Early intervention changes trajectory for depressed preschoolers
Peer-Reviewed Publication
Updates every hour. Last Updated: 12-Jul-2025 08:11 ET (12-Jul-2025 12:11 GMT/UTC)
Van Andel Institute scientists and collaborators have discovered a potential treatment target that may re-energize dysfunctional or “exhausted” immune cells in their fight against cancer.
The target is an immune checkpoint called PTGIR, which regulates the number and cancer-fighting powers of T cells, the soldiers of the immune system. Too much PTGIR puts a brake on T cells and reduces their ability to release cancer-killing molecules.
The findings, published in the journal Nature Immunology, could help improve cancer immunotherapies by paving the way for new immune checkpoint inhibitors or engineered T cell therapies that block PTGIR signaling and re-invigorate T cells.
USC researchers have identified a new brain imaging benchmark that may improve how researchers classify biologically meaningful changes associated with Alzheimer’s disease, especially in Hispanic and non-Hispanic white populations. Using an advanced brain imaging scan called tau PET, the research team studied over 675 older adults from the Health and Aging Brain Study–Health Disparities (HABS-HD) aiming to identify the optimal brain signal that distinguishes individuals with clinically-relevant biological markers of AD from those who are aging normally. They compared tau PET scans of study participants who were cognitively impaired with those who were not impaired based on cognitive tests to establish a tau cut-point that would indicate a higher risk for Alzheimer’s disease. The team used a new imaging tracer called 18F-PI-2620, to measure tau protein buildup in the brain. They found that when tau levels in the medial temporal lobe—a region deep in the brain—exceeded a certain threshold, it strongly indicated cognitive impairment related to AD. But the tau cut-point was only effective when another abnormal protein, amyloid, was also present in those with cognitive impairment, and it only worked for Hispanic and non-Hispanic White participants. In non-Hispanic Black participants, the tau cut-point did not perform as expected. This suggests that other pathologies or conditions may be driving cognitive decline in this group. The findings reflect a growing focus in AD research on making sure diagnostic tools work for everyone—not just in narrow clinical trial populations.
A new study from the University of Michigan Rogel Health Cancer Center, published in Science, sheds light on how two distinct classes of mutations in the FOXA1 gene—commonly altered in prostate cancer—drive tumor initiation formation and therapeutic resistance.