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Cerebral multi-morbidity is common in older people with dementia, including people with dementia with Lewy bodies (DLB). We describe the first Australian-based, longitudinal observational biomarker study of DLB.
To investigate the frequency and influence of Alzheimer’s disease (AD) pathology (amyloid-β and tau) and cerebrovascular disease on clinical symptoms and disease outcome in DLB.
The study will recruit 100 people with mild to moderate probable DLB, who will undergo comprehensive clinical and cognitive assessments. Scales targeting DLB-specific clinical features (such as cognitive fluctuations and rapid eye movement sleep behaviour disorder) are administered. Biomarker protocols incorporate blood sampling (including ApoE genotyping and systemic inflammatory markers), molecular imaging (amyloid-β [18F-NAV 4694], tau [18F-MK6240], VMAT2 [18F-AV133] PET scans), 3-tesla magnetic resonance imaging and optional lumbar puncture. Clinical assessments are completed 6 - monthly and imaging 18-monthly. Participants are also invited to register for post-mortem brain tissue donation.
Thirty participants with probable DLB have been enrolled to date (mean age 75.4 years, range 64-82; 87% male). All participants have mild to moderate cognitive impairment (mean MMSE 25, range 17-30). Approximately 64% of the participants were amyloid-β positive. Study procedure tolerability has been excellent with no adverse events reported.
There is significant overlap of AD-related proteinopathies in people with DLB. Understanding the impact of multi-morbidity is essential in the development of effective treatment strategies. This study supports the feasibility of intensive, longitudinal biomarker studies in DLB in the Australian setting.
Neurofibrillary tangles (NFT) formed by tau proteins, a pathological hallmark of Alzheimer’s disease, are a common co-pathology in people with Lewy body dementias, which include dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD).
To investigate the prevalence of tau in Lewy body dementia, and its association with clinical outcomes.
A systematic search was conducted on Medline, Embase and PubMed using the search term: (“dementia with Lewy bodies” OR “diffuse Lewy body disease”) AND (“tau protein” OR “tauopathy” OR “neurofibrillary tangle”). A total of 42 articles met the inclusion criteria for data extraction. Random-effect meta-analyses were performed to obtain pooled estimates for prevalence, and risk ratios (RR) or standardised mean difference (SMD) for clinical outcomes measures.
Braak NFT stage ≥III was observed in 67% (n=1399, 95%CI 59%-76%) of DLB and 52% (n=429, 95%CI 26%-78%) of PDD at autopsy. Abnormal CSF phosphorylated-tau levels were present in 27% (n=705, 95%CI 23%-30%) of DLB and 15% (n=172, 95%CI 5%-24%) of PDD cases. Higher tau burden in DLB was associated with reduced likelihood of manifesting visual hallucinations (RR 0.56; 95%CI 0.40-0.77) and motor parkinsonism (RR 0.62; 95%CI 0.40-0.98), lower diagnostic accuracy of DLB during life (RR 0.49; 95%CI 0.38-0.64) and worse cognition prior to death (SMD 0.60; 95%CI 0.44-0.76).
Tau is more common in DLB than PDD and may negatively impact clinical diagnostic accuracy in people with DLB. Prospective longitudinal studies are needed to understand the roles of co-morbid neuropathologies in Lewy body dementias.
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