Agata Adamczyk’s research while affiliated with Mossakowski Medical Research Institute, Polish Academy of Sciences and other places

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Publications (1)

SARS-CoV-2 structure. Structural elements of the virus, including the spike (S) glycoprotein (homotrimer), membrane (M) protein, envelope (E) protein, and internal components, such as the viral single-stranded RNA and nucleocapsid (N) protein. Created in BioRender. B, L. (2024) BioRender.com/q94f155, accessed on 16 September 2024.
The number of published papers from 2019 to 2024 (until October 28.) containing the combined keywords “alpha-synuclein” and “COVID-19”. The results are presented as the proportion of citations per 100,000 in PubMed for each year. Data sourced using PubMed by Year: http://esperr.github.io/pubmed-by-year, accessed on 28 October 2024.
Timeline summarizing the research history on the relationship between α-synuclein and COVID-19 infection, highlighting key findings, significant years, and influential authors. References: 2020: [36,37,38]; 2021: [39,40,41]; 2022 [42,43,44,45]; 2023 [46,47,48,49]; 2024 [50,51]. Created in BioRender. Pan, I. (2024) https://BioRender.com/r11e475, accessed on 30 October 2024.
Key neuroinvasive pathways that SARS-CoV-2 may use to reach the CNS. SARS-CoV-2 may potentially gain access to the brain through three primary routes. (A) Vagus nerve fibers: SARS-CoV-2 can be transmitted via the respiratory system through saliva droplets or nasal discharge toward the lungs, as well as through the gastrointestinal tract via swallowed saliva or the consumption of contaminated food, where the virus is known to replicate. ACE2 expression is high in both the lungs and gastrointestinal epithelium, making these tracts vulnerable to SARS-CoV-2 entry. The vagus nerve extends from the brainstem to various organs, including the lungs and digestive tract. Consequently, the virus may travel retrogradely along nerve fibers from the respiratory and gastric epithelium via the vagus nerve to the brainstem. (B) Olfactory nerve pathway: SARS-CoV-2 can enter the nasal cavity, travel into the nasal submucosa, and infect olfactory sensory neurons in the nasal epithelium. The virus may then travel along olfactory nerve fibers, reaching the olfactory bulb by moving upstream. This pathway could explain symptoms such as anosmia and may be a key route for the virus to spread to other parts of the CNS. (C) Disrupted blood–brain barrier (BBB): SARS-CoV-2 infection can trigger a strong immune response, leading to inflammation that may increase the permeability of the blood–brain barrier, facilitating the virus’s entry into the CNS. ACE2, expressed on endothelial cells, pericytes, and some neurons in the brain, could mediate viral entry into the brain. Created in BioRender. Pan, I. (2024) https://BioRender.com/r11e475, accessed on 30 October 2024.
SARS-CoV-2–induced alterations in α-synuclein. (A) Potential direct interactions between the SARS-CoV-2 spike (S) protein and α-synuclein. The S protein may directly interact with α-synuclein, potentially altering its structure and increasing its propensity to misfold and aggregate. This interaction could encourage the formation of toxic α-synuclein oligomers or fibrils, which are harmful to neurons. (B) SARS-CoV-2–induced activation of α-synuclein’s immunomodulatory function. α-Synuclein plays a role in the immune system, including the modulation of inflammatory responses. When SARS-CoV-2 infects a cell, it initiates inflammatory signaling that involves microglial activation and the release of high levels of pro-inflammatory cytokines and chemokines. This inflammatory response may lead to α-synuclein accumulation and neuronal damage. Conversely, non-toxic multimers of α-synuclein could help prevent viral spread. Created in BioRender. Pan, I. (2024) https://BioRender.com/r11e475, accessed on 30 October 2024.
SARS-CoV-2 Infection and Alpha-Synucleinopathies: Potential Links and Underlying Mechanisms
  • Literature Review
  • Full-text available

November 2024

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48 Reads

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1 Citation

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Grzegorz Arkadiusz Czapski

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Agata Adamczyk

Alpha-synuclein (α-syn) is a 140-amino-acid, intrinsically disordered, soluble protein that is abundantly present in the brain. It plays a crucial role in maintaining cellular structures and organelle functions, particularly in supporting synaptic plasticity and regulating neurotransmitter turnover. However, for reasons not yet fully understood, α-syn can lose its physiological role and begin to aggregate. This altered α-syn disrupts dopaminergic transmission and causes both presynaptic and postsynaptic dysfunction, ultimately leading to cell death. A group of neurodegenerative diseases known as α-synucleinopathies is characterized by the intracellular accumulation of α-syn deposits in specific neuronal and glial cells within certain brain regions. In addition to Parkinson’s disease (PD), these conditions include dementia with Lewy bodies (DLBs), multiple system atrophy (MSA), pure autonomic failure (PAF), and REM sleep behavior disorder (RBD). Given that these disorders are associated with α-syn-related neuroinflammation—and considering that SARS-CoV-2 infection has been shown to affect the nervous system, with COVID-19 patients experiencing neurological symptoms—it has been proposed that COVID-19 may contribute to neurodegeneration in PD and other α-synucleinopathies by promoting α-syn misfolding and aggregation. In this review, we focus on whether SARS-CoV-2 could act as an environmental trigger that facilitates the onset or progression of α-synucleinopathies. Specifically, we present new evidence on the potential role of SARS-CoV-2 in modulating α-syn function and discuss the causal relationship between SARS-CoV-2 infection and the development of parkinsonism-like symptoms.

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