Deficiencies in interferon-stimulated gene 15 (ISG15), a protein that normally regulates the immune response, causes mild but persistent inflammation. However, its absence also provides an unexpected advantage by increasing resistance to viral infections. Inspired by this condition and using mRNA technology, scientists at Columbia University and the Icahn School of Medicine at Mount Sinai have developed a broad-spectrum antiviral platform.
Deficiencies in interferon-stimulated gene 15 (ISG15), a protein that normally regulates the immune response, causes mild but persistent inflammation. However, its absence also provides an unexpected advantage by increasing resistance to viral infections. Inspired by this condition and using mRNA technology, scientists at Columbia University and the Icahn School of Medicine at Mount Sinai have developed a broad-spectrum antiviral platform.
A little-known tissue composed of a cluster of immune cells could offer novel insights into the development of neurological disorders. Meninges' immune system changes with age and neurodegeneration. Are they protecting the brain or fueling disease?
The difference between the origin of Alzheimer's disease (AD) and its symptoms is an obstacle to finding effective treatments. Scientists focused on amyloid-β (Aβ) plaques and tau aggregates to slow neurodegeneration and cognitive decline. Without identifying what causes AD, approved treatments do not provide much benefit.
A little-known tissue composed of a cluster of immune cells could offer novel insights into the development of neurological disorders. Meninges' immune system changes with age and neurodegeneration. Are they protecting the brain or fueling disease? Mapping and analyzing the so-called ectopic lymphoid structures (ELSs) in the meninges at different ages in preclinical models of neurodegenerative diseases such as Alzheimer's may help clarify whether they are good, bad, or ugly, as in the iconic film by Sergio Leone.
Experimental drugs that directly inhibit the NSD2 enzyme have shown potential as an effective strategy against hard-to-treat cancers, such as lung and pancreatic tumors driven by KRAS mutations. The therapeutic mechanism involves reversing a histone H3 methylation that promotes open chromatin and the expression of oncogenes.
Experimental drugs that directly inhibit the NSD2 enzyme have shown potential as an effective strategy against hard-to-treat cancers, such as lung and pancreatic tumors driven by KRAS mutations. The therapeutic mechanism involves reversing a histone H3 methylation that promotes open chromatin and the expression of oncogenes.
In the tumor microenvironment, cancer cells activate various signaling pathways to promote their growth. This includes the formation of blood vessels. However, the circulatory system is not the only one attracted to the tumor. Researchers at Sanford Research have uncovered a mechanism to circumvent the immune response that would destroy them.
The difference between the origin of Alzheimer's disease (AD) and its symptoms is an obstacle to finding effective treatments. Scientists focused on amyloid-β (Aβ) plaques and tau aggregates to slow neurodegeneration and cognitive decline. Without identifying what causes AD, approved treatments do not provide much benefit. However, new findings suggest that restoring lithium levels in the brain could prevent and treat AD. Not just any lithium would work, just the forms that do not bind to Aβ.
In the tumor microenvironment, cancer cells activate various signaling pathways to promote their growth. This includes the formation of blood vessels. However, the circulatory system is not the only one attracted to the tumor. Researchers at Sanford Research have uncovered a mechanism to circumvent the immune response that would destroy them.
