, that provide for targeted intervention.

This invention relates to the finding that testis development related protein (TDRP; also termed Immunomoodulin or Imood herein) is a circulatory anxiogenic factor that modulates anxiety-like behaviour in mammalian models through the regulation of the immune system. Methods of treatment of mental disorders, such as anxiety, and TDRP antagonists for use in such methods are provided. Methods of diagnosing or monitoring a mental disorder in an individual by determining levels of TDRP in a sample and methods of screening for compounds that reduce levels of TDRP are provided.

This invention relates to polynucleotides comprising a nucleotide sequence encoding a PPT1 polypeptide or a fragment thereof, vectors (viral or non-viral vectors) comprising the same, and methods of using the same for delivery of the open reading frame to a cell or a subject and to treat infantile neuronal lipofuscinosis (infantile Batten disease). The polynucleotides comprise an optimized CLN1 open reading frame.

Provided herein are methods for enhancing survival of a neuron, for inhibiting degeneration of a neuron, and for inhibiting abnormal protein accumulation in a neuron, optionally a motor neuron, comprising, consisting or consisting essentially of increasing the level of cyclin F in the neuron regardless of the neuron's level or activity of endogenous cyclin F. Optionally the neuron is in a subject with a neurodegenerative condition or at risk of developing a neurodegenerative condition, typically a neurodegenerative condition associated with a neuronal TDP-43 proteinopathy.

The present discloses relates to a composition, a kit or a method using an eIF4E inhibitor for diagnosis or treatment of a condition associated with increased activity of eIF4E.

This disclosure relates to an animal model of human disease. More specifically, this disclosure relates to a rodent model of mood disorders such as unipolar depression and an anxiety disorder. Disclosed herein are genetically modified rodent animals that carry a humanized G protein-coupled receptor 156 (GPR156) gene that encodes a mutant human GPR156 protein comprising Asp at an amino acid position corresponding to position 533 in a full length wild type human GPR156 protein.

This disclosure relates to an animal model of human disease. More specifically, this disclosure relates to a rodent model of mood disorders such as unipolar depression and an anxiety disorder. Disclosed herein are genetically modified rodent animals that carry a humanized G protein-coupled receptor 156 (GPR156) gene that encodes a mutant human GPR156 protein comprising Asp at an amino acid position corresponding to position 533 in a full length wild type human GPR156 protein.