ArticleAnnals of neurology2021
Lewy Body Disease is a Contributor to Logopenic Progressive Aphasia Phenotype.
Article in Annals of neurology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
23 citing papers in PubMed, 34 citations in OpenAlex.
- Plasma eMTBR-tau243 as a disease biomarker across Alzheimer's disease clinical phenotypes.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- FDG-PET in the Evaluation of Primary Progressive Aphasia: A Narrative Review.Medicina (Kaunas, Lithuania) · 2026Review
- Imposter in the brain: aetiological, clinical and neuroimaging characteristics of Capgras syndrome.Brain : a journal of neurology · 2026Article
- Early Behavioral and Cognitive Changes in Patients With Pathologically Confirmed Alzheimer Disease, Lewy Body Dementia, and Mixed Dementia.Neurology open access · 2026Article
- Neuropathology of Lewy body dementia: Lewy-related pathology, α-synuclein oligomers, and comorbid pathologies.Molecular neurodegeneration · 2025Review
- Brain Perfusion, Atrophy, and Dopaminergic Changes in Amyloid Negative Logopenic Primary Progressive Aphasia.Scientific reports · 2025Article
- Primary Progressive Aphasia Lacking Core Features of Nonfluent and Semantic Variants: Clinical, Neuroimaging, and Neuropathologic Features.Neurology · 2024Observational
- Clinicoradiological and neuropathological evaluation of primary progressive aphasia.Journal of neurology, neurosurgery, and psychiatry · 2024Article
- Symptom-based staging for logopenic variant primary progressive aphasia.European journal of neurology · 2024Article
- Primary progressive aphasia: six questions in search of an answer.Journal of neurology · 2024Review
- Behavioral and Neuropsychiatric Differences Across Two Atypical Alzheimer's Disease Variants: Logopenic Progressive Aphasia and Posterior Cortical Atrophy.Journal of Alzheimer's disease : JAD · 2024Article
- Initial non-amnestic symptoms relate to faster rate of functional and cognitive decline compared to amnestic symptoms in neuropathologically confirmed dementias.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2023Article
- Review
- Aphasic mild cognitive impairment in prodromal dementia with Lewy bodies.Frontiers in neurology · 2023Article
- Atypical Alzheimer's disease phenotypes with normal or borderline PET biomarker profiles.Journal of neurology · 2022Article
- Neuropathological fingerprints of survival, atrophy and language in primary progressive aphasia.Brain : a journal of neurology · 2022Article
- Association of Variation in Behavioral Symptoms With Initial Cognitive Phenotype in Adults With Dementia Confirmed by Neuropathology.JAMA network open · 2022Article
- Unclassified fluent variants of primary progressive aphasia: distinction from semantic and logopenic variants.Brain communications · 2022Article
- Mental arithmetic modulates temporal variabilities of finger-tapping tasks in a tempo-dependent manner.PeerJ · 2022Article
- Neuropathology and molecular diagnosis of Synucleinopathies.Molecular neurodegeneration · 2021Review
Corrections and comments
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Authors and funding
22 authors at 6 institutions in 2 countries.
Funding
Abstract
objectiveThe objective of this study was to describe clinical features, [
methodsThis is a clinicopathologic case-control study of 45 patients, including 20 prospectively recruited patients with LPA among whom 6 were diagnosed with LPA-DLBD. We analyzed clinical features and compared FDG-PET metabolism in LPA-DLBD to an independent group of patients with clinical pDLB and regional α-synuclein burden on digital pathology to a second independent group of autopsied patients with DLBD pathology and antemortem pDLB (DLB-DLBD).
resultsAll patients with LPA-DLBD were men. Neurological, speech, and neuropsychological characteristics were similar across LPA-DLBD, LPA-Alzheimer's disease (LPA-AD), and LPA-frontotemporal lobar degeneration (LPA-FTLD). Genetic screening of AD, DLBD, and FTLD linked genes were negative with the exception of APOE ε4 allele present in 83% of LPA-DLBD patients. Seventy-five percent of the patients with LPA-DLBD showed a parietal-dominant pattern of hy pometabolism; LPA-FTLD - temporal-dominant pattern, whereas LPA-AD showed heterogeneous patterns of hypometabolism. LPA-DLBD had more asymmetrical hypometabolism affecting frontal lobes, with relatively spared occipital lobe in the nondominantly affected hemisphere, compared to pDLB. LPA-DLBD had minimal atrophy on gross brain examination, higher cortical Lewy body counts, and higher α-synuclein burden in the middle frontal and inferior parietal cortices compared to DLB-DLBD.
interpretationWhereas AD is the most frequent underlying pathology of LPA, DLBD can also be present and may contribute to the LPA phenotype possibly due to α-synuclein-associated functional impairment of the dominant parietal lobe. ANN NEUROL 2021;89:520-533.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.