Brain scans reveal tau buildup in late-onset psychosis
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 in Molecular Psychiatry suggests that, for many patients, these symptoms may be linked to brain changes also seen in dementia.
A recent study published in Molecular Psychiatry reveals a significant association between brain changes linked to Alzheimer's disease and late-onset psychosis. Using positron emission tomography (PET) scans, researchers found that approximately 65% of patients who experienced psychosis after age 40 showed abnormal buildup of tau, a protein associated with Alzheimer's disease.
In comparison, only 15% of healthy older adults exhibited tau PET positivity. Additionally, 35% of patients had amyloid PET positivity, compared to just 2% of controls. These findings provide the first direct evidence of diverse tau-related brain changes in living patients with late-onset psychosis, challenging previous assumptions that these symptoms were solely psychiatric in nature.
Lead researcher Manabu Kubota emphasized that while patients may display similar symptoms, their clinical course and response to treatment can vary greatly. The study identified distinct tau patterns, with some patients showing amyloid-positive Alzheimer's-type tau pathology and others displaying amyloid-negative forms of tau-related neurodegeneration.
Notably, greater tau accumulation in the parietal lobes of amyloid-positive patients correlated with poorer executive function, suggesting a potential link between tau buildup and cognitive impairment. This research suggests that PET-based assessments could aid in earlier diagnosis and personalized treatment of late-onset psychosis by identifying underlying biological mechanisms, moving beyond symptom-based approaches.
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