Mutations within the MS4A gene cluster have been linked to changes in protein levels that affect disease risk.

Using super-resolution microscopy, scientists learned how mutant tau causes a memory-related protein to clump up in mouse neurons.

Exposing mice to an hour of 40-hertz stimuli every day for a week reduced levels of amyloid-β plaques and tau protein, and improved cognition.

An enzyme of the bacteria Porphyromonas gingivalis has been found in the brains of patients with the disorder, and causes neurodegeneration in mice.

Tau proteins disrupt the movement of molecules into and out of neuronal cells’ nuclei.

A study explores how nuclear pore complexes are disrupted in Alzheimer’s disease.

Levels of tau, amyloid-β 42, and IL-10 extracted from extracellular vesicles that started out in the brain were higher in military personal suffering head injuries compared with healthy soldiers.

A proposed definition of the disease emphasizes signs of neurodegeneration and the presence of β-amyloid and tau, rather than cognitive symptoms.

The findings suggest that faster synthesis, rather than decreased clearance, causes the protein to build up in neurons.