ArticleJournal of Alzheimer's disease : JAD2021
Genetics Contributes to Concomitant Pathology and Clinical Presentation in Dementia with Lewy Bodies.
Article in Journal of Alzheimer's disease : JAD, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers, 2 of them syntheses that pooled it.
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Who cites it
18 citing papers in PubMed, 2 syntheses or guidelines pooled it, 24 citations in OpenAlex.
- Association between the LRP1B and APOE loci and the development of Parkinson's disease dementia.Brain : a journal of neurology · 2023Pooled it
- Effect of GBA gene variants on clinical characteristics of dementia with Lewy bodies: a review and meta-analyses.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2022Pooled it
- Synuclein Disorder-Related Genetic Determinants of Mild Behavioural Impairment in a Pre-Clinical Community Cohort.International journal of geriatric psychiatry · 2026Article
- Characteristics and mechanisms of cognitive impairment in Parkinson disease.Nature reviews. Neurology · 2026Review
- Genetic testing of common and rare variants in dementia patients from a memory clinic : Dementia-related genetic testing in memory clinic.Alzheimer's research & therapy · 2025Article
- Comorbid Pathologies and Their Impact on Dementia with Lewy Bodies-Current View.International journal of molecular sciences · 2025Review
- Genetic risk and plasma biomarkers of dementia with Lewy bodies in a Chinese population.NPJ Parkinson's disease · 2025Article
- Identification of Common Brain Protein and Genetic Loci Between Parkinson's Disease and Lewy Body Dementia.CNS neuroscience & therapeutics · 2025Article
- Effect of GBA1 Mutations and APOE Polymorphisms on Survival and Progression Among Ashkenazi Jews with Dementia with Lewy Bodies.Movement disorders : official journal of the Movement Disorder Society · 2024Article
- Clinical, mechanistic, biomarker, and therapeutic advances in GBA1-associated Parkinson's disease.Translational neurodegeneration · 2024Review
- Associations of cholinergic system integrity with cognitive decline in GBA1 and LRRK2 mutation carriers.NPJ Parkinson's disease · 2024Article
- Causal influences of neuropsychiatric disorders on Alzheimer's disease.Translational psychiatry · 2024Article
- Apolipoprotein E Gene in α-Synucleinopathies: A Narrative Review.International journal of molecular sciences · 2024Review
- Genetic background of cognitive decline in Parkinson's disease.Frontiers in cognition · 2024Review
- Brain age in genetic and idiopathic Parkinson's disease.Brain communications · 2024Article
- Lysosomal polygenic risk is associated with the severity of neuropathology in Lewy body disease.Brain : a journal of neurology · 2023Article
- GBA-associated PD: chances and obstacles for targeted treatment strategies.Journal of neural transmission (Vienna, Austria : 1996) · 2022Review
- Genetic susceptibility and environmental factors in dementia with Lewy bodies: Converging pathogenic mechanisms.Frontiers in neurologyReview
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundDementia with Lewy bodies (DLB) is a complex, progressive neurodegenerative disease with considerable phenotypic, pathological, and genetic heterogeneity.
objectiveWe tested if genetic variants in part explain the heterogeneity in DLB.
methodsWe tested the effects of variants previously associated with DLB (near APOE, GBA, and SNCA) and polygenic risk scores for Alzheimer's disease (AD-PRS) and Parkinson's disease (PD-PRS). We studied 190 probable DLB patients from the Alzheimer's dementia cohort and compared them to 2,552 control subjects. The p-tau/Aβ1-42 ratio in cerebrospinal fluid was used as in vivo proxy to separate DLB cases into DLB with concomitant AD pathology (DLB-AD) or DLB without AD (DLB-pure). We studied the clinical measures age, Mini-Mental State Examination (MMSE), and the presence of core symptoms at diagnosis and disease duration.
resultsWe found that all studied genetic factors significantly associated with DLB risk (all-DLB). Second, we stratified the DLB patients by the presence of concomitant AD pathology and found that APOE ɛ4 and the AD-PRS associated specifically with DLB-AD, but less with DLB-pure. In addition, the GBA p.E365K variant showed strong associated with DLB-pure and less with DLB-AD. Last, we studied the clinical measures and found that APOE ɛ4 associated with reduced MMSE, higher odds to have fluctuations and a shorter disease duration. In addition, the GBA p.E365K variant reduced the age at onset by 5.7 years, but the other variants and the PRS did not associate with clinical features.
conclusionThese finding increase our understanding of the pathological and clinical heterogeneity in DLB.
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