ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2017
Hippocampal α-Synuclein in Dementia with Lewy Bodies Contributes to Memory Impairment and Is Consistent with Spread of Pathology.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers, 1 of them a synthesis that pooled it.
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Who cites it
78 citing papers in PubMed, 1 synthesis or guideline pooled it, 134 citations in OpenAlex.
- Hippocampal subfield volumes in mild cognitive impairment and alzheimer's disease: a systematic review and meta-analysis.Brain imaging and behavior · 2023Pooled it
- Activated microglial phenotypes in the hippocampal CA2 subfield are implicated in Lewy body disease progression.Acta neuropathologica · 2026Article
- Seven tesla MRI reveals amygdala and hippocampal subfield atrophy in dementia with Lewy bodies.Alzheimer's research & therapy · 2026Article
- Microglial reactivity in the hippocampal CA2 is associated with advanced neuronal α-synucleinopathy.bioRxiv : the preprint server for biology · 2026Article
- Imaging spatial transcriptomics reveals molecular patterns underlying accumulation of p-Ser129 α-synuclein in a transgenic mouse model.NPJ Parkinson's disease · 2026Article
- Genetic factors and comorbid pathologies interact to drive regional mitophagy alterations in Lewy body dementia.Acta neuropathologica · 2025Article
- Primary age-related tauopathy.Acta neuropathologica · 2025Review
- High-Fat Diet Alters Behavior and Hippocampal Gene Expression.International journal of molecular sciences · 2025Article
- Alpha-synuclein abundance and localization are regulated by the RNA-binding protein PUMILIO1.Cell reports · 2025Article
- Reliability and modeling of digital histological measurements in Alzheimer's disease neuropathologic change and Lewy body disease.Journal of neuropathology and experimental neurology · 2025Article
- Dementia with Lewy bodies and Parkinson disease dementia - the same or different and is it important?Nature reviews. Neurology · 2025Review
- Pathological α-synuclein elicits granulovacuolar degeneration independent of tau.Translational neurodegeneration · 2025Article
- Potential therapeutic effects of curcumin, with or without L-DOPA, on motor and cognitive functions and hippocampal changes in rotenone-treated rats.Metabolic brain disease · 2025Article
- Co-pathologies modify hippocampal protein accumulation patterns in neurodegenerative diseases.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- AIMP2 accumulation in brain leads to cognitive deficits and blood secretion in Parkinson's disease.Journal of translational medicine · 2024Article
- Alpha-synuclein-induced stress sensitivity renders the Parkinson's disease brain susceptible to neurodegeneration.Acta neuropathologica communications · 2024Article
- A topographical atlas of α-synuclein dosage and cell type-specific expression in adult mouse brain and peripheral organs.NPJ Parkinson's disease · 2024Article
- Neuroimaging of autobiographical memory in dementia with Lewy bodies: a story of insula.Brain communications · 2024Article
- Amygdala-predominant α-synuclein pathology is associated with exacerbated hippocampal neuron loss in Alzheimer's disease.Brain communications · 2024Article
- Pathobiology of Cognitive Impairment in Parkinson Disease: Challenges and Outlooks.International journal of molecular sciences · 2023Review
18 more citing papers are in PubMed but not listed here.
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7 authors at 3 institutions in 1 country.
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Abstract
Despite considerable research to uncover them, the anatomic and neuropathologic correlates of memory impairment in dementia with Lewy bodies (DLB) remain unclear. While some studies have implicated Lewy bodies in the neocortex, others have pointed to α-synuclein pathology in the hippocampus. We systematically examined hippocampal Lewy pathology and its distribution in hippocampal subfields in 95 clinically and neuropathologically characterized human cases of DLB, finding that α-synuclein pathology was highest in two hippocampal-related subregions: the CA2 subfield and the entorhinal cortex (EC). While the EC had numerous classic somatic Lewy bodies, CA2 contained mainly Lewy neurites in presumed axon terminals, suggesting the involvement of the EC → CA2 circuitry in the pathogenesis of DLB symptoms. Clinicopathological correlations with measures of verbal and visual memory supported a role for EC Lewy pathology, but not CA2, in causing these memory deficits. Lewy pathology in CA1-the main output region for CA2-correlated best with results from memory testing despite a milder pathology. This result indicates that CA1 may be more functionally relevant than CA2 in the context of memory impairment in DLB. These correlations remained significant after controlling for several factors, including concurrent Alzheimer's pathology (neuritic plaques and neurofibrillary tangles) and the interval between time of testing and time of death. Our data suggest that although hippocampal Lewy pathology in DLB is predominant in CA2 and EC, memory performance correlates most strongly with CA1 burden.
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