ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2025
Impact of hippocampal α-synuclein oligomers on cognitive trajectory in patients with dementia with Lewy bodies.
Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Seeing Invisible Oligomers: Rethinking α-Synuclein Pathology Through Proximity Ligation Assay.Movement disorders : official journal of the Movement Disorder Society · 2026Review
- Molecular profiling of alpha-synuclein pathology and seeding activity in Parkinson's disease.Acta neuropathologica · 2026Article
- Neuropathology of Lewy body dementia: Lewy-related pathology, α-synuclein oligomers, and comorbid pathologies.Molecular neurodegeneration · 2025Review
- Facilitated α-synuclein oligomer sharing among glial cells by a centrally acting connexin inhibitor attenuates a rapidly progressive multiple system atrophy-cerebellar type model by reducing the neuronal α-synuclein burden.Acta neuropathologica communications · 2025Article
- Impact of hippocampal α-synuclein oligomers on cognitive trajectory in patients with dementia with Lewy bodies.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
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Authors and funding
9 authors.
Funding
Abstract
introductionIncreasing evidence indicates that α-synuclein (αSYN) oligomers are toxic. We sought to determine whether αSYN oligomers were associated with faster cognitive decline in prospectively-followed patients with dementia with Lewy bodies (DLB).
methodsEight autopsy-confirmed patients with DLB were selected based on rapid or slow cognitive decline determined by the rate of change of Mini-Mental State Examination (MMSE) scores. Quantitative neuropathologic analysis of αSYN oligomers, Lewy-related pathology, phosphorylated tau, and amyloid-β was conducted in hippocampal subfields (CA1-4 and subiculum) and the entorhinal cortex.
resultsDLB with rapid cognitive decline showed greater CA1 αSYN oligomer burden (p = 0.029) and tau burden (p = 0.029) than DLB with slow decline. The groups showed comparable burden of Lewy-related pathology and amyloid-β pathology in the hippocampal formation and entorhinal cortex. DISCUSSION: Hippocampal accumulation of αSYN oligomers and phosphorylated tau is associated with rapid cognitive decline in DLB. Therapeutic strategies targeting αSYN oligomers warrant further investigation. HIGHLIGHTS: Proximity ligation assay (PLA) and digital pathology for oligomer quantification. Abundant α-synuclein (αSYN) oligomers in CA1 of patients with dementia with Lewy bodies (DLB) with rapid decline. First human brain study linking αSYN oligomers to cognitive trajectory. Potential therapeutic implications of targeting αSYN oligomers in DLB.
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