ArticleJournal of neural transmission (Vienna, Austria : 1996)2014
A quantitative study of α-synuclein pathology in fifteen cases of dementia associated with Parkinson disease.
Article in Journal of neural transmission (Vienna, Austria : 1996), 2014. 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.
- Hippocampal subfields: volume, neuropathological vulnerability and cognitive decline in Alzheimer's and Parkinson's disease.Alzheimer's research & therapy · 2025Article
- Chronic stress induces depression-like behaviors and Parkinsonism via upregulating α-synuclein.NPJ Parkinson's disease · 2025Article
- Synaptic mechanisms underlying onset and progression of memory deficits caused by hippocampal and midbrain synucleinopathy.NPJ Parkinson's disease · 2023Article
- Quantifying regional α -synuclein, amyloid β, and tau accumulation in lewy body dementia.Annals of clinical and translational neurology · 2022Article
- Exposure of α-Synuclein Aggregates to Organotypic Slice Cultures Recapitulates Key Molecular Features of Parkinson's Disease.Frontiers in neurology · 2022Article
- The Human Hippocampus in Parkinson's Disease: An Integrative Stereological and Proteomic Study.Journal of Parkinson's disease · 2021Article
- Do multiple system atrophy and Parkinson's disease show distinct patterns of volumetric alterations across hippocampal subfields? An exploratory study.European radiology · 2019Article
- Neuropathology and pathogenesis of extrapyramidal movement disorders: a critical update-I. Hypokinetic-rigid movement disorders.Journal of neural transmission (Vienna, Austria : 1996) · 2019Review
- Baseline concentration of misfolded α-synuclein aggregates in cerebrospinal fluid predicts risk of cognitive decline in Parkinson's disease.Neuropathology and applied neurobiology · 2019Article
- Hippocampal CA2 Lewy pathology is associated with cholinergic degeneration in Parkinson's disease with cognitive decline.Acta neuropathologica communications · 2019Article
- Gintonin Mitigates MPTP-Induced Loss of Nigrostriatal Dopaminergic Neurons and Accumulation of α-Synuclein via the Nrf2/HO-1 Pathway.Molecular neurobiology · 2019Article
- Expression of α-synuclein is regulated in a neuronal cell type-dependent manner.Anatomical science international · 2019Review
- Differential α-synuclein expression contributes to selective vulnerability of hippocampal neuron subpopulations to fibril-induced toxicity.Acta neuropathologica · 2018Article
- Critical appraisal of pathology transmission in the α-synuclein fibril model of Lewy body disorders.Experimental neurology · 2018Article
- The BSSG rat model of Parkinson's disease: progressing towards a valid, predictive model of disease.The EPMA journal · 2017Review
- Laminar degeneration of frontal and temporal cortex in Parkinson disease dementia.Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology · 2017Article
- Synucleinopathies: common features and hippocampal manifestations.Cellular and molecular life sciences : CMLS · 2017Review
- Hippocampal α-Synuclein in Dementia with Lewy Bodies Contributes to Memory Impairment and Is Consistent with Spread of Pathology.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Article
- A quantitative study of tau pathology in 11 cases of chronic traumatic encephalopathy.Neuropathology and applied neurobiology · 2017Article
- The Retina in Multiple System Atrophy: Systematic Review and Meta-Analysis.Frontiers in neurology · 2017Review
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
The α-synuclein-immunoreactive pathology of dementia associated with Parkinson disease (DPD) comprises Lewy bodies (LB), Lewy neurites (LN), and Lewy grains (LG). The densities of LB, LN, LG together with vacuoles, neurons, abnormally enlarged neurons (EN), and glial cell nuclei were measured in fifteen cases of DPD. Densities of LN and LG were up to 19 and 70 times those of LB, respectively, depending on region. Densities were significantly greater in amygdala, entorhinal cortex (EC), and sectors CA2/CA3 of the hippocampus, whereas middle frontal gyrus, sector CA1, and dentate gyrus were least affected. Low densities of vacuoles and EN were recorded in most regions. There were differences in the numerical density of neurons between regions, but no statistical difference between patients and controls. In the cortex, the density of LB and vacuoles was similar in upper and lower laminae, while the densities of LN and LG were greater in upper cortex. The densities of LB, LN, and LG were positively correlated. Principal components analysis suggested that DPD cases were heterogeneous with pathology primarily affecting either hippocampus or cortex. The data suggest in DPD: (1) ratio of LN and LG to LB varies between regions, (2) low densities of vacuoles and EN are present in most brain regions, (3) degeneration occurs across cortical laminae, upper laminae being particularly affected, (4) LB, LN and LG may represent degeneration of the same neurons, and (5) disease heterogeneity may result from variation in anatomical pathway affected by cell-to-cell transfer of α-synuclein.
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