The biological processes giving rise to the central nervous system symptoms of long COVID remain a mystery. But multiple studies suggest they do not appear to be a result of a direct viral infection of brain tissue. The latest such research, which appeared online in Nature Neuroscience on Feb. 16, 2024, demonstrated that local immune response in brain tissues persisted long after SARS-CoV-2 virus had disappeared.

At the recent Macula Society Meeting, researchers from the Molecular Insight Research Foundation reported on the creation of a novel murine model of North Carolina macular dystrophy.

Immunesensor Therapeutics Inc. has presented preclinical data on the stimulator of interferon genes (STING) agonist IMSA-101 which is designed to modify the tumor microenvironment in solid tumors and thus improve the trafficking and infiltration of CAR T-cell therapy into the tumor.

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.

The biological processes giving rise to the central nervous system symptoms of long COVID remain a mystery. But multiple studies suggest they do not appear to be a result of a direct viral infection of brain tissue. The latest such research, which appeared online in Nature Neuroscience on Feb. 16, 2024, demonstrated that local immune response in brain tissues persisted long after SARS-CoV-2 virus had disappeared.

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.