Guillain–Barré Syndrome in COVID-19—The Potential Role of NCAM-1 and Immunotherapy
Abstract
:1. Introduction
1.1. Models of Pathophysiology
1.1.1. Molecular Mimicry
1.1.2. Inflammation
1.2. Correlation with COVID-19
2. Case Presentation
2.1. Methods
2.2. Case Report
2.3. Clinical Presentation Discussion
3. Discussion
NCAM-1 as a Potential Link between GBS and COVID-19
4. Conclusions
Author Contributions
Funding
Institutional Review Board Statement
Informed Consent Statement
Data Availability Statement
Conflicts of Interest
Abbreviations
KLK6 | Kallikrein-6 |
TOT TAU | Total tau protein |
NCAM-1 | Neural cell adhesion molecule 1 |
TDP43 | TAR DNA-binding protein 43 |
NFL | Neurofilament light chain |
NRGN | Neurogranin |
FGF21 | Fibroblast growth factor 21 |
TREM2 | Triggering receptor expressed on myeloid cells 2 |
BLC | B lymphocyte chemoattractant |
YKL40/CHI3L1 | Chitinase-3-like protein 1 |
RAGE | Receptor for advanced glycation endproducts |
TNF-α | Tumor necrosis factor alpha |
AMAN | Acute motor axonal neuropathy |
AIDP | Acute inflammatory demyelinating polyneuropathy |
COVID-19 | Coronavirus disease 2019 |
GBS | Guillain–Barré syndrome |
CSF | Cerebrospinal fluid |
ApoE | Apolipoprotein E |
IL-37 | Interleukin 37 |
IL-17A | Interleukin 17A |
IFN-γ | Interferon gamma |
SARS-CoV-2 | Severe acute respiratory syndrome coronavirus 2 |
CRP | C-reactive protein |
RT-PCR | Reverse transcription polymerase chain reaction |
PLEX | Plasmapheresis |
EMG | Electromyography |
IgG | Immunoglobulin G |
IL-6 | Interleukin 6 |
MS | Multiple sclerosis |
AD | Alzheimer’s Disease |
PD | Parkinson’s Disease |
ALS | Amyotrophic lateral sclerosis |
FTD | Frontotemporal dementia |
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Biomarker | Blood | CSF | Reference Ranges | General Description | |||
---|---|---|---|---|---|---|---|
T1 | T2 | T3 | T4 | Relevance to COVID-19 | |||
KLK6 | 923.7 | 3953.6 | 3442.7 | 465.2 | 14,849.4 | unknown | Serum protease, neuroinflammation, linked to multiple sclerosis (MS), elevated in Alzheimer’s disease (AD) when tau also elevated, decreased in Parkinson’s disease (PD), degraded in respiratory disease, regulates myelin volume. No association with GBS or COVID-19 [21] |
Amyloid B1-41 | BDL | BDL | BDL | BDL | BDL | unknown | Was not found in the literature [22] |
Amyloid B1-42 | 4.2 | 7.8 | 12.6 | 16.1 | 29.3 | 0–400 pg/mL (SIMOA) | Lower in AD, no relation to COVID-19 found [22] |
TOT TAU | BDL | 121.7 | BDL | 114.1 | BDL | 100–300 in GBS, 0–360 pg(SIMOA) | Higher values associated with worse prognosis in GBS [22,23,24,25,26] |
NCAM-1 | 57,758.5 | 51,593.3 | 57,231.2 | 119,018.3 | 22,356.6 | 246.03 pg/mL control, 153 in autism | Also called CD56, helps synapse formation, found to be low in autism, high in MS, hypothetically associated with COVID-19 pathogenesis [27,28,29,30] |
TAU PT181 | BDL | BDL | BDL | BDL | BDL | unknown | Another marker for tau, no association found with GBS or COVID-19 [23,24] |
TDP43 | ND | 4045.3 | 1620.1 | 5583.8 | BDL | unknown | Elevated in amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), not GBS. No association with COVID-19 seen [5] |
NFL | 41.85 | 93.15 | 38.61 | 192.9 | unknown | Elevated in AD, GBS, and ALS, in addition to non-survivors of COVID-19 [31,32,33] | |
NRGN | 6052.2 | 11,867.6 | 5743.6 | 11,040.7 | 1048.9 | unknown | Neurogranin: decreased in schizophrenia, increased in AD, no association found with COVID-19 or GBS [23] |
