Presumptive Molecular Interconnections Between COVID-19 And Huntington’s Disease

Year 2024, Volume: 14 Issue: 1, 169 - 175, 28.03.2024

Duygu Sarı Ak , Omar Alomari , Ülkan Kılıç

https://doi.org/10.33808/clinexphealthsci.1256952

Abstract

Objective: The healthcare system worldwide has faced unparalleled challenges as a result of the coronavirus disease of 2019 (COVID-19) pandemic. While respiratory tract disease is the most common symptom of COVID-19, there is increasing evidence of neurological damage caused by the virus. To guide the clinical management of the disease, it is essential to elucidate the mechanisms underlying the
pathophysiology of COVID-19. Various research indicate that COVID-19 patients exhibit reduced levels of brain-derived neurotrophic factor (BDNF), which is also a hallmark of Huntington’s disease, a neurodegenerative disorder. The objective of this study is to investigate the possible links between COVID-19 and Huntington’s disease. This aim is motivated by the need to guide the clinical management of COVID-19, especially given the increasing evidence of neurological damage caused by the virus, including reduced levels of BDNF, a hallmark also observed in Huntington’s disease.
Methods: The comprehensive literature review conducted for both COVID-19 and Huntington’s disease, focusing on the genes associated with both conditions. These genes were then analyzed using the STRING database to determine protein-protein interactions, aiming to elucidate the mechanisms underlying the pathophysiology of COVID-19 and its potential connections to Huntington’s disease.
Results: The outcomes of the study indicate that there could be molecular-level interactions between COVID-19 and Huntington’s disease, based on the literature research and STRING database analysis. Although the primary mechanism behind these interactions is not yet fully understood, the hypothesis suggests that BDNF and its high-affinity receptor TrkB may play a crucial role. Additionally, the study highlights olfactory dysfunction as a common symptom of COVID-19, which is also linked with various neurodegenerative conditions, including Huntington’s disease.
Conclusion: This work emphasizes the connection between COVID-19 and neurodegenerative diseases, particularly through the lens of olfactory dysfunction, a common symptom shared by COVID-19 and Huntington’s disease. The potential molecular interactions observed suggest that COVID-19 could exacerbate neurodegenerative processes. This underscores the critical need for further research focused on olfactory dysfunction as a key symptom, to better understand and manage the implications of COVID-19 in patients with neurodegenerative conditions.

Keywords

olfactory dysfunction, amyloid- β, α-synuclein, BDNF, ACE2, NTRK2

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