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Updated May 16, 2024 7 subscribers

COVID, AMYLOID, AND INFLAMMATION

Literature collection of the CovAmInf workgroup.

Editors Joshua T. Berryman Abdul Mannan Baig Artemi Bendandi Daniel Bonhenry Mattheos A.G. Koffas

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Links between COVID-19 and Parkinson's disease/Alzheimer's disease: reciprocal impacts, medical care strategies and underlying mechanisms (2023)

Pei Huang, Lin-Yuan Zhang, Yu-Yan Tan, Sheng-Di Chen

PubMed: 36717892  DOI: 10.1186/s40035-023-00337-1 

This review captures some of the big studies and meta-studies on neurodegenerative disease and PD. Bullet points include:

  • SARS-CoV2 infection can initiate Parkinson's disease, and can also initiate transient PD-like symptoms. Mechanism is not clear but infection of neurons seems likely. H1N1 Influenza infection of neurons causes alpha synuclein buildup.
  • The converse does not seem to hold, or not strongly: during the peak of the pandemic, PD patients were at increased mortality risk whether they were diagnosed with covid or not.
  • It is stated that dopamine agonist (antipsychotics) increase covid mortality risk, however most antipsychotics are dopamine antagonists... and the example given, of clozapine, is more related to serotonin and GABA receptors. The most I can take from this section is that there is a big crossover between neurotransmitter chemistry and neuroinflammation, therefore covid. Some PD medications (amantadine) are protective against covid, although it is unclear if this has anything to do with their neurological action.
  • Vitamin D is protective against PD and Covid separately or together.
  • SARS-CoV-2 harms by (neuro)inflammation, coagulation, and straightforward viral activity of infecting cells and lysing them.
  • Alpha synuclein is expressed in response to SARS-CoV-2 nucleocapsid protein.
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