562. <i>IN VIVO</i> ASSESSMENTS OF TAU PATHOLOGIES IN PATIENTS WITH LATE-ONSET PSYCHOSIS: A PET STUDY
Abstract Background Late-onset psychosis (LOP) has distinct clinical features compared to younger-onset psychosis. While previous postmortem and epidemiological studies have suggested a link between the neural substrates of LOP and neurodegenerative processes, particularly tauopathies, research examining tau accumulation in the living brain of patients with LOP remains limited. Aims & Objectives This study aimed to investigate the putative neuropathology of LOP by combining amyloid PET and tau PET with Florzolotau (18F) (18F-florzolotau), which can detect various tauopathies in vivo. Method Thirty-seven patients with LOP (mean age = 69.9 years) and 47 controls underwent PET with 11C-PiB and 18F-florzolotau to evaluate amyloid beta and tau accumulation. Multivariate analysis of covariance (MANCOVA) was performed to examine the effects of diagnosis on standardized uptake value ratios (SUVRs) of 18F-florzolotau for four gray matter regions (frontal, temporal, parietal, and occipital cortices), controlling for age and sex. Correlations between these SUVRs and total scores of Mini-Mental State Examination (MMSE) and Frontal Assessment Battery (FAB) were investigated. Results Patients showed a significantly higher proportion of amyloid positivity (13 patients versus one control). MANCOVA demonstrated significant effects of diagnosis on 18F-florzolotau SUVRs (p = 0.004), and post-hoc analyses showed a higher SUVR in the parietal cortex of the patients. The diagnostic effects on SUVRs remained significant when MANCOVA was restricted exclusively to amyloid-negative participants (p = 0.002). There were no significant correlations between SUVR values in these regions and total MMSE or FAB scores. Discussion & Conclusions This in vivo clinical PET study suggests a potential association between the neuropathology of LOP and diverse tau pathologies. These findings contribute to a better understanding of the pathogenesis of LOP, and may facilitate the development of molecular-targeted therapeutic interventions.
Authors
- K Takahata
- Makoto Higuchi (ORCID: https://orcid.org/0000-0002-3934-5810)
- Mitsumoto Onaya (ORCID: https://orcid.org/0009-0000-4104-5035)
- Hironobu Endo
- Hiroyuki Uchida (ORCID: https://orcid.org/0000-0002-0628-7036)
- Hisashi Suzuki (ORCID: https://orcid.org/0000-0002-7162-8730)
- Kiwamu Matsuoka (ORCID: https://orcid.org/0000-0003-3263-0958)
- Yoshiharu Momota
- Chie Seki (ORCID: https://orcid.org/0000-0002-3222-7125)
- Kazunori Kawamura (ORCID: https://orcid.org/0000-0001-6786-678X)
- Manabu Kubota (ORCID: https://orcid.org/0000-0001-9507-1845)
- Kenji Tagai (ORCID: https://orcid.org/0000-0002-4551-1491)
- Muru Zhang
- Takahiko Tokuda (ORCID: https://orcid.org/0000-0002-7411-4911)
- M. Ichihashi
- Yasuharu Yamamoto
- S. Kurose
- H Tahakashi
Institutions
- Jikei University School of Medicine (JP)
- Keio University (JP)
- Kyoto University (JP)
- Nara Medical University Hospital (JP)
- National Institutes for Quantum Science and Technology (JP)
- Institute of Behavioral Sciences (JP)
- Psychiatric Medical Center (AM)
- Nara Medical University (JP)
Publication Details
- Journal
- The International Journal of Neuropsychopharmacology
- Published
- 2025-08-01
- DOI
- https://doi.org/10.1093/ijnp/pyaf052.314
- Primary Topic
- Prion Diseases and Protein Misfolding
- Type
- article
- Field-Weighted Citation Impact
- 0.00