Study connects late-life psychosis to abnormal tau protein buildup

Hallucinations and delusions that appear for the first time in midlife or later are often treated as psychiatric symptoms whose biological cause is unclear. The study, published online in Molecular Psychiatry on August 2, 2026, suggests that, for many patients, these symptoms may be linked to brain changes also seen in dementia.

Using positron emission tomography, or PET, the research team found that about 65% of patients who developed psychosis after age 40 showed abnormal buildup of tau, a protein associated with Alzheimer's disease and other forms of dementia. By comparison, tau PET positivity was seen in about 15% of healthy older controls. The study also found amyloid PET positivity in 35% of patients, compared with 2% of controls.

The findings provide the first in vivo evidence that diverse tau-related brain changes may be involved in late-onset psychosis. Until now, earlier epidemiological and postmortem studies had suggested a possible relationship between late-life psychotic symptoms and neurodegeneration, but direct evidence in the living brain had been limited.

Patients can show the same symptoms, such as hallucinations or delusions, but their clinical course and response to treatment can be very different. This study started from a clinical question: whether hidden biological differences in the brain could explain those differences."