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SARS-CoV-2-Mimicking Pseudoviral Particles Accelerate α-Synuclein Aggregation In Vitro.

Gianluca ZilioAnna MasatoMichele SandreAlberto CaregnatoFrancesca MoretAgnieszka Katarzyna MaciolaAngelo AntoniniMarco BrucaleLaura CendronNicoletta PlotegherLuigi Bubacco
Published in: ACS chemical neuroscience (2023)
Since the SARS-CoV-2 virus started spreading worldwide, evidence pointed toward an impact of the infection on the nervous system. COVID-19 patients present neurological manifestations and have an increased risk of developing brain-related symptoms in the long term. In fact, evidence in support of the neuroinvasive potential of SARS-CoV-2 has emerged. Considering that viral parkisonism was observed as a consequence of encephalopathies caused by viral infections, it has been already suggested that COVID-19 could affect the dopaminergic neurons and contribute to neurodegeneration in Parkinson's disease (PD), by promoting the formation of amyloid fibrils constituted by the PD-related protein α-synuclein. Here, we observe not only that SARS-CoV-2 viral spike protein and nucleocapsid protein can alone promote α-synuclein aggregation but also that the spike protein organization in a corona shape on the viral envelope may be crucial in triggering fast amyloid fibrils formation, thus possibly contributing to PD pathogenesis.
Keyphrases
  • sars cov
  • respiratory syndrome coronavirus
  • protein protein
  • amino acid
  • binding protein
  • spinal cord
  • white matter
  • risk assessment
  • physical activity
  • climate change
  • blood brain barrier
  • brain injury
  • depressive symptoms