Immunoglobulin G (IgG), an antibody that participates in the response to infection, could have a specific role in metabolism. During aging, it accumulates in certain tissues inducing metabolic dysfunction and fibrosis of fat tissue. This effect could be prevented through an intracellular receptor that contributes to the delivery of IgG. A team of researchers from Columbia University and Peking University (PKU) demonstrated that reducing excess IgG improved the metabolic health of aged mice and increased their life expectancy.

Pompe disease is a disorder caused by deficiency of the lysosomal acid α-glucosidase (GAA) enzyme, which leads to the accumulation of glycogen within the lysosomes, overall in skeletal and cardiac muscle.

Pompe disease is caused by a deficiency in the lysosomal enzyme acid α-glucosidase (GAA) that leads to accumulation of glycogen in the lysosomes, mainly seen in skeletal and cardiac muscles. Researchers from Duke University have developed a new murine model of Pompe disease, which recapitulates human infantile-onset disease. This model harbors the c.1826dupA mutation in the murine Gaa gene, which resembles the human GAA c.1826dupA (p.Y609*) mutation seen in infantile-onset Pompe disease.

Researchers from the Yale University School of Medicine have developed a novel murine model of Gaucher disease type I with the aim to investigate the impact of GBA1 deficiency on hematopoiesis and the immune system, in order to elucidate potential therapeutic targets.