The DOI matches its Crossref record; 52 of the 52 references it cites were found in a registry or an index.
Accumulation of α-synuclein/NACP is a cytopathological feature common to Lewy body disease and multiple system atrophy
Abstract
Recently, we have shown that the precursor of the non-Abeta component of Alzheimer's disease amyloid (NACP), also known as alpha-synuclein, is a major component of Lewy bodies (LBs) as well as neuronal and glial cytoplasmic inclusions in multiple system atrophy (MSA). To elucidate whether the accumulation of NACP is specific to LB disease and MSA, we further studied 83 autopsied cases with various neurological disorders, using anti-NACP antibodies. In LB disease, NACP immunoreactivity was present in all of the LBs and Lewy neurites in both the central and peripheral nervous systems, the pale bodies in the substantia nigra, and dystrophic neurites in the hippocampal CA2/3 region. Immunoelectron microscopy revealed that the reaction product was localized within filamentous structures and associated granular structures. In MSA, NACP immunoreactivity was found in the intracytoplasmic inclusions of both neuronal and oligodendroglial cells, neuronal intranuclear inclusions, and swollen neuronal processes. No NACP immunoreactivity was found in a variety of other neuronal or glial inclusions in other disorders, including Alzheimer's disease, Pick's disease, progressive supranuclear palsy, corticobasal degeneration, motor neuron disease and triplet-repeat diseases. These findings strongly suggest that the accumulation of NACP is a cytopathological feature common to LB disease and MSA.
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“MSA is a synucleinopathy, however, unlike PD and dementia with Lewy bodies, in which α-syn accumulates and aggregates in neurons, MSA is characterized neuropathologically by α-syn-positive glial cytoplasmic inclusions (GCIs) in oligodendroglia [1, 42, 54, 58, 59].”
From Novel oligodendroglial alpha synuclein viral vector models of multiple system atrophy: studies in rodents and nonhuman primates (2017) · cites this paper as [58]
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Metadata
- Authors
- Wakabayashi, K., Hayashi, S., Kakita, A., Yamada, M., Toyoshima, Y., Yoshimoto, M., & Takahashi, H.
- Affiliations
- Brain Research Institute, Niigata University (JP)
- Taisho Pharmaceutical (Japan) (JP)
- ORCID
- Venue
- Acta Neuropathologica
- Published
- 1998-11-01
- Volume
- 96
- Issue
- 5
- Pages
- 445-452
- ISSN
- 0001-6322 (ISSN-L)
- 1432-0533
- OpenAlex
- W2016816471
- Cited by
- 347
- References
- 52
- Citations by year
- 2026: 1 · 2025: 9 · 2024: 9 · 2023: 11 · 2022: 8 · 2021: 13 · 2020: 10 · 2019: 8 · 2018: 4 · 2017: 11 · 2016: 7 · 2015: 6 · 2014: 4 · 2013: 6 · 2012: 9
- FWCI
- 22.57
- Type
- journal article
- Language
- en
- Open access
- closed
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Acta Neuropathologica (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nuclear Receptors and Signaling
- Keywords
- alpha-synuclein, Lewy bodies, multiple system atrophy, Lewy body disease, Lewy neurites, substantia nigra, dystrophic neurites, neuronal intranuclear inclusions, oligodendroglial inclusions, cytopathology, immunoreactivity, immunoelectron microscopy
- MeSH terms
- Humans, Immunohistochemistry, Nerve Degeneration, Nerve Tissue Proteins, Nervous System Diseases, Parkinson Disease, Microscopy, Immunoelectron, Lewy Bodies, Cellular Senescence, Multiple System Atrophy, Synucleins, alpha-Synuclein
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