Brain scans find tau buildup in nearly two-thirds of patients with late-onset psychosis
Psychosis that starts later in life may sometimes be an early sign of neurodegenerative disease. In a study of 37 patients, about a third had Alzheimer’s-type amyloid, and half of the rest showed other forms of tau buildup.
A Japanese study discovered that individuals experiencing psychosis after the age of 40 were significantly more likely to exhibit protein buildup associated with Alzheimer's disease and other forms of dementia, compared to healthy older adults. The research, published in Molecular Psychiatry, utilized a radioactive tracer called florzolotau to detect tau proteins in the brains of participants.
The tracer enabled researchers to identify both the type of tau buildup seen in Alzheimer's disease and other tau-related neurodegenerative diseases.
The study focused on 37 patients with late-onset psychosis and 47 healthy older adults, with an average age of 70 for the patients and 66 for the healthy participants. Late-onset psychosis, which involves symptoms such as hallucinations and delusions, typically begins in later life, sometimes after age 60. Patients with late-onset psychosis often display more prominent persecutory delusions, fewer negative symptoms, and less disorganized thinking than those with earlier-onset psychosis.
The research team found that 35% of the patients tested positive for amyloid-beta, a protein linked to Alzheimer's, while only 2% of the healthy participants tested positive. More strikingly, 65% of the patients tested positive for tau buildup, compared to only 15% of the healthy participants. Of the 13 patients who tested positive for amyloid-beta, all had developed psychosis after age 60.
Among the remaining 24 patients who tested positive for tau but not amyloid-beta, half exhibited tau buildup without amyloid, suggesting the presence of other tau-related diseases.
The researchers observed that the patients' tau patterns varied significantly, with the parietal cortex showing more tau tracer activity in the patients. This region is involved in attention and integrating information. However, the differences in tau levels between patients whose symptoms began before or after age 60 were not significant when amyloid-negative participants were considered.
Among the 13 amyloid-positive patients, those with higher parietal tau levels tended to score lower on a test of executive function, which controls planning and behavior. The tau levels were not linked to the severity of patients' psychiatric symptoms.
The study's findings suggest that late-onset psychosis may be associated with heterogeneous tau-related neurodegenerative processes. Although the authors propose that late-onset psychosis could be an early stage of a dementing illness, further long-term follow-up of patients is necessary to confirm this hypothesis. The study's limitations include its small sample size and the need for further confirmation of the specific tau-related diseases through autopsy data.
Additionally, the interpretation of tau patterns in non-Alzheimer's patients relies on the tracer's ability to distinguish different types of tau.
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