Abstract: The present disclosure provides antibodies and antigen-binding fragments thereof that bind to human artemin. Methods for using anti-artemin antibodies and antigen-binding fragments are also provided.

Abstract: 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.

Abstract: Non-human animal genomes, non-human animal cells, and non-human animals comprising a humanized TRKB locus and methods of making and using such non-human animal genomes, non-human animal cells, and non-human animals are provided. Non-human animal cells or non-human animals comprising a humanized TRKB locus express a human TRKB protein or a chimeric transthyretin protein, fragments of which are from human TRKB. Methods are provided for using such non-human animals comprising a humanized TRKB locus to assess in vivo efficacy of human-TRKB-targeting reagents such as nuclease agents designed to target human TRKB.

Abstract: The present disclosure provides antibodies and antigen-binding fragments thereof that bind to human artemin. Methods for using anti-artemin antibodies and antigen-binding fragments are also provided.

Abstract: 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.

Abstract: Non-human animal genomes, non-human animal cells, and non-human animals comprising a humanized TRKB locus and methods of making and using such non-human animal genomes, non-human animal cells, and non-human animals are provided. Non-human animal cells or non-human animals comprising a humanized TRKB locus express a human TRKB protein or a chimeric transthyretin protein, fragments of which are from human TRKB. Methods are provided for using such non-human animals comprising a humanized TRKB locus to assess in vivo efficacy of human-TRKB-targeting reagents such as nuclease agents designed to target human TRKB.

Abstract: An animal model for motor neuron dysfunction in disease, e.g., amyotrophic lateral sclerosis (ALS), comprising a genetically modified non-human animal that comprises a genetically modified DR6 allele and exhibits normal phenotypes at birth and for a few weeks or months after birth. However, as the non-human animal ages, it develops motor neuron dysfunction that presents as one or more ALS-like symptoms, which may progress rapidly after onset. Methods of identifying candidate agents that may be used to prevent, delay or treat ALS are also provided.

Abstract: The present invention provides antibodies that bind specifically to TrkB and methods of using the same. According to certain embodiments, the antibodies of the invention are agonist antibodies that are neuroprotective, as shown by their effect on enhancing the survival of retinal ganglion cells in vitro. As such, these agonist antibodies may be used to treat diseases or disorders of the eye, such as, but not limited to glaucoma. In addition, other neuronal diseases or disorders may benefit from treatment with these agonist antibodies, including any disease or disorder characterized in part by neuronal damage. In certain embodiments, the invention includes antibodies that bind TrkB and mediate cell signaling. The antibodies of the invention may be fully human, non-naturally occurring antibodies.

Abstract: The present invention provides antibodies that bind to human GFR?3 and methods of using same. According to certain embodiments of the invention, the antibodies are fully human antibodies that bind to human GFR?3. The antibodies of the invention are useful for the treatment of diseases and disorders associated with one or more GFR?3 biological activities, including the treatment of acute or chronic pain conditions, or inflammatory conditions.

Abstract: 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.

Abstract: The present invention provides antibodies that bind to human GFR?3 and methods of using same. According to certain embodiments of the invention, the antibodies are fully human antibodies that bind to human GFR?3. The antibodies of the invention are useful for the treatment of diseases and disorders associated with one or more GFR?3 biological activities, including the treatment of acute or chronic pain conditions, or inflammatory conditions.

Abstract: An animal model for motor neuron dysfunction in disease, e.g., amyotrophic lateral sclerosis (ALS), comprising a genetically modified non-human animal that comprises a genetically modified DR6 allele and exhibits normal phenotypes at birth and for a few weeks or months after birth. However, as the non-human animal ages, it develops motor neuron dysfunction that presents as one or more ALS-like symptoms, which may progress rapidly after onset. Methods of identifying candidate agents that may be used to prevent, delay or treat ALS are also provided.

Abstract: The present invention provides antibodies that bind specifically to TrkB and methods of using the same. According to certain embodiments, the antibodies of the invention are agonist antibodies that are neuroprotective, as shown by their effect on enhancing the survival of retinal ganglion cells in vitro. As such, these agonist antibodies may be used to treat diseases or disorders of the eye, such as, but not limited to glaucoma. In addition, other neuronal diseases or disorders may benefit from treatment with these agonist antibodies, including any disease or disorder characterized in part by neuronal damage. In certain embodiments, the invention includes antibodies that bind TrkB and mediate cell signaling. The antibodies of the invention may be fully human, non-naturally occurring antibodies.

Abstract: An animal model for motor neuron dysfunction in disease, e.g., amyotrophic lateral sclerosis (ALS), comprising a genetically modified non-human animal that comprises a genetically modified DR6 allele and exhibits normal phenotypes at birth and for a few weeks or months after birth. However, as the non-human animal ages, it develops motor neuron dysfunction that presents as one or more ALS-like symptoms, which may progress rapidly after onset. Methods of identifying candidate agents that may be used to prevent, delay or treat ALS are also provided.

Abstract: The present invention provides antibodies that bind to human GFR?3 and methods of using same. According to certain embodiments of the invention, the antibodies are fully human antibodies that bind to human GFR?3. The antibodies of the invention are useful for the treatment of diseases and disorders associated with one or more GFR?3 biological activities, including the treatment of acute or chronic pain conditions, or inflammatory conditions.

Abstract: The present invention provides antibodies that bind to human GFR?3 and methods of using same. According to certain embodiments of the invention, the antibodies are fully human antibodies that bind to human GFR?3. The antibodies of the invention are useful for the treatment of diseases and disorders associated with one or more GFR?3 biological activities, including the treatment of acute or chronic pain conditions, or inflammatory conditions.

Abstract: The present invention provides antibodies that bind to human GFR?3 and methods of using same. According to certain embodiments of the invention, the antibodies are fully human antibodies that bind to human GFR?3. The antibodies of the invention are useful for the treatment of diseases and disorders associated with one or more GFR?3 biological activities, including the treatment of acute or chronic pain conditions, or inflammatory conditions.

Abstract: The present invention provides antibodies that bind to human GFR?3 and methods of using same. According to certain embodiments of the invention, the antibodies are fully human antibodies that bind to human GFR?3. The antibodies of the invention are useful for the treatment of diseases and disorders associated with one or more GFR?3 biological activities, including the treatment of acute or chronic pain conditions, or inflammatory conditions.

Abstract: An animal model for motor neuron dysfunction in disease, e.g., amyotrophic lateral sclerosis (ALS), comprising a genetically modified non-human animal that comprises a genetically modified DR6 allele and exhibits normal phenotypes at birth and for a few weeks or months after birth. However, as the non-human animal ages, it develops motor neuron dysfunction that presents as one or more ALS-like symptoms, which may progress rapidly after onset. Methods of identifying candidate agents that may be used to prevent, delay or treat ALS are also provided.

Abstract: The invention provides methods of treating, inhibiting, or ameliorating a disease characterized by aberrant deposition of beta amyloid in a subject in need thereof, comprising administering to a subject a therapeutic amount of an interleukin 1 (IL-1) antagonist, wherein the disease, or condition is treated, inhibited, or ameliorated, or wherein the onset or progression of the disease, or at least one symptom of the disease, is delayed. The IL-1 antagonist is an IL-1 trap, preferably comprising a sequence selected from the group consisting of SEQ ID NO: 2, 4, 6, 8, 10, 12, 14, 16, 18, 20, 22, 24, 26, and 28 and capable of binding and inhibiting IL-1. The therapeutic methods are useful for treating a human adult suffering from Alzheimer's Disease or cerebral amyloid angiopathy.