ArticleAnnals of clinical and translational neurology2022
Quantifying regional α -synuclein, amyloid β, and tau accumulation in lewy body dementia.
Article in Annals of clinical and translational neurology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 42 citations in OpenAlex.
- Cognitive impairment in Parkinson disease correlates with loss of cholinergic axon projections to cortex in an autopsy study.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Amyloid exacerbates tau and alpha-synuclein pathologies, behavioral impairments, and neuroinflammation in a mixed dementia model.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Characteristics and mechanisms of cognitive impairment in Parkinson disease.Nature reviews. Neurology · 2026Review
- Longitudinal brain morphometry in Parkinson's disease clinical subtypes: Distinct signatures forecast behavioral change within subtypes.Parkinsonism & related disorders · 2026Article
- Alpha-synuclein deposition patterns in Alzheimer's disease: association with cortical amyloid beta and variable tau load.Acta neuropathologica · 2025Article
- Identification of small molecule dimethyoxyphenyl piperazine inhibitors of alpha-synuclein fibril growth.Scientific reports · 2025Article
- Article
- Tackling a disease on a global scale, the Global Parkinson's Genetics Program, GP2: A new generation of opportunities.American journal of human genetics · 2025Review
- Combining GWAS Summary Data and Proteomics Identified Potential Drug Targets in Dementia.Molecular neurobiology · 2025Article
- PINK1 deficiency permits the development of Lewy body dementia with coexisting Aβ pathology.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Clinical Evolution of Neuropsychiatric Symptoms in Alzheimer's Disease and Dementia With Lewy Bodies in a Post-Mortem Cohort.International journal of geriatric psychiatry · 2025Article
- Blood-brain barrier breakdown in dementia with Lewy bodies.Fluids and barriers of the CNS · 2024Article
- Structure of alpha-synuclein fibrils derived from human Lewy body dementia tissue.Nature communications · 2024Article
- Tau maturation in the clinicopathological spectrum of Lewy body and Alzheimer's disease.Annals of clinical and translational neurology · 2024Article
- Mild cognitive impairment in Parkinson's disease: current view.Frontiers in cognition · 2024Review
- The molecular spectrum of amyloid-beta (Aβ) in neurodegenerative diseases beyond Alzheimer's disease.Brain pathology (Zurich, Switzerland) · 2024Article
- Mild cognitive impairment in dementia with Lewy bodies: an update and outlook.Journal of neural transmission (Vienna, Austria : 1996) · 2023Review
- Morphological characteristics differentiate dementia with Lewy bodies from Parkinson disease with and without dementia.Journal of neural transmission (Vienna, Austria : 1996) · 2023Article
- Dual Anta-Inhibitors Targeting Protein Kinase CK1δ and AMolecules (Basel, Switzerland) · 2023Article
- Review
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Authors and funding
14 authors at 1 institution in 2 countries.
Funding
Abstract
objectiveParkinson disease (PD) is defined by the accumulation of misfolded α-synuclein (α-syn) in Lewy bodies and Lewy neurites. It affects multiple cortical and subcortical neuronal populations. The majority of people with PD develop dementia, which is associated with Lewy bodies in neocortex and referred to as Lewy body dementia (LBD). Other neuropathologic changes, including amyloid β (Aβ) and tau accumulation, occur in some LBD cases. We sought to quantify α-syn, Aβ, and tau accumulation in neocortical, limbic, and basal ganglia regions.
methodsWe isolated insoluble protein from fresh frozen postmortem brain tissue samples for eight brains regions from 15 LBD, seven Alzheimer disease (AD), and six control cases. We measured insoluble α-syn, Aβ, and tau with recently developed sandwich ELISAs.
resultsWe detected a wide range of insoluble α-syn accumulation in LBD cases. The majority had substantial α-syn accumulation in most regions, and dementia severity correlated with neocortical α-syn. However, three cases had low neocortical levels that were indistinguishable from controls. Eight LBD cases had substantial Aβ accumulation, although the mean Aβ level in LBD was lower than in AD. The presence of Aβ was associated with greater α-syn accumulation. Tau accumulation accompanied Aβ in only one LBD case.
interpretationLBD is associated with insoluble α-syn accumulation in neocortical regions, but the relatively low neocortical levels in some cases suggest that other changes contribute to impaired function, such as loss of neocortical innervation from subcortical regions. The correlation between Aβ and α-syn accumulation suggests a pathophysiologic relationship between these two processes.
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