Phosphorylation of the protein Tau is a key post-translational feature in tauopathies like Alzheimer’s disease (AD), which leads to microtubule dysfunction and Tau accumulation. Recent findings have suggested the blockade of the adenosine A2A receptor as an approach that improves the outcome in amyloid and Tau models.

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.

Ischemic stroke triggers a strong neuroinflammatory response, with microglial activation and neutrophil infiltration contributing to blood-brain barrier disruption and worsening neuronal damage.

Subtyping is what made precision medicine in cancer a reality. And for successful drug discovery in all its stages, finding subtypes in Alzheimer’s disease is all but imperative.

Nitrogen-containing heteroaromatic-based inhibitors for cytochrome P450 (CYP) in various species contain a crucial coordination between the nitrogen atom and the heme iron. Previous studies suggested that 1,3-oxazole could bind heme-iron with a strength comparable to pyridine, highlighting its potential as a novel heme-iron binding moiety.

Neucore Bio Inc. announced it has been awarded a US$304,000 National Science Foundation Small Business Technology Transfer grant to evaluate scalable manufacturing of exosome-based gene delivery methods.

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.