The DOI matches its Crossref record; 35 of the 35 references it cites were found in a registry or an index.
α-Synuclein-positive structures in cases with sporadic Alzheimer’s disease: morphology and its relationship to tau aggregation
Abstract
Alzheimer's disease (AD) and Parkinson's disease share common clinical and pathological features. In this study, we examined the relationship between AD pathology and alpha-synuclein aggregation. The frequency and distribution of alpha-synuclein-positive structures were systematically investigated in 27 cases with sporadic AD by alpha-synuclein immuno-histochemistry. Thirteen (48.2%) of 27 cases had various alpha-synuclein-positive structures as well as Lewy bodies. The frequency and density of senile plaques and neurofibrillary tangles were not significantly different between cases with alpha-synuclein structures and those without. alpha-Synuclein-positive structures were found most frequently in the amygdala. The alpha-synuclein-positive inclusions that are different from Lewy bodies were observed at the highest rate in the hippocampus. The discovery of alpha-synuclein as the constituent of Lewy bodies facilitated the detection of Lewy-related structures even in AD cases with widespread and numerous neurofibrillary tangles. alpha-Synuclein-positive inclusions except for Lewy bodies are exposed, and the distribution of them indicates that Lewy body formation may be influenced by the degree of tau aggregation. This study also supports the suggestion that cases with AD pathology can be classified into two groups according to the existence or absence of alpha-synuclein aggregation.
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“co-morbid αSyn pathology has been reported in more than half of all autopsy-confirmed AD cases [22–24]”
From α-synuclein in the pathophysiology of Alzheimer’s disease (2019) · cites this paper as [24]
In the citing paper
“co-morbid αSyn pathology has been reported in more than half of all autopsy-confirmed AD cases [22–24]”
From α-synuclein in the pathophysiology of Alzheimer’s disease (2019) · cites this paper as [24]
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Cites
McKhann, G., Drachman, D., Folstein, M., Katzman, R., Price, D., & Stadlan, E. M. (1984) · Neurology · doi:10.1212/wnl.34.7.939 · Cited by 27,915
Neuropathological stageing of Alzheimer-related changes.
Braak, H., & Braak, E. (1991) · Acta Neuropathologica · doi:10.1007/bf00308809 · Cited by 16,123
Spillantini, M. G., Schmidt, M. L., Lee, V. M.-Y., Trojanowski, J. Q., Jakes, R., & Goedert, M. (1997) · Nature · doi:10.1038/42166 · Cited by 8,382
Mirra, S. S., Heyman, A., McKeel, D., Sumi, S. M., Crain, B. J., Brownlee, L. M., Vogel, F. S., Hughes, J. P., Belle, G. V., Berg, L., et al. (1991) · Neurology · doi:10.1212/wnl.41.4.479 · Cited by 4,961
McKeith, I. G., Galasko, D., Kosaka, K., Perry, E. K., Dickson, D. W., Hansen, L. A., Salmon, D. P., Lowe, J., Mirra, S. S., Byrne, E. J., et al. (1996) · Neurology · doi:10.1212/wnl.47.5.1113 · Cited by 3,960
(1998) · Europe PMC (PubMed Central) · Cited by 1,594
HYMAN, B. T., & TROJANOWSKI, J. Q. (1997) · Journal of Neuropathology and Experimental Neurology · doi:10.1097/00005072-199710000-00002 · Cited by 1,542
Conway, K. A., Harper, J. D., & Lansbury, P. T. (1998) · Nature Medicine · doi:10.1038/3311 · Cited by 1,520
Molecular cloning of cDNA encoding an unrecognized component of amyloid in Alzheimer disease.
Uéda, K., Fukushima, H., Masliah, E., Xia, Y., Iwai, A., Yoshimoto, M., Otero, D. A., Kondo, J. D. M., Ihara, Y., & Saitoh, T. (1993) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.90.23.11282 · Cited by 1,502
(1964) · The Medical Journal of Australia · doi:10.5694/j.1326-5377.1964.tb115841.x · Cited by 1,411
Cited by
Sorted by citations
Conformational constraints for amyloid fibrillation: the importance of being unfolded
Uversky, V. N., & Fink, A. L. (2004) · Biochimica et Biophysica Acta (BBA) - Proteins and Proteomics · doi:10.1016/j.bbapap.2003.12.008 · Cited by 1,022
Neuroinflammation as a common feature of neurodegenerative disorders
Guzman-Martinez, L., Maccioni, R. B., Andrade, V., Navarrete, L. P., Pastor, M. G., & Ramos-Escobar, N. (2019) · Frontiers in Pharmacology · doi:10.3389/fphar.2019.01008 · Cited by 702
Plasma exosomal α-synuclein is likely CNS-derived and increased in Parkinson’s disease
Shi, M., Liu, C., Cook, T. J., Bullock, K. M., Zhao, Y., Ginghina, C., Li, Y., Aro, P., Dator, R., He, C., et al. (2014) · Acta Neuropathologica · doi:10.1007/s00401-014-1314-y · Cited by 676
Neuropathology of sporadic Parkinson's disease: Evaluation and changes of concepts
Jellinger, K. A. (2011) · Movement Disorders · doi:10.1002/mds.23795 · Cited by 480
Colocalization of Tau and Alpha-Synuclein Epitopes in Lewy Bodies
Ishizawa, T., Mattila, P. M., Davies, P., Wang, D., & Dickson, D. W. (2003) · Journal of Neuropathology & Experimental Neurology · doi:10.1093/jnen/62.4.389 · Cited by 402
Metadata
- Authors
- Arai, Y., Yamazaki, M., Mori, O., Muramatsu, H., Asano, G., & Katayama, Y.
- Affiliations
- Nippon Medical School (JP)
- Corresponding author
- Yamazaki, Mineo
- Venue
- Brain Research
- Publisher
- Elsevier BV
- Published
- 2001-01
- Volume
- 888
- Issue
- 2
- Pages
- 287-296
- ISSN
- 0006-8993 (ISSN-L)
- OpenAlex
- W2072878433
- Cited by
- 173
- References
- 35
- Citations by year
- 2026: 7 · 2025: 16 · 2024: 11 · 2023: 8 · 2022: 13 · 2021: 13 · 2020: 7 · 2019: 8 · 2018: 2 · 2016: 4 · 2014: 6 · 2013: 5 · 2012: 2
- FWCI
- 5.98
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Brain Research (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- alpha-synuclein, sporadic Alzheimer's disease, Lewy bodies, tau aggregation, neurofibrillary tangles, amyloid plaques, amygdala, hippocampus, Alzheimer's disease classification
- MeSH terms
- Aged, Aged, 80 and over, Alzheimer Disease, Brain, Inclusion Bodies, Female, Humans, Immunohistochemistry, Male, Middle Aged, Nerve Tissue Proteins, Neurites, Neurofibrillary Tangles, tau Proteins, Microscopy, Confocal, Synucleins, alpha-Synuclein, Plaque, Amyloid
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