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Cited by 367Parkinson's Disease Mechanisms and TreatmentsNeuroinflammation and Neurodegeneration MechanismsNuclear Receptors and Signaling

The DOI matches its Crossref record; 31 of the 32 references it cites were found in a registry or an index.

α-Synucleinopathy phenotypes

Open access
McCann, Heather, Stevens, Claire H., Cartwright, Heidi, Halliday, Glenda M.·2014·Parkinsonism & Related Disorders
DOI 10.1016/s1353-8020(13)70017-8
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Abstract

α-Synucleinopathies are neurodegenerative diseases characterised by the abnormal accumulation of α-synuclein aggregates in neurons, nerve fibres or glial cells. While small amounts of these α-synuclein pathologies can occur in some neurologically normal individuals who do not have associated neurodegeneration, the absence of neurodegeneration in such individuals precludes them from having a degenerative α-synucleinopathy, and it has yet to be established whether such individuals have a form of preclinical disease. There are three main types of α-synucleinopathy, Parkinson's disease (PD), dementia with Lewy bodies (DLB), and multiple system atrophy (MSA), with other rare disorders also having α-synuclein pathologies, such as various neuroaxonal dystrophies. Multiple clinical phenotypes exist for each of the three main α-synucleinopathies, with these phenotypes differing in the dynamic distribution of their underlying neuropathologies. Identifying the factors involved in causing different α-synuclein phenotypes may ultimately lead to more targeted therapeutics as well as more accurate clinical prognosis.

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Figure 2 Diagram illustrating the different pathological types of cases meeting clinical criteria for Parkinson's disease with dementia (PDD), dementia with Lewy bodies (DLB) and Alzheimer's disease (AD). Lewy-related pathologies (LRP) identified in sections from the temporal cortex and amygdala stained for α-synuclein immunohistochemistry and counterstained with cresyl violet. Plaques are identified in sections from temporal cortex stained for amyloid β immunohistochemistry and counterstained with cresyl violet. Neurofibrillary tangles (NFTs) identified in sections from the temporal cortex stained with a modified Bielschowsky silver stain.
Figure 2 Diagram illustrating the different pathological types of cases meeting clinical criteria for Parkinson's disease with dementia (PDD), dementia with Lewy bodies (DLB) and Alzheimer's disease (AD). Lewy-related pathologies (LRP) identified in sections from the temporal cortex and amygdala stained for α-synuclein immunohistochemistry and counterstained with cresyl violet. Plaques are identified in sections from temporal cortex stained for amyloid β immunohistochemistry and counterstained with cresyl violet. Neurofibrillary tangles (NFTs) identified in sections from the temporal cortex stained with a modified Bielschowsky silver stain.CC-BY-NC-ND · From the PDF
Figure 3 Photomicrographs of the substantia nigra (SN in A-D), putamen (E-H) and cerebellum (I-L) of representative controls (A, E, I) and cases with early and mild (B, F, J) or late and severe (C, G, K) MSA. Cases with MSA-P have substantial degeneration in the putamen (F, G) in addition to the substantia nigra (B, C), while cases with MSA-C have substantial degeneration in the cerebellum (J, K) in addition to the substantia nigra (B, C), as shown in haematoxylin and eosin stained sections. αSynuclein immunoreactive glial cytoplasmic inclusions are observed in all regions of neurodegeneration in MSA (D, H, L). cp=cerebral peduncle.
Figure 3 Photomicrographs of the substantia nigra (SN in A-D), putamen (E-H) and cerebellum (I-L) of representative controls (A, E, I) and cases with early and mild (B, F, J) or late and severe (C, G, K) MSA. Cases with MSA-P have substantial degeneration in the putamen (F, G) in addition to the substantia nigra (B, C), while cases with MSA-C have substantial degeneration in the cerebellum (J, K) in addition to the substantia nigra (B, C), as shown in haematoxylin and eosin stained sections. αSynuclein immunoreactive glial cytoplasmic inclusions are observed in all regions of neurodegeneration in MSA (D, H, L). cp=cerebral peduncle.CC-BY-NC-ND · From the PDF

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Metadata

Authors
McCann, H., Stevens, C. H., Cartwright, H., & Halliday, G. M.
Affiliations
  • Neuroscience Research Australia (AU)
  • UNSW Sydney (AU)
Corresponding author
Halliday, Glenda M.
ORCID
Venue
Parkinsonism & Related Disorders
Publisher
Elsevier BV
Published
2014-01
Volume
20
Pages
S62-S67
ISSN
1353-8020 (ISSN-L)
DOI
10.1016/s1353-8020(13)70017-8
OpenAlex
W2057784346
Cited by
364
References
32
Citations by year
2026: 8 · 2025: 23 · 2024: 55 · 2023: 28 · 2022: 37 · 2021: 43 · 2020: 37 · 2019: 32 · 2018: 23 · 2017: 27 · 2016: 29 · 2015: 17 · 2014: 5
FWCI
2.22
Type
journal article
Language
en
Open access
Licence
Locations
  • Parkinsonism & Related Disorders (publishedVersion)
  • PubMed (publishedVersion)
  • UNSWorks (University of New South Wales, Sydney, Australia) (submittedVersion, cc-by-nc-nd)
  • Research Online (University of Wollongong) (submittedVersion)
  • UNSWorks (UNSW Sydney) (submittedVersion, cc-by-nc-nd)
Funders
National Health and Medical Research Council (630434)
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
synucleinopathies, alpha-synuclein aggregation
MeSH terms
Humans, Parkinson Disease, Phenotype, Multiple System Atrophy, Lewy Body Disease, alpha-Synuclein

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