Serum and CSF alpha-synuclein levels do not change in COVID-19 patients with neurological symptoms
SARS-CoV-2 infection can associate diverse neurological manifestations. Several studies have provided proof to support the theory of neurotropic involvement of SARS-CoV-2. Alpha-synuclein has been described as a native antiviral factor within neurons, and upregulation of this protein can be seen in...
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| Veröffentlicht in: | Journal of neurology 2021-09, Vol.268 (9), p.3116-3124 |
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| creator | Blanco-Palmero, V. A. Azcárate-Díaz, F. J. Ruiz-Ortiz, M. Laespada-García, M. I. Rábano-Suárez, P. Méndez-Guerrero, A. Aramendi-Ramos, M. Eguiburu, J. L. Pérez-Rivilla, A. Marchán-López, A. Rubio-Fernández, M. Carro, E. González de la Aleja, J. |
| description | SARS-CoV-2 infection can associate diverse neurological manifestations. Several studies have provided proof to support the theory of neurotropic involvement of SARS-CoV-2. Alpha-synuclein has been described as a native antiviral factor within neurons, and upregulation of this protein can be seen in animals that suffered other neuroinvasive infections. To assess if increased expression of this protein takes place in COVID-19 patients with neurological symptoms, we analyzed serum total alpha-synuclein levels in three groups: seven COVID-19 patients with myoclonus, Parkinsonism and/or encephalopathy; thirteen age- and sex-matched COVID-19 patients without neurological involvement and eight age- and sex-matched healthy controls. We did not find differences among them. In a subset of four patients, the change in serum alpha-synuclein before and after the onset of neurological symptoms was not significant either. Cerebrospinal fluid alpha-synuclein levels were also similar between neurological COVID-19 and healthy controls. Overall, these results cannot support the hypothesis of alpha-synuclein upregulation in humans with neurological symptoms in COVID-19. Further research taking into account a larger group of COVID-19 patients including the whole spectrum of neurological manifestations and disease severity is needed. |
| doi_str_mv | 10.1007/s00415-021-10444-6 |
| format | Article |
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A. ; Azcárate-Díaz, F. J. ; Ruiz-Ortiz, M. ; Laespada-García, M. I. ; Rábano-Suárez, P. ; Méndez-Guerrero, A. ; Aramendi-Ramos, M. ; Eguiburu, J. L. ; Pérez-Rivilla, A. ; Marchán-López, A. ; Rubio-Fernández, M. ; Carro, E. ; González de la Aleja, J.</creator><creatorcontrib>Blanco-Palmero, V. A. ; Azcárate-Díaz, F. J. ; Ruiz-Ortiz, M. ; Laespada-García, M. I. ; Rábano-Suárez, P. ; Méndez-Guerrero, A. ; Aramendi-Ramos, M. ; Eguiburu, J. L. ; Pérez-Rivilla, A. ; Marchán-López, A. ; Rubio-Fernández, M. ; Carro, E. ; González de la Aleja, J.</creatorcontrib><description>SARS-CoV-2 infection can associate diverse neurological manifestations. Several studies have provided proof to support the theory of neurotropic involvement of SARS-CoV-2. Alpha-synuclein has been described as a native antiviral factor within neurons, and upregulation of this protein can be seen in animals that suffered other neuroinvasive infections. To assess if increased expression of this protein takes place in COVID-19 patients with neurological symptoms, we analyzed serum total alpha-synuclein levels in three groups: seven COVID-19 patients with myoclonus, Parkinsonism and/or encephalopathy; thirteen age- and sex-matched COVID-19 patients without neurological involvement and eight age- and sex-matched healthy controls. We did not find differences among them. In a subset of four patients, the change in serum alpha-synuclein before and after the onset of neurological symptoms was not significant either. Cerebrospinal fluid alpha-synuclein levels were also similar between neurological COVID-19 and healthy controls. Overall, these results cannot support the hypothesis of alpha-synuclein upregulation in humans with neurological symptoms in COVID-19. Further research taking into account a larger group of COVID-19 patients including the whole spectrum of neurological manifestations and disease severity is needed.</description><identifier>ISSN: 0340-5354</identifier><identifier>EISSN: 1432-1459</identifier><identifier>DOI: 10.1007/s00415-021-10444-6</identifier><identifier>PMID: 33606070</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>alpha-Synuclein ; Animals ; Basal ganglia ; Brain Diseases ; Central nervous system diseases ; Cerebrospinal fluid ; Coronaviruses ; COVID-19 ; Encephalopathy ; Humans ; Invasiveness ; Medicine ; Medicine & Public Health ; Movement disorders ; Myoclonus ; Neurology ; Neurons ; Neuroradiology ; Neurosciences ; Original Communication ; SARS-CoV-2 ; Severe acute respiratory syndrome coronavirus 2 ; Synuclein</subject><ispartof>Journal of neurology, 2021-09, Vol.268 (9), p.3116-3124</ispartof><rights>Springer-Verlag GmbH, DE part of Springer Nature 2021</rights><rights>2021. Springer-Verlag GmbH, DE part of Springer Nature.