FGF21 | BDL | BDL | BDL | BDL | BDL | unknown | Neuroprotectant, involved in carbohydrate metabolism, no link with GBS or COVID [34] |
CLUSTERIN | 11,039.5 | 1673.9 | 28,787,864.31 | 56,444,777.02 | 29,957.99667 | unknown | Increased in AD, no evidence for role in GBS or COVID-19 [35] |
TREM2 | 109.5 | 144.6 | 286.51 | 1833.17 | 728.849106 | unknown | Associated with a risk for AD, can suppress inflammation but also trigger it, no clear association with GBS or COVID-19 [36] |
BLC | 325.1 | 6462.4 | 155.89 | 200.75 | BDL | unknown | B lymphocyte chemoattractant. Associated with adenocarcinoma. Also called CXCL13 or BCA-1. Other types but not this type associated with GBS [37] |
YKL40 | 8684.5 | 14,853.5 | 17,258.11 | 18,389.31 | 15,090.6293 | healthy: 80 ng/mL, severe COVID 300 | Also called chitinase-3-like protein 1 (CHI3L1), elevated in AD, not GBS, associated with worse mortality in lung COVID-19 disease [38,39] |
RAGE | 146.3 | 124.8 | 67.87 | 61.70 | 24.0432183 | serum pg/mL AIDP > 1000, AMAN < 1000 | Binds to pro-inflammatory pathways, higher in neurodegenerative disease, lower in AMAN subtype of GBS, higher in AIDP, higher in asymptomatic COVID-19, lower in severe COVID-19 in enzyme-linked immunosorbent assay in ng/mL [2,10,40,41,42] |
FERRITIN | 383,593.2 | 207,231.3 | 218,048.4 | 709,040.7 | 51,863.9 | unknown | Increased levels seen in patients that showed inflammation during episode of malaria and COVID-19. Similar results were seen in a patient who presented with GBS associated with COVID-19 [43,44,45] |
DDIMER | 110,928.0 | 34,814.4 | 25,904.3 | 6,737,038.6 | 720,348.9 | unknown | Elevated d-dimer plasma levels are associated with inflammatory reactions to pneumonia and severe COVID-19. No association with GBS [46] |
IL-6 | 1.6 | 22.8 | 5.0 | 0.7 | <1.04736328125 | unknown | Uncontrolled inflammation may occur following the increased activation of serum IL-6, similarly to how its role in a “cytokine storm” has been correlated with critical COVID-19 development. It plays both a pro-inflammatory and protective role in GBS [47,48] |
TNF-α | 0.0 | 0.5 | 0.0 | 0.0 | 0.1 | unknown | Gene polymorphisms prevent efficacious immune response against viruses such as hepatitis B and predict susceptibility to GBS, while decreased levels due to antibiotics (azithromycin specifically) are seen in COVID-19 patients [49] |
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Laudanski, K.; Yakhkind, A.; Restrepo, M.; Draham, L.; Lang, A.E. Guillain–Barré Syndrome in COVID-19—The Potential Role of NCAM-1 and Immunotherapy. BioMed 2021, 1, 80-92. https://doi.org/10.3390/biomed1010006
Laudanski K, Yakhkind A, Restrepo M, Draham L, Lang AE. Guillain–Barré Syndrome in COVID-19—The Potential Role of NCAM-1 and Immunotherapy. BioMed. 2021; 1(1):80-92. https://doi.org/10.3390/biomed1010006
Chicago/Turabian StyleLaudanski, Krzysztof, Aleksandra Yakhkind, Mariana Restrepo, Lindsay Draham, and Adam Edward Lang. 2021. "Guillain–Barré Syndrome in COVID-19—The Potential Role of NCAM-1 and Immunotherapy" BioMed 1, no. 1: 80-92. https://doi.org/10.3390/biomed1010006
APA StyleLaudanski, K., Yakhkind, A., Restrepo, M., Draham, L., & Lang, A. E. (2021). Guillain–Barré Syndrome in COVID-19—The Potential Role of NCAM-1 and Immunotherapy. BioMed, 1(1), 80-92. https://doi.org/10.3390/biomed1010006