Commentary on “Alcohol use disorder as a potential risk factor for <scp>COVID</scp>‐19 severity: A narrative review”

Chang, Sulie L.; Bishir, Muhammed

doi:10.1111/acer.14978

Cited by 4 publications

(2 citation statements)

References 19 publications

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“…The pathway map was constructed from ethanol to AGTR1 to ACE2 to the Infection by SARS coronavirus. As previously conducted in our laboratory, we used IPA's Molecule Activity Predictor (MAP) tool to simulate ethanol activation mimicking alcohol consumption in the pathway (Alabed et al, 2021; Chang & Bishir, 2022; Kota et al, 2022). Alcohol consumption affected a set of intermediary molecules leading to an overall AGTR1 activation followed by the activation of ACE2 and subsequent activation of infection by SARS coronavirus.…”

Section: Gene Total Analyses No Aud Analyses Trima Average Aud Z‐scor...mentioning

confidence: 99%

Commentary on “Repeated ethanol exposure and withdrawal alters angiotensin‐converting enzyme 2 expression in discrete brain regions: Implications for SARS‐CoV‐2 neuroinvasion”

Chang

Zhang

2023

Alcohol: Clinical and Experimental Research

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Section: Gene Total Analyses No Aud Analyses Trima Average Aud Z‐scor...mentioning

confidence: 99%

Commentary on “Repeated ethanol exposure and withdrawal alters angiotensin‐converting enzyme 2 expression in discrete brain regions: Implications for SARS‐CoV‐2 neuroinvasion”

Chang

Zhang

2023

Alcohol: Clinical and Experimental Research

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“…To determine the quantitative impact of these qualitative relationships found using the MAP tool, downstream effect analysis was performed as described previously [20,[33][34][35][36]. The analysis determines the significance of a molecule's effect on either another molecule or a signaling pathway by quantifying the relationship between the nodes on IPA.…”

Section: Quantitative Analysis Of Covid-19 On Snca Expression and The...mentioning

confidence: 99%

Meta-Analysis of the Mechanisms Underlying COVID-19 Modulation of Parkinson’s Disease

Zhang,

Bishir,

Barbhuiya

et al. 2023

IJMS

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Coronavirus disease-19 (COVID-19) is caused by the infection of severe acute respiratory syndrome-coronavirus-2 (SARS-CoV-2). The virus enters host cells through receptor-mediated endocytosis of angiotensin-converting enzyme-2 (ACE2), leading to systemic inflammation, also known as a “cytokine storm”, and neuroinflammation. COVID-19’s upstream regulator, interferon-gamma (IFNG), is downregulated upon the infection of SARS-CoV-2, which leads to the downregulation of ACE2. The neuroinflammation signaling pathway (NISP) can lead to neurodegenerative diseases, such as Parkinson’s disease (PD), which is characterized by the formation of Lewy bodies made primarily of the α-synuclein protein encoded by the synuclein alpha (SNCA) gene. We hypothesize that COVID-19 may modulate PD progression through neuroinflammation induced by cytokine storms. This study aimed to elucidate the possible mechanisms and signaling pathways involved in COVID-19-triggered pathology associated with neurodegenerative diseases like PD. This study presents the analysis of the pathways involved in the downregulation of ACE2 following SARS-CoV-2 infection and its effect on PD progression. Through QIAGEN’s Ingenuity Pathway Analysis (IPA), the study identified the NISP as a top-five canonical pathway/signaling pathway and SNCA as a top-five upstream regulator. Core Analysis was also conducted on the associated molecules between COVID-19 and SNCA to construct a network connectivity map. The Molecule Activity Predictor tool was used to simulate the infection of SARS-CoV-2 by downregulating IFNG, which leads to the predicted activation of SNCA, and subsequently PD, through a dataset of intermediary molecules. Downstream effect analysis was further used to quantify the downregulation of ACE2 on SNCA activation.

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Network meta-analysis on alcohol-mediated modulation of Alzheimer’s disease in the diseases of inflammation including COVID-19

Bishir

Rengifo

Huang

et al. 2023

NeuroImmune Pharmacology and Therapeutics

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Objectives Cross sectional surveys have reported that alcohol consumption has skyrocketed during the COVID-19 pandemic. Chronic alcohol use triggers systemic inflammation which leads to neuroinflammation and neurodegeneration. In the present study, we hypothesize that alcohol consumption and cytokine elevation during inflammatory conditions synergistically increase amyloid-beta precursor protein (APP) expression and worsens Alzheimer’s disease (AD) pathology. Methods QIAGEN Ingenuity Pathway Analysis (IPA) was employed to conduct network meta-analysis on the molecular mechanisms underlying ethanol (EtOH) influence on APP expression and AD in inflammatory conditions including COVID-19, inflammation of respiratory system, organ, absolute anatomical region, body cavity, joint, respiratory system component, gastrointestinal tract, large intestine, liver, central nerve system, and lung. IPA tools were utilized to identify the molecules associated with EtOH, inflammatory conditions and the common molecules between them. Results Simulation activity of EtOH, mimicking exposure to alcohol, upregulated the APP expression and augmented AD pathology in all inflammatory conditions including COVID-19. Our studies identified six molecules including ADORA2A, Cytokine, IFN-gamma, IL1-beta, Immunoglobulin and TNF, which concurrently contribute to increased APP expression and AD progression upon EtOH simulation in all diseases studied. Conclusions The present study has revealed molecular mechanisms underlying alcohol augmentation of AD in COVID-19 and other diseases of inflammation.

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Commentary on “Alcohol use disorder as a potential risk factor for COVID‐19 severity: A narrative review”

Cited by 4 publications

References 19 publications

Commentary on “Repeated ethanol exposure and withdrawal alters angiotensin‐converting enzyme 2 expression in discrete brain regions: Implications for SARS‐CoV‐2 neuroinvasion”

Commentary on “Repeated ethanol exposure and withdrawal alters angiotensin‐converting enzyme 2 expression in discrete brain regions: Implications for SARS‐CoV‐2 neuroinvasion”

Meta-Analysis of the Mechanisms Underlying COVID-19 Modulation of Parkinson’s Disease

Network meta-analysis on alcohol-mediated modulation of Alzheimer’s disease in the diseases of inflammation including COVID-19

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