4.3 Article

Tau in dementia with Lewy bodies

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SAGE PUBLICATIONS LTD
DOI: 10.1177/00048674231177219

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Tau; dementia with Lewy bodies; Alzheimer's disease; positron emission tomography; phosphorylated tau

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This study found that tau protein is commonly present in individuals with dementia with Lewy bodies and may be associated with worse cognition. The levels of plasma p-tau181 correlated with tau deposition and amyloid-beta binding, suggesting its potential as a marker for identifying co-morbid Alzheimer's disease-related pathology in dementia with Lewy bodies. Further research is needed to evaluate the clinical implications of tau in larger longitudinal studies.
Objective: 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. Methods: 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 (F-18-MK6240 and F-18-NAV4694). Plasma p-tau181 levels were measured using Simoa technology. Results: 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 (rho = 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 (rho = 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. Conclusions: 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.

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