The invention provides methods for treating, preventing or reversing retinal degeneration. The methods administering to the subject a vector that expresses a Cadherin-related family member 1 (CDHR1) polypeptide. The invention also provides gene therapy vectors that expresses a CDHR1 polypeptide, host cells that express the gene therapy vectors, and pharmaceutical compositions comprising the gene therapy vector.

In some aspects, the disclosure relates to compositions and methods useful for the diagnosis and treatment of diseases associated with a metabolic imbalance in a subject (e.g.,cancer). In some embodiments, the methods comprise administering to a subject an N-acetylaspartate (NAA)-depleting agent or an N-acetylaspartate (NAA)-increasing agent based upon the subject's metabolic profile.

A transgenic mouse has a genome that includes the entire gene region of human transforming growth factor beta-1 (human TGF1) located downstream of a mouse Podocin promoter such that expression of the human TGF1 is controlled by the mouse Podocin promoter. The human TGF1 contains 7 exons and 6 introns, the human TGF1 is expressed in a kidney of the mouse as non-active TGF1 and becomes active TGF1 extracellularly, and the transgenic mouse spontaneously develops renal fibrosis.

Provided are a non-human model animal of a retinal vascular disease that can favorably show symptoms similar to those of human retinal vascular diseases such as human diabetic retinopathy, and a method for producing the non-human model animal. In particular, provided are a non-human model animal that is suitable for establishing a method for treating, preventing, or diagnosing retinal edema, which causes highly impaired vision, and a method for producing the non-human model animal. A method for screening a drug for treating and preventing a retinal vascular disease, the method using a non-human model animal, is provided. Provided are a non-human model animal of a retinal vascular disease in which constitutively active Akt is expressed, a method for producing a non-human model animal of a retinal vascular disease in which constitutively active Akt is expressed, and a method for screening a drug for treating or preventing a retinal vascular disease.

An embodiment of the present invention provides a novel method for diagnosing, treating, or preventing a mood disorder. The method includes the step of measuring, by using a fusion protein, a level of the anti-fusion protein antibody in a biological sample.

The present disclosure provides non-human animal models of non-alcoholic fatty liver disease (NAFLD). Also provided are methods for producing the non-human animal models and uses of the non-human animal models to screen and evaluate agents for treating or preventing NAFLD.

Disclosed herein are novel compositions and methods for the treatment of age-related diseases, mitochondrial diseases, the improvement of stress resistance, the improvement of resistance to hypoxia and the extension of life span. Also described herein are methods for the identification of agents useful in the foregoing methods.

Methods and compositions are provided for the treatment of diseases or disorders associated with mitochondrial dysfunction.

The invention relates to methods for treatment and prevention of cancer by administering agents that increase levels of NAD+, such as NAD+ precursors or agents involved in NAD+ biosynthesis.

The present invention provides compositions for use in recovering and/or ameliorating deterioration of physiological functions due to aging. Provided are: a cell overexpressing GDF6 protein or an miR-17 family member; a composition for use in treating a senescence-related condition, containing GDF6 protein; a composition for use in treating a senescence-related condition, containing a human expression vector for GDF6 protein or an miR-17 family member; and a composition for use in treating a senescence-related condition, containing a cell secreting GDF6 protein.

Disclosed is a method of treating, reducing, or preventing pruritis in a mammal, the method comprising administering at least one natriuretic polypeptide b (Nppb) blocking agent to a mammal in an amount effective to treat or prevent pruritis in the mammal. An in vitro method of identifying a compound that inhibits Nppb activity is also disclosed.

An isogenic murine animal model for liver disease resulting from a Western (high fat, high sugar) diet is provided. This phenotypically and genotypically stable model sequentially develops steatosis (4-8 weeks), steatohepatitis (12-16 weeks), progressive fibrosis (16 week onwards) and spontaneous HCC (32-52 weeks), but only when fed a diet high in fat and sugar. The mice also develop obesity, insulin resistance and dyslipidemia, and the mouse hepatic transcriptome is concordant with the human NASH transcriptome at early and late time points, including activation of lipogenic, inflammatory and apoptotic signaling. The mouse HCC gene signature resembles S1 and S2 human HCC subclasses. This simple model of NASH and HCC that mirrors the development of human disease in terms of its triggers, serology, phenotype, histology, transcriptome and outcomes has utility in new target discovery, biomarker discovery, diagnostic test development, and screening and development of drugs for the corresponding liver conditions.