Knight Initiative for Brain Resilience

Scientists including Knight Initiative Director Tony Wyss-Coray are trying to find out whether plasma can slow aging.

The genetic variant APOE4, carried by one-fifth of the world’s people, substantially boosts Alzheimer’s risk. But scientists have been puzzled about how to reverse that risk: punch up the gene variant’s potency, or smack it down? Now we know, thanks to research funded by the Knight Initiative for Brain Resilience.

A new study finds links between two popular models of the disease—and the results could change how researchers think about treatment.

Knight Initiative researchers are uncovering the fine points of how our brains learn to move. In the long run, their findings could help devise better treatments for Parkinson's disease.

A study of killifish reveals how protein dysfunction develops in vertebrate brain cells, a key driver of aging – shedding light on cognitive decline and diseases like Alzheimer’s, Parkinson’s, and ALS.

Stanford researchers reviewed over 400 therapy evaluations and discovered a crucial mismatch: Mouse studies test disease prevention, while human trials test treatment of existing disease.

Knight Initiative researchers used a new lab model of aging human neurons to show that as cells age, lysosomes fall into disrepair and waste builds up—feeding a damaging cycle that could lead to Alzheimer’s.

Blood and cerebrospinal fluid markers tied to inflammation and metabolism sort some patients into subgroups, according to Knight Initiative researchers, a step toward predicting progression and tailoring care.

The technique, which used genetically healthy donor cells, prolonged life and function in mice with a disease similar to Tay-Sachs. It may help with other neurodegenerative diseases like Alzheimer’s.

Fat-filled microglia may play a role in the damage caused by Alzheimer’s, especially for those who carry two copies a particular gene.