Autonomic dysfunction in genetic forms of synucleinopathies Article Swipe
Viorica Chelban
,
Ekawat Vichayanrat
,
Lucia Schottlaende
,
Valeria Iodice
,
Henry Houlden
·
YOU?
·
· 2018
· Open Access
·
· DOI: https://doi.org/10.1002/mds.27343
YOU?
·
· 2018
· Open Access
·
· DOI: https://doi.org/10.1002/mds.27343
The discovery of genetic links between alpha‐synuclein and PD has opened unprecedented opportunities for research into a new group of diseases, now collectively known as synucleinopathies. Autonomic dysfunction, including cardiac sympathetic denervation, has been reported in familial forms of synucleinopathies that have Lewy bodies at the core of their pathogenesis. SNCA mutations and multiplications, LRRK2 disease with Lewy bodies as well as other common, sporadic forms of idiopathic PD, MSA, pure autonomic failure, and dementia with Lewy bodies have all been associated with dysautonomia. By contrast, in familial cases of parkinsonism without Lewy bodies, such as in PARK2 , the autonomic profile remains normal throughout the course of the disease. The degeneration of the central and peripheral autonomic systems in genetic as well as sporadic forms of neurodegenerative synucleinopathies correlates with the accumulation of alpha‐synuclein immunoreactive‐containing inclusions. Given that dysautonomia has a significant impact on the quality of life of sufferers and autonomic symptoms are generally treatable, a prompt diagnostic testing and treatment should be provided. Moreover, new evidence suggests that autonomic dysfunction can be used as an outcome prediction factor in some forms of synucleinopathies or premotor diagnostic markers that could be used in the future to define further research avenues. In this review, we describe the autonomic dysfunction of genetic synucleinopathies in comparison to the dysautonomia of sporadic forms of alpha‐synuclein accumulation and provide the reader with an up‐to‐date overview of the current understanding in this fast‐growing field. © 2018 International Parkinson and Movement Disorder Society
Related Topics
Concepts
Synucleinopathies
Dysautonomia
Dementia with Lewy bodies
Pure autonomic failure
Neuroscience
Parkinson's disease
Lewy body
Medicine
Alpha-synuclein
Disease
Pathology
Psychology
Dementia
Internal medicine
Orthostatic vital signs
Blood pressure
Metadata
- Type
- review
- Language
- en
- Landing Page
- https://doi.org/10.1002/mds.27343
- OA Status
- gold
- Cited By
- 25
- References
- 154
- Related Works
- 10
- OpenAlex ID
- https://openalex.org/W2790064437
All OpenAlex metadata
Raw OpenAlex JSON
- OpenAlex ID
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https://openalex.org/W2790064437Canonical identifier for this work in OpenAlex
- DOI
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https://doi.org/10.1002/mds.27343Digital Object Identifier
- Title
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Autonomic dysfunction in genetic forms of synucleinopathiesWork title
- Type
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reviewOpenAlex work type
- Language
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enPrimary language
- Publication year
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2018Year of publication
- Publication date
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2018-03-01Full publication date if available
- Authors
-
Viorica Chelban, Ekawat Vichayanrat, Lucia Schottlaende, Valeria Iodice, Henry HouldenList of authors in order
- Landing page
-
https://doi.org/10.1002/mds.27343Publisher landing page
- Open access
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YesWhether a free full text is available
- OA status
-
goldOpen access status per OpenAlex
- OA URL
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https://ibn.idsi.md/vizualizare_articol/131866Direct OA link when available
- Concepts
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Synucleinopathies, Dysautonomia, Dementia with Lewy bodies, Pure autonomic failure, Neuroscience, Parkinson's disease, Lewy body, Medicine, Alpha-synuclein, Disease, Pathology, Psychology, Dementia, Internal medicine, Orthostatic vital signs, Blood pressureTop concepts (fields/topics) attached by OpenAlex
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25Total citation count in OpenAlex
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2025: 2, 2024: 3, 2023: 4, 2022: 4, 2021: 3Per-year citation counts (last 5 years)
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154Number of works referenced by this work
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10Other works algorithmically related by OpenAlex
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| abstract_inverted_index.correlates | 130 |
| abstract_inverted_index.diagnostic | 160, 189 |
| abstract_inverted_index.idiopathic | 68 |
| abstract_inverted_index.peripheral | 117 |
| abstract_inverted_index.prediction | 180 |
| abstract_inverted_index.throughout | 105 |
| abstract_inverted_index.treatable, | 157 |
| abstract_inverted_index.dysfunction | 173, 210 |
| abstract_inverted_index.inclusions. | 137 |
| abstract_inverted_index.significant | 143 |
| abstract_inverted_index.sympathetic | 31 |
| abstract_inverted_index.accumulation | 133, 224 |
| abstract_inverted_index.collectively | 23 |
| abstract_inverted_index.degeneration | 112 |
| abstract_inverted_index.denervation, | 32 |
| abstract_inverted_index.dysautonomia | 140, 218 |
| abstract_inverted_index.dysfunction, | 28 |
| abstract_inverted_index.parkinsonism | 91 |
| abstract_inverted_index.International | 243 |
| abstract_inverted_index.dysautonomia. | 84 |
| abstract_inverted_index.opportunities | 13 |
| abstract_inverted_index.pathogenesis. | 50 |
| abstract_inverted_index.understanding | 236 |
| abstract_inverted_index.unprecedented | 12 |
| abstract_inverted_index.fast‐growing | 239 |
| abstract_inverted_index.up‐to‐date | 231 |
| abstract_inverted_index.multiplications, | 54 |
| abstract_inverted_index.alpha‐synuclein | 7, 135, 223 |
| abstract_inverted_index.neurodegenerative | 128 |
| abstract_inverted_index.synucleinopathies | 40, 129, 186, 213 |
| abstract_inverted_index.synucleinopathies. | 26 |
| abstract_inverted_index.immunoreactive‐containing | 136 |
| cited_by_percentile_year.max | 97 |
| cited_by_percentile_year.min | 94 |
| corresponding_author_ids | https://openalex.org/A5014701168 |
| countries_distinct_count | 2 |
| institutions_distinct_count | 5 |
| corresponding_institution_ids | https://openalex.org/I4210121123, https://openalex.org/I4210151618, https://openalex.org/I45129253 |
| citation_normalized_percentile.value | 0.83941321 |
| citation_normalized_percentile.is_in_top_1_percent | False |
| citation_normalized_percentile.is_in_top_10_percent | False |