Title:Central Effects of Ivermectin in Alleviation of Covid-19-induced Dysautonomia
Volume: 23
Issue: 13
Author(s): Hayder M. Al-kuraishy, Ali I. Al-Gareeb, Athanasios Alexiou*Gaber El-Saber Batiha*
Affiliation:
- Department of Science and Engineering, Novel Global Community Educational Foundation, Hebersham, Australia
- AFNP Med, Wien, Austria
- Department of Pharmacology and Therapeutics, Faculty of Veterinary Medicine, Damanhour University, Damanhour 22511, AlBeheira, Egypt
Keywords:
Covid-19, GABA-ergic neurons, ivermectin, dysautonomia, nicotinic acetylcholine receptor, neuroinflammation.
Abstract: Covid-19 may be associated with various neurological disorders, including dysautonomia,
a dysfunction of the autonomic nervous system (ANS). In Covid-19, hypoxia, immunoinflammatory
abnormality, and deregulation of the renin-angiotensin system (RAS) may increase
sympathetic discharge with dysautonomia development. Direct SARS-CoV-2 cytopathic effects and
associated inflammatory reaction may lead to neuroinflammation, affecting different parts of the
central nervous system (CNS), including the autonomic center in the hypothalamus, causing dysautonomia.
High circulating AngII, hypoxia, oxidative stress, high pro-inflammatory cytokines, and
emotional stress can also provoke autonomic deregulation and high sympathetic outflow with the
development of the sympathetic storm. During SARS-CoV-2 infection with neuro-invasion,
GABA-ergic neurons and nicotinic acetylcholine receptor (nAChR) are inhibited in the hypothalamic
pre-sympathetic neurons leading to sympathetic storm and dysautonomia. Different therapeutic
modalities are applied to treat SARS-CoV-2 infection, like antiviral and anti-inflammatory drugs.
Ivermectin (IVM) is a robust repurposed drug widely used to prevent and manage mild-moderate
Covid-19. IVM activates both GABA-ergic neurons and nAChRs to mitigate SARS-CoV-2 infection-
induced dysautonomia. Therefore, in this brief report, we try to identify the potential role of
IVM in managing Covid-19-induced dysautonomia.