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Title: | Tau in dementia with Lewy bodies. | Austin Authors: | Chin, Kai Sin;Churilov, Leonid ;Doré, Vincent ;Villemagne, Victor L ;Rowe, Christopher C ;Yassi, Nawaf;Watson, Rosie | Affiliation: | Department of Medicine, The Royal Melbourne Hospital, The University of Melbourne, Parkville, VIC, Australia Department of Medicine and Neurology, Melbourne Brain Centre at the Royal Melbourne Hospital, The University of Melbourne, Parkville, VIC, Australia. Molecular Imaging and Therapy Medicine (University of Melbourne) Population Health and Immunity Division, The Walter and Eliza Hall Institute of Medical Research, Parkville, VIC, Australia Department of Aged Care, The Royal Melbourne Hospital, Parkville, VIC, Australia Health and Biosecurity Flagship, The Australian eHealth Research Centre, CSIRO, Clayton South, VIC, Australia Department of Psychiatry, University of Pittsburgh, Pittsburgh, PA, USA. |
Issue Date: | Feb-2024 | Date: | 2023 | Publication information: | The Australian and New Zealand Journal of Psychiatry 2024-02; 58(2) | Abstract: | Neurofibrillary tangles are present in a proportion of people with dementia with Lewy bodies and may be associated with worse cognition. Recent advances in biomarkers for Alzheimer's disease include second-generation tau positron emission tomography as well as the detection of phosphorylated tau at threonine 181 (p-tau181) in plasma. This study aimed to investigate tau in people with dementia with Lewy bodies using a second-generation tau positron emission tomography tracer as well as plasma p-tau181. Twenty-seven participants (mean age 74.7 ± 5.5) with clinically diagnosed probable dementia with Lewy bodies underwent comprehensive clinical assessment and positron emission tomography imaging (18F-MK6240 and 18F-NAV4694). Plasma p-tau181 levels were measured using Simoa technology. Five dementia with Lewy bodies participants (18.5%) had an abnormal tau positron emission tomography (increased tau uptake in the temporal meta-region-of-interest). Higher plasma p-tau181 concentrations correlated with higher tau deposition in the temporal region (ρ = 0.46, 95% confidence interval = [0.10, 0.72]) and classified abnormal tau positron emission tomography in dementia with Lewy bodies with an area under the curve of 0.95 (95% confidence interval = [0.86, 0.99]). Plasma p-tau181 also correlated positively with cortical amyloid-beta binding (ρ = 0.68, 95% confidence interval = [0.40, 0.84]) and classified abnormal amyloid-beta positron emission tomography in dementia with Lewy bodies with an area under the curve of 0.91 (95% confidence interval = [0.79, 0.99]). There was no association found between tau deposition and any of the clinical variables. Tau is a common co-pathology in dementia with Lewy bodies. Plasma p-tau181 correlated with abnormal tau and amyloid-beta positron emission tomography and may potentially be used as a marker to identify co-morbid Alzheimer's disease-related pathology in dementia with Lewy bodies. The clinical implications of tau in dementia with Lewy bodies need to be further evaluated in larger longitudinal studies. | URI: | https://ahro.austin.org.au/austinjspui/handle/1/33024 | DOI: | 10.1177/00048674231177219 | ORCID: | 0000-0002-3384-3499 |
Journal: | The Australian and New Zealand Journal of Psychiatry | Start page: | 48674231177219 | PubMed URL: | 37264610 | ISSN: | 1440-1614 | Type: | Journal Article | Subjects: | Alzheimer’s disease Tau dementia with Lewy bodies phosphorylated tau positron emission tomography |
Appears in Collections: | Journal articles |
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