ArticleThe American journal of pathology1999
Non-Abeta component of Alzheimer's disease amyloid (NAC) revisited. NAC and alpha-synuclein are not associated with Abeta amyloid.
Article in The American journal of pathology, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.
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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.
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Who cites it
57 citing papers in PubMed, 180 citations in OpenAlex.
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- Toward common treatment strategies: convergent proteinopathies and mitochondrial dysfunction in Alzheimer's and Parkinson's diseases.Frontiers in neuroscience · 2026Review
- Dissecting the Molecular Determinants of α-synuclein Phase Separation and Condensate Aging: The Pivotal Role of β-Sheet-Rich Motifs.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- Parkinson's disease mutant Miro1 causes mitochondrial dysfunction and dopaminergic neuron loss.Brain : a journal of neurology · 2025Article
- Differential role of C-terminal truncations on alpha-synuclein pathology and Lewy body formation.NPJ Parkinson's disease · 2025Article
- Novel in situ seeding immunodetection assay uncovers neuronal-driven alpha-synuclein seeding in Parkinson's disease.NPJ Parkinson's disease · 2025Article
- Broken but not beaten: Challenge of reducing the amyloids pathogenicity by degradation.Journal of advanced research · 2025Review
- Molecular Insights into α-Synuclein Fibrillation: A Raman Spectroscopy and Machine Learning Approach.ACS chemical neuroscience · 2025Article
- Strategies of positron emission tomography (PET) tracer development for imaging of tau and α-synuclein in neurodegenerative disorders.RSC medicinal chemistry · 2025Review
- Generation of G51D and 3D mice reveals decreased α-synuclein tetramer-monomer ratios promote Parkinson's disease phenotypes.NPJ Parkinson's disease · 2024Article
- Development and validation of an expanded antibody toolset that captures alpha-synuclein pathological diversity in Lewy body diseases.NPJ Parkinson's disease · 2023Article
- Monitoring α-synuclein aggregation.Neurobiology of disease · 2023Review
- Opportunities and challenges of alpha-synuclein as a potential biomarker for Parkinson's disease and other synucleinopathies.NPJ Parkinson's disease · 2022Review
- Immunohistochemical Demonstration of the pGlu79 α-Synuclein Fragment in Alzheimer's Disease and Its Tg2576 Mouse Model.Biomolecules · 2022Article
- Lipase regulation of cellular fatty acid homeostasis as a Parkinson's disease therapeutic strategy.NPJ Parkinson's disease · 2022Article
- Extracellular Alpha-Synuclein: Mechanisms for Glial Cell Internalization and Activation.Biomolecules · 2022Review
- Alpha-synuclein research: defining strategic moves in the battle against Parkinson's disease.NPJ Parkinson's disease · 2021Review
- Reverse engineering Lewy bodies: how far have we come and how far can we go?Nature reviews. Neuroscience · 2021Review
- Case Report: Synucleinopathy Associated WithFrontiers in veterinary science · 2021Article
- The emerging role of α-synuclein truncation in aggregation and disease.The Journal of biological chemistry · 2020Review
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
alpha-Synuclein (alphaSN), also termed the precursor of the non-Abeta component of Alzheimer's disease (AD) amyloid (NACP), is a major component of Lewy bodies and Lewy neurites pathognomonic of Parkinson's disease (PD) and dementia with Lewy bodies (DLB). A fragment of alphaSN termed the non-Abeta component of AD amyloid (NAC) had previously been identified as a constituent of AD amyloid plaques. To clarify the relationship of NAC and alphaSN with Abeta plaques, antibodies were raised to three domains of alphaSN. All antibodies produced punctate labeling of human cortex and strong labeling of Lewy bodies. Using antibodies to alphaSN(75-91) to label cortical and hippocampal sections of pathologically proven AD cases, we found no evidence for NAC in Abeta amyloid plaques. Double labeling of tissue sections in mixed DLB/AD cases revealed alphaSN in dystrophic neuritic processes, some of which were in close association with Abeta plaques restricted to the CA1 hippocampal region. In brain homogenates alphaSN was predominantly recovered in the cytosolic fraction as a 16-kd protein on Western analysis; however, significant amounts of aggregated and alphaSN fragments were also found in urea extracts of SDS-insoluble material from DLB and PD cases. NAC antibodies identified an endogenous fragment of 6 kd in the cytosolic and urea-soluble brain fractions. This fragment may be produced as a consequence of alphaSN aggregation or alternatively may accelerate aggregation of the full-length alphaSN.
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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.