ArticleNature medicine2023
Cognitive effects of Lewy body pathology in clinically unimpaired individuals.
Article in Nature medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 115 papers, 1 of them a synthesis that pooled it.
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Who cites it
115 citing papers in PubMed, 1 synthesis or guideline pooled it, 152 citations in OpenAlex.
- Genome-wide association study provides insights into the genetic basis of Lewy body dementia.Molecular psychiatry · 2025Pooled it
- Different functional connectivity gradients reflect aging and Alzheimer's disease.Nature neuroscience · 2026Article
- Brain pathology in relation to somatic diseases: Exploring the body-brain crosstalk.Journal of internal medicine · 2026Review
- Pre-dementia clinical trajectories associated with neuronal α-synuclein neuropathologic change: a retrospective cohort study.Research square · 2026Article
- CSF p-tau205: a biomarker of Alzheimer's disease progression and biological staging.Molecular psychiatry · 2026Article
- APOEε4 attenuates early TREM2-mediated microglial responses and influences disease trajectories in dementia with Lewy bodies.Research square · 2026Article
- Spatial multi-omics identifies early synaptic pruning and context-specific dopaminergic vulnerability in synucleinopathies.Nature communications · 2026Article
- Deep learning-based MRI analysis reveals Lewy body co-pathology accelerates brain aging in Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Estimating the time course of biomarker changes in Alzheimer's disease.Brain : a journal of neurology · 2026Article
- Definition of treatment-resistant late-life depression: Conclusions from a European Task Force Delphi process.European psychiatry : the journal of the Association of European Psychiatrists · 2026Article
- ATNIVS biomarker heterogeneity in real-world patients receiving lecanemab.The journal of prevention of Alzheimer's disease · 2026Article
- Co-pathologies and biological processes beyond amyloid-beta and tau in people with Alzheimer's disease: Evidence from clinical cohort studies.Journal of internal medicine · 2026Review
- Parkinson's Disease and Salivary Issues: A Survey.Gerodontology · 2026Article
- Use of machine learning and voice for multiclass classification of Parkinson's disease, chronic obstructive pulmonary disease, and healthy controls.Scientific reports · 2026Article
- Seed Amplification Assays for Parkinson's Disease: A Review of α-Synuclein Assays in Body Fluids and Tissues.Journal of neurochemistry · 2026Review
- A deep joint-learning proteomics model for diagnosis of six conditions associated with dementia.Nature medicine · 2026Article
- Effects of α-synuclein pathology on synaptic dysfunction and clinical outcomes in normal aging.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Discordance of Dopaminergic Dysfunction and Subcortical Atrophy by α-Synuclein Status in Sporadic and Genetic Parkinson's Disease.Movement disorders : official journal of the Movement Disorder Society · 2026Article
- Proteomic signatures of the APOE ε4 and APOE ε2 genetic variants and Alzheimer's disease.Nature aging · 2026Article
- Stable episodic memory and high education do not influence the rate of Alzheimer's disease pathology as measured by plasma p-tau217.bioRxiv : the preprint server for biology · 2026Article
55 more citing papers are in PubMed but not listed here.
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Authors and funding
15 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
α-Synuclein aggregates constitute the pathology of Lewy body (LB) disease. Little is known about the effects of LB pathology in preclinical (presymptomatic) individuals, either as isolated pathology or coexisting with Alzheimer's disease (AD) pathology (β-amyloid (Aβ) and tau). We examined the effects of LB pathology using a cerebrospinal fluid α-synuclein-seed amplification assay in 1,182 cognitively and neurologically unimpaired participants from the BioFINDER study: 8% were LB positive, 26% Aβ positive (13% of those were LB positive) and 16% tau positive. LB positivity occurred more often in the presence of Aβ positivity but not tau positivity. LB pathology had independently negative effects on cross-sectional and longitudinal global cognition and memory and on longitudinal attention/executive function. Tau had cognitive effects of a similar magnitude, but these were less pronounced for Aβ. Participants with both LB and AD (Aβ and tau) pathology exhibited faster cognitive decline than those with only LB or AD pathology. LB, but not AD, pathology was associated with reduced sense of smell. Only LB-positive participants progressed to clinical LB disease over 10 years. These results are important for individualized prognosis, recruitment and choice of outcome measures in preclinical LB disease trials, but also for the design of early AD trials because >10% of individuals with preclinical AD have coexisting LB pathology.
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