</rights><rights>Springer-Verlag GmbH, DE part of Springer Nature 2021.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c474t-b8f3f17219a4604d776c2a1194731ebdbc5df79ec8ba88d3285cef79a56c8bac3</citedby><cites>FETCH-LOGICAL-c474t-b8f3f17219a4604d776c2a1194731ebdbc5df79ec8ba88d3285cef79a56c8bac3</cites><orcidid>0000-0002-1721-6217</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00415-021-10444-6$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00415-021-10444-6$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>230,314,776,780,881,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33606070$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Blanco-Palmero, V. A.</creatorcontrib><creatorcontrib>Azcárate-Díaz, F. J.</creatorcontrib><creatorcontrib>Ruiz-Ortiz, M.</creatorcontrib><creatorcontrib>Laespada-García, M. I.</creatorcontrib><creatorcontrib>Rábano-Suárez, P.</creatorcontrib><creatorcontrib>Méndez-Guerrero, A.</creatorcontrib><creatorcontrib>Aramendi-Ramos, M.</creatorcontrib><creatorcontrib>Eguiburu, J. L.</creatorcontrib><creatorcontrib>Pérez-Rivilla, A.</creatorcontrib><creatorcontrib>Marchán-López, A.</creatorcontrib><creatorcontrib>Rubio-Fernández, M.</creatorcontrib><creatorcontrib>Carro, E.</creatorcontrib><creatorcontrib>González de la Aleja, J.</creatorcontrib><title>Serum and CSF alpha-synuclein levels do not change in COVID-19 patients with neurological symptoms</title><title>Journal of neurology</title><addtitle>J Neurol</addtitle><addtitle>J Neurol</addtitle><description>SARS-CoV-2 infection can associate diverse neurological manifestations. Several studies have provided proof to support the theory of neurotropic involvement of SARS-CoV-2. Alpha-synuclein has been described as a native antiviral factor within neurons, and upregulation of this protein can be seen in animals that suffered other neuroinvasive infections. To assess if increased expression of this protein takes place in COVID-19 patients with neurological symptoms, we analyzed serum total alpha-synuclein levels in three groups: seven COVID-19 patients with myoclonus, Parkinsonism and/or encephalopathy; thirteen age- and sex-matched COVID-19 patients without neurological involvement and eight age- and sex-matched healthy controls. We did not find differences among them. In a subset of four patients, the change in serum alpha-synuclein before and after the onset of neurological symptoms was not significant either. Cerebrospinal fluid alpha-synuclein levels were also similar between neurological COVID-19 and healthy controls. Overall, these results cannot support the hypothesis of alpha-synuclein upregulation in humans with neurological symptoms in COVID-19. 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Alpha-synuclein has been described as a native antiviral factor within neurons, and upregulation of this protein can be seen in animals that suffered other neuroinvasive infections. To assess if increased expression of this protein takes place in COVID-19 patients with neurological symptoms, we analyzed serum total alpha-synuclein levels in three groups: seven COVID-19 patients with myoclonus, Parkinsonism and/or encephalopathy; thirteen age- and sex-matched COVID-19 patients without neurological involvement and eight age- and sex-matched healthy controls. We did not find differences among them. In a subset of four patients, the change in serum alpha-synuclein before and after the onset of neurological symptoms was not significant either. Cerebrospinal fluid alpha-synuclein levels were also similar between neurological COVID-19 and healthy controls. Overall, these results cannot support the hypothesis of alpha-synuclein upregulation in humans with neurological symptoms in COVID-19. Further research taking into account a larger group of COVID-19 patients including the whole spectrum of neurological manifestations and disease severity is needed.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>33606070</pmid><doi>10.1007/s00415-021-10444-6</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0002-1721-6217</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | alpha-Synuclein Animals Basal ganglia Brain Diseases Central nervous system diseases Cerebrospinal fluid Coronaviruses COVID-19 Encephalopathy Humans Invasiveness Medicine Medicine & Public Health Movement disorders Myoclonus Neurology Neurons Neuroradiology Neurosciences Original Communication SARS-CoV-2 Severe acute respiratory syndrome coronavirus 2 Synuclein |
| title | Serum and CSF alpha-synuclein levels do not change in COVID-19 patients with neurological symptoms |
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