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 Mercer University have presented a middle cerebral artery/ferric chloride (MCA/FeCl3) thromboembolic mouse model of COVID-19-induced stroke and cerebrovascular complications.
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.
It has been shown that vascular endothelial growth factor A (VEGF-A) induces blood-brain barrier disruption and vasogenic edema and it is up-regulated in stroke. When bound to its receptor, VEGF promotes angiogenesis and neuroprotection, in addition to inducing vasogenic edema. VST Bio Ltd. and Yale University have presented data on their monoclonal antibody against syndecan-2, named VST-002, that completely blocks VEGF-driven vasogenic edema while preserving neuroprotective effects.
Japanese researchers have developed a new rat model of thromboembolic ischemic stroke that did not require arterial ligation of the external carotid artery, which makes the research for thrombolytic agents more complicated.
It is known that CX3C chemokine receptor 1 (CX3CR1) expressed on macrophages plays a crucial role in inner hair cell ribbon synaptic repair and spiral ganglion neuron survival after synaptopathic noise-induced trauma.
Bleeding of unknown cause is a group of rare disorders that are still difficult to accurately diagnose. A case report on a patient with hematoma in the perineal region after her first delivery was presented.
The most common genetic cause of hereditary deafness in humans are mutations in the GJB2 gene, especially the 35delG and 235delC mutations. At the recent ARO meeting, researchers from Ear Nose and Throat Hospital of Fudan University presented the creation of a novel mouse model for studying the pathogenic mechanisms of hereditary deafness resulting from these mutations.
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