Serum and CSF alpha-synuclein levels do not change in COVID-19 patients with neurological symptoms

Blanco-Palmero, Víctor Antonio; Azcárate-Díaz, Francisco Javier; Ruiz-Ortiz, Mariano; Laespada-García, María Isabel; Rábano-Suárez, Pablo; Méndez-Guerrero, Antonio; Aramendi-Ramos, M.; Eguiburu, J. L.; Pérez‐Rivilla, Alfredo; Marchán‐López, Álvaro; Rubio‐Fernández, Marcos; Carro, Eva; Aleja, Jesús González de la

doi:10.1007/s00415-021-10444-6

Cited by 18 publications

(15 citation statements)

References 36 publications

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“…41 These results allow to postulate that SARS-CoV-2 infection can trigger the aggregation mechanisms of α-Syn leading to cellular vulnerability and degeneration of dopaminergic neurons. This hypothesis has not been confirmed by a clinical study, as Blanco-Palmero and colleagues 45 did not find a significant change in serum α-Syn concentration in patients with Covid-19 and neurological disorders, compared with age-and sex-matched Covid-19 patients free of neurological symptoms and healthy controls. 45 However, the authors mentioned two limitations: (1) the study involved a small number of patients and (2) the serum sample analyzed in Covid-19 with neurological symptoms was extracted later in the course of the disease (31 days after symptom onset) than in Covid-19 patients without neurological symptoms (12 days).…”

Section: Sars-cov-2 and Pdmentioning

confidence: 83%

“…This hypothesis has not been confirmed by a clinical study, as Blanco-Palmero and colleagues 45 did not find a significant change in serum α-Syn concentration in patients with Covid-19 and neurological disorders, compared with age-and sex-matched Covid-19 patients free of neurological symptoms and healthy controls. 45 However, the authors mentioned two limitations: (1) the study involved a small number of patients and (2) the serum sample analyzed in Covid-19 with neurological symptoms was extracted later in the course of the disease (31 days after symptom onset) than in Covid-19 patients without neurological symptoms (12 days). Further clinical studies taking into account these two parameters, as well as experimental studies using SARS-CoV-2 infection animal models, are needed.…”

Section: Sars-cov-2 and Pdmentioning

confidence: 83%

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Covid‐19 Infection and Parkinsonism: Is There a Link?

Bouali‐Benazzouz

Benazzouz

2021

Movement Disorders

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A BS TRACT: Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is an opportunistic pathogen that infects the upper respiratory tract in humans and causes serious illness, including fatal pneumonia and neurological disorders. Several studies have reported that SARS-CoV-2 may worsen the symptoms of Parkinson's disease (PD), with the potential to increase mortality rates in patients with advanced disease. The potential risk of SARS-CoV-2 to induce PD has also been suggested because the virus can enter the brain, where it can trigger cellular processes involved in neurodegeneration. In this review, we will discuss the potential of SARS-CoV-2 to exacerbate and cause certain neurological disorders, including PD. We will then elucidate its impact on the brain while examining its pathways and mechanisms of action.

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Section: Sars-cov-2 and Pdmentioning

confidence: 83%

Section: Sars-cov-2 and Pdmentioning

confidence: 83%

Covid‐19 Infection and Parkinsonism: Is There a Link?

Bouali‐Benazzouz

Benazzouz

2021

Movement Disorders

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“…These cases were included into a primary group and further analysed in detail. This primary group did not include cases of people undergoing mechanical ventilation, or with significant organic damage to the central nervous system, or in the absence of information as to the identification of the pathogen; a total of 53 cases [12,13,27,40,46,[55][56][57][58][59][60][61][62][63][64]. 46 of them were intubated, three patients did not have a SARS-CoV-2 confirmation test, in two patients the primary diagnosis was a stroke, one case presented with subacute thyroiditis, and one case concerned a patient with multiple system atrophy.…”

Section: Resultsmentioning

confidence: 99%

Autoimmune mediated hyperkinetic movement disorders in SARS-CoV-2 infection — a systematic review

Hirschfeld

2021

Neurol Neurochir Pol.

