ArticleActa neuropathologica2010
Cell type specific sequestration of choline acetyltransferase and tyrosine hydroxylase within Lewy bodies.
Article in Acta neuropathologica, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 45 citations in OpenAlex.
- Modeling Parkinson's pathology in human iPSC dopaminergic neurons uncovers key mechanisms of Lewy body formation and heterogeneity.Science advances · 2026Article
- α-Synuclein Pathology in Synucleinopathies: Mechanisms, Biomarkers, and Therapeutic Challenges.International journal of molecular sciences · 2025Review
- Liganded magnetic nanoparticles for magnetic resonance imaging of α-synuclein.NPJ Parkinson's disease · 2025Article
- Visual hallucinations in Parkinson's disease: spotlight on central cholinergic dysfunction.Brain : a journal of neurology · 2025Review
- Kisspeptin-10 Mitigates α-Synuclein-Mediated Mitochondrial Apoptosis in SH-SY5Y-Derived Neurons via a Kisspeptin Receptor-Independent Manner.International journal of molecular sciences · 2023Article
- The roles of connectivity and neuronal phenotype in determining the pattern of α-synuclein pathology in Parkinson's disease.Neurobiology of disease · 2022Review
- Neuropathology and molecular diagnosis of Synucleinopathies.Molecular neurodegeneration · 2021Review
- Alpha-Synuclein Post-translational Modifications: Implications for Pathogenesis of Lewy Body Disorders.Frontiers in aging neuroscience · 2021Review
- Neuropathology and pathogenesis of extrapyramidal movement disorders: a critical update-I. Hypokinetic-rigid movement disorders.Journal of neural transmission (Vienna, Austria : 1996) · 2019Review
- Hippocampal CA2 Lewy pathology is associated with cholinergic degeneration in Parkinson's disease with cognitive decline.Acta neuropathologica communications · 2019Article
- Parkinson's Disease Is Not Simply a Prion Disorder.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017Review
- Pathology of Neurodegenerative Diseases.Cold Spring Harbor perspectives in biology · 2017Review
- Selective neuronal vulnerability in Parkinson disease.Nature reviews. Neuroscience · 2017Review
- Embryonic development of selectively vulnerable neurons in Parkinson's disease.NPJ Parkinson's disease · 2017Review
- Neuropathological Staging of Brain Pathology in Sporadic Parkinson's disease: Separating the Wheat from the Chaff.Journal of Parkinson's disease · 2017Review
- Potential Pathways of Abnormal Tau and α-Synuclein Dissemination in Sporadic Alzheimer's and Parkinson's Diseases.Cold Spring Harbor perspectives in biology · 2016Review
- α-synuclein interacts with SOD1 and promotes its oligomerization.Molecular neurodegeneration · 2015Article
- Cutaneous neuropathy in Parkinson's disease: a window into brain pathology.Acta neuropathologica · 2014Article
- The Lewy body in Parkinson's disease and related neurodegenerative disorders.Molecular neurobiology · 2013Review
- Sequence variants in eukaryotic translation initiation factor 4-gamma (eIF4G1) are associated with Lewy body dementia.Acta neuropathologica · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Lewy bodies (LBs), the pathological hallmark of Lewy body disease (LBD), contain α-synuclein, as well as other proteins. In this study, we examined the relationship of α-synuclein to two rate-limiting enzymes in neurotransmitter synthesis, tyrosine hydroxylase (TH) and choline acetyltransferase (ChAT). Double-labeling immunohistochemistry for α-synuclein and TH revealed TH immunoreactivity within LBs in catecholaminergic neurons in the substantia nigra and locus coeruleus, but not within LBs in cholinergic neurons in the pedunculopontine nucleus and nucleus basalis of Meynert. In contrast, ChAT immunoreactivity within LBs was detected in cholinergic, but not within LBs in catecholaminergic neurons. The amygdala was devoid of TH and ChAT positive LBs, although a few Lewy neurites contained ChAT immunoreactivity. Further analysis revealed two distinct patterns of neurotransmitter immunoreactivity within LBs. One pattern had diffuse co-localization of TH or ChAT with α-synuclein as in cortical-type LBs, while the other had intense TH or ChAT immunoreactivity in the LB core surrounded by a peripheral rim of α-synuclein as in brainstem-type LBs. Levels of both TH and ChAT were higher in brainstem-type LBs than in the cytoplasm of the same neuron or in neurons from the same case devoid of LBs. Given the fact that LB-containing neurons have decreases in cytoplasmic TH and ChAT immunoreactivity, these results suggest LBs may disrupt cholinergic and catecholaminergic neurotransmitter production by sequestration of the rate-limiting enzymes for acetylcholine and catecholamine synthesis.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.