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P4‐341: THE PREVALENCE AND INFLUENCE OF TAU IN LEWY BODY DEMENTIA
Author(s) -
Chin Kai Sin,
Yassi Nawaf,
Masters Colin L.,
Watson Rosie
Publication year - 2019
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2019.06.4011
Subject(s) - dementia with lewy bodies , lewy body , dementia , tauopathy , pathological , medicine , lewy body disease , pathology , disease , alzheimer's disease , psychology , neurodegeneration
Background: Lewy body dementias (LBD), including dementia with Lewy bodies (DLB) and Parkinson’s disease dementia (PDD), are common forms of neurodegenerative dementia in older adults. Neurofibrillary tangles (NFT) formed by tau proteins, a pathological hallmark of Alzheimer’s disease, are a common co-pathology in LBD. However, the influence of tau in people with LBD is not completely understood. We aimed to investigate the prevalence and influence of tau on clinical outcomes in people with LBD.Methods: A systematic literature search was conducted using three major electronic databases (Medline, Embase and PubMed). The search terms were (“dementia with Lewy bodies” OR “diffuse Lewy body disease”) AND (“tau protein” OR “tauopathy” OR “neurofibrillary tangle”). After screening all titles and abstracts, relevant studies which investigated the influence of tau pathology on clinical outcomes (clinical phenotypes, cognition, rate of decline and survival) in LBD were included in this review. Results: Fiftytwo studies were identified, which included 34 neuropathologic, 15 cerebrospinal fluid (CSF) and three PET imaging studies. Pooled prevalence data from 16 neuropathologic studies showed that at least 60.0% (744/1249) of DLB patients had a Braak NFT stage of IV or higher, whilst 52.0% (223/429) of PDD patients had a Braak NFT stage of III or more. In six CSF studies, pathologically elevated total tau and phosphorylated-tau levels were detected in 27.9% (194/696) and 28.0% (185/661) of DLB, and 22.5% (55/ 244) and 15.4% (26/169) of PDD patients, respectively. Despite the significant heterogeneity in study designs, people with LBD and high tau burden seemed to be less likely to manifest the core clinical features of DLB, resulting in lower clinical diagnostic accuracy. Some, but not all studies found that a greater tau burden was associated with worse cognition, greater rate of decline and shorter survival, particularly in DLB. Conclusions: Tau pathology is common in people with LBD. Understanding the role and significance of co-morbid neuropathological change in LBD is important as it might improve the clinical diagnosis, have implication on disease progression and prognosis, and help to develop effective treatment options. Longitudinal studies, utilizing in vivo, diseasespecific biomarkers are needed.