New study links tau protein to mitochondrial dysfunction in Alzheimer’s

Scientists led by Stanford investigators reported that tau protein interferes with mitochondrial electron transport, forcing electrons to flow backward and produce harmful reactive oxygen species. This reverse electron transport triggers cellular stress and inflammatory responses that contribute to neurodegeneration. Experiments showed that pharmacologically blocking the backward flow rescued mitochondrial function and markedly improved learning and memory in both fruit flies and mouse models of Alzheimer’s disease.

Analyses of cultured human neurons and post-mortem brain tissue from patients indicated that the same mitochondrial defect may occur in humans. The findings point to a novel therapeutic target, and two of the study’s authors have founded a biotech startup to pursue drug development based on this approach.