ArticlePloS one2019
Faster cognitive decline in dementia due to Alzheimer disease with clinically undiagnosed Lewy body disease.
Article in PloS one, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 62 citations in OpenAlex.
- Alpha-Synuclein in Neurodegeneration: From Shared Biology to Disease-Specific Phenotypes.Cells · 2026Review
- Alpha-synuclein co-pathology in a real-world early Alzheimer's disease cohort.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Targeting protein aggregate co-pathologies in neurodegeneration: a viable therapeutic strategy?Molecular neurodegeneration advances · 2026Review
- Deep learning for FDG-PET classification in patients with Alzheimer's disease, dementia with Lewy bodies and their mixed pathology: a solution for diagnostic heterogeneity.Frontiers in aging neuroscience · 2026Article
- Tau, amyloid-β and α-synuclein co-pathologies synergistically enhance neuroinflammation and neuropathology.bioRxiv : the preprint server for biology · 2025Article
- Neuropathology of Lewy body dementia: Lewy-related pathology, α-synuclein oligomers, and comorbid pathologies.Molecular neurodegeneration · 2025Review
- Celebrating neuropathology's contributions to Alzheimer's Disease Research Centers.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- The effect of Lewy body (co-)pathology on the clinical and imaging phenotype of amnestic patients.Brain : a journal of neurology · 2025Article
- Lipid profiling of Parkinson's disease brain highlights disruption in Lysophosphatidylcholines, and triacylglycerol metabolism.NPJ Parkinson's disease · 2025Article
- Early Motor Signs in Pathologically Verified Alzheimer's Disease and Lewy Body Disease.Movement disorders clinical practice · 2025Article
- Associations between neuropsychiatric symptoms and pathology in clinicopathologically defined Alzheimer's disease, Alzheimer's disease with Lewy bodies, and dementia with Lewy bodies.Journal of Alzheimer's disease : JAD · 2025Article
- Characterizing visual read tau-PET-negative participants with Alzheimer's disease dementia.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Comorbidities in early-onset sporadic versus presenilin-1 mutation-associated Alzheimer disease dementia: Evidence for dependency on Alzheimer disease neuropathological changes.Journal of neuropathology and experimental neurology · 2025Article
- Parkinson Disease Neuropathological Comorbidities: Prevalences from Younger-Old to Older-Old, With Comparison to Non-Demented, Non-Parkinsonian Subjects.medRxiv : the preprint server for health sciences · 2025Article
- Association of CSF α-synuclein seed amplification assay positivity with disease progression and cognitive decline: A longitudinal Alzheimer's Disease Neuroimaging Initiative study.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Pilot implementation of the revised criteria for staging of Alzheimer's disease by the Alzheimer's Association Workgroup in a tertiary memory clinic.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Clinicopathological Heterogeneity of Lewy Body Diseases: The Profound Influence of Comorbid Alzheimer's Disease.medRxiv : the preprint server for health sciences · 2024Article
- In vivo detection of Alzheimer's and Lewy body disease concurrence: Clinical implications and future perspectives.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Review
- Alzheimer Disease Cerebrospinal Fluid Biomarkers in a Tertiary Neurology Practice.Mayo Clinic proceedings · 2024Article
- Disease progression modelling reveals heterogeneity in trajectories of Lewy-type α-synuclein pathology.Nature communications · 2024Article
Corrections and comments
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Authors and funding
36 authors at 7 institutions in 3 countries.
Funding
Abstract
backgroundNeuropathology has demonstrated a high rate of comorbid pathology in dementia due to Alzheimer's disease (ADD). The most common major comorbidity is Lewy body disease (LBD), either as dementia with Lewy bodies (AD-DLB) or Alzheimer's disease with Lewy bodies (AD-LB), the latter representing subjects with ADD and LBD not meeting neuropathological distribution and density thresholds for DLB. Although it has been established that ADD subjects with undifferentiated LBD have a more rapid cognitive decline than those with ADD alone, it is still unknown whether AD-LB subjects, who represent the majority of LBD and approximately one-third of all those with ADD, have a different clinical course.
methodsSubjects with dementia included those with "pure" ADD (n = 137), AD-DLB (n = 64) and AD-LB (n = 114), all with two or more complete Mini Mental State Examinations (MMSE) and a full neuropathological examination.
resultsLinear mixed models assessing MMSE change showed that the AD-LB group had significantly greater decline compared to the ADD group (β = -0.69, 95% CI: -1.05, -0.33, p<0.001) while the AD-DLB group did not (β = -0.30, 95% CI: -0.73, 0.14, p = 0.18). Of those with AD-DLB and AD-LB, only 66% and 2.1%, respectively, had been diagnosed with LBD at any point during their clinical course. Compared with clinically-diagnosed AD-DLB subjects, those that were clinically undetected had significantly lower prevalences of parkinsonism (p = 0.046), visual hallucinations (p = 0.0008) and dream enactment behavior (0.013).
conclusionsThe probable cause of LBD clinical detection failure is the lack of a sufficient set of characteristic core clinical features. Core DLB clinical features were not more common in AD-LB as compared to ADD. Clinical identification of ADD with LBD would allow stratified analyses of ADD clinical trials, potentially improving the probability of trial success.
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