UAB researchers discover the mechanism by which neurofibrillary tangles spread through the brain of Alzheimer’s patients is via connected neurons, and these findings reveal a major disease etiology that could lead to new therapies that slow Alzheimer’s disease progression.

A UAB research team defines the criteria these immunotherapies must meet to advance both conceptually and in trials, which are still at a very preliminary stage

They should have high selective precision and be programmable, sustained over time, and controllable throughout the pathologies. Macrophages, microglia and regulatory T cells would be appropriate effector cells for these treatments

Gladstone Institutes investigator Ryan Corces, PhD, has been named a 2026 winner of the Pershing Square Foundation’s MIND Prize, a prestigious award recognizing next-frontier thinkers who are uncovering a deeper understanding of the brain and cognition. The 2026 Prize winners each receive $750,000 over three years to support breakthroughs in research on neurodegenerative diseases, including Alzheimer’s disease and other aging-related dementias, which affect millions of people worldwide. With funding from the MIND Prize, he will investigate why many families in which multiple members have Alzheimer’s disease do not have gene variants known to cause the condition.

For the millions of people who carry the gene APOE4, which is the strongest known genetic risk factor for Alzheimer’s disease, their brain activity may begin changing long before any memory problems appear. Now, researchers at Gladstone Institutes have uncovered a precise chain of molecular events behind those early changes and identified a potential way to reverse them. Published in the journal Nature Aging, their new study in mouse models reveals how APOE4 triggers increased production of the protein Nell2, which makes neurons shrink and become hyperactive. The more hyperactive the neurons were in early life, the more severe were the memory problems the mice developed later in life.