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Introduction. Various neurological symptoms have been confirmed in the course of SARS-CoV-2 infection. Some of these are undoubtedly the aftermath of the developing inflammation and increased coagulation processes. However, there is also a group of symptoms that derive from possible autoimmune processes. These include primary hyperkinetic movement disorders such as myoclonus, ataxia, opsoclonus, and tremors. This study systematically reviews scientific reports presenting patients with hyperkinetic movement disorders as one of the neurological symptoms. Material and methods.The available literature was systematically reviewed as per the recommendations of Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). The PubMed database was used in the range from 1 April, 2020, to 31 July, 2021.Results. The PubMed database search identified 102 cases of patients with SARS-CoV-2 infection who developed hyperkinetic movement disorders. After excluding patients undergoing mechanical ventilation (n = 46) and a few other cases (n = 7), a group of 49 non-intubated patients was obtained. The mean age of the patients was 57.92 years, and 75.51% of the patients were male. The most common hyperkinetic movement disorders were ataxia (83.67%), myoclonus (67.35%), and tremor (30.61%). Symptoms appeared on average within two weeks of the first symptoms of infection. Most patients had symptoms significantly reduced or withdrawn (67.44%) or early partial improvement (30.23%). Conclusions.Based on the meta-analysis, it can be concluded that hyperkinetic movement disorders in the course of SARS--CoV-2 infection are an early symptom with a potential autoimmune background. They have a good prognosis with the applied treatment. Further observations are needed to determine their frequency and the most effective methods of treatment.

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“…This finding prompted the hypothesis that α-synuclein is upregulated during infection as an antiviral factor in neurons, where it is proposed to act as a natural antimicrobial peptide to restrict viral infection in the brain (61,62). However, a recent study indicated that there were no alterations in a-synuclein levels in serum and CSF of COVID-19 patients with neurological symptoms (63). These findings suggest that the reported cases of parkinsonism after SARS-CoV-2 infection could be a consequence of an increased proinflammatory environment, mediated by blood brain barrier (BBB) disruption (64), peripheral cell infiltration (65), and microglial activation (66).…”

Section: Discussionmentioning

confidence: 99%

SARS-CoV-2 drives NLRP3 inflammasome activation in human microglia through spike-ACE2 receptor interaction

Albornoz

Amarilla

Modhiran

et al. 2022

Preprint

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Coronavirus disease-2019 (COVID-19) is primarily a respiratory disease, however, an increasing number of reports indicate that SARS-CoV-2 infection can also cause severe neurological manifestations, including precipitating cases of probable Parkinson's disease. As microglial NLRP3 inflammasome activation is a major driver of neurodegeneration, here we interrogated whether SARS-CoV-2 can promote microglial NLRP3 inflammasome activation utilising a model of human monocyte-derived microglia. We identified that SARS-CoV-2 isolates can bind and enter microglia, triggering inflammasome activation in the absence of viral replication. Mechanistically, microglial NLRP3 could be both primed and activated with SARS-CoV-2 spike glycoprotein in a NFκB and ACE2-dependent manner. Notably, virus- and spike protein-mediated inflammasome activation in microglia was significantly enhanced in the presence of α-synuclein fibrils, which was entirely ablated by NLRP3-inhibition. These results support a possible mechanism of microglia activation by SARS-CoV-2, which could explain the increased vulnerability to developing neurological symptoms akin to Parkinson's disease in certain COVID-19 infected individuals, and a potential therapeutic avenue for intervention.

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Serum and CSF alpha-synuclein levels do not change in COVID-19 patients with neurological symptoms

Cited by 18 publications

References 36 publications

Covid‐19 Infection and Parkinsonism: Is There a Link?

Covid‐19 Infection and Parkinsonism: Is There a Link?

Autoimmune mediated hyperkinetic movement disorders in SARS-CoV-2 infection — a systematic review

SARS-CoV-2 drives NLRP3 inflammasome activation in human microglia through spike-ACE2 receptor interaction

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