Common Inflammatory Mechanisms in COVID-19 and Parkinson’s Diseases: The Role of Microbiome, Pharmabiotics and Postbiotics in Their Prevention

Abstract

In the last decade, metagenomic studies have shown the key role of the gut microbiome in maintaining immune and neuroendocrine systems. Malfunction of the gut microbiome can induce inflammatory processes, oxidative stress, and cytokine storm. Dysfunction of the gut microbiome can be caused by short-term (virus infection and other infectious diseases) or long-term (environment, nutrition, and stress) factors. Here, we reviewed the inflammation and oxidative stress in neurodegenerative diseases and coronavirus infection (COVID-19). Here, we reviewed the renin-angiotensin-aldosterone system (RAAS) involved in the processes of formation of oxidative stress and inflammation in viral and neurodegenerative diseases. Moreover, the coronavirus uses ACE2 receptors of the RAAS to penetrate human cells. The coronavirus infection can be the trigger for neurodegenerative diseases by dysfunction of the RAAS. Pharmabiotics, postbiotics, and nextgeneration probiotics, are considered as a means to prevent oxidative stress, inflammatory processes, neurodegenerative and viral diseases through gut microbiome regulation.

Parkinson’s Disease in Light of the COVID-19 Pandemic

“…The etiology of PD is not completely understood [ 3 , 19 ]. Currently, it is believed that PD affects numerous systems of the human organism [ 3 , 20 ].…”

“…The virus's targeting of various cell types has been partially attributed to the fact that SARS-CoV-2 utilizes angiotensin-converting-enzyme 2 (ACE2) type 1 transmembrane receptors localized on the epithelial and endothelial cells of the respiratory system, as well as on immune cells, to enter and replicate within the human organism. Interestingly, ACE2 receptors are widespread within brain structures, the central nervous system, and visual tracts, which may explain the many neurological symptoms in coronavirus disease 2019 (COVID- 19) infection [1][2][3]. Interaction with ACE2 receptors of the vascular endothelial cells leads to disruption of the blood-brain barrier, with consequent cerebral edema and microhemorrhages.…”

“…In addition, SARS-CoV-2 may exert direct neuronal damage due to the affinity of the spike S1 protein of the virus towards ACE2 receptors expressed on neurons. There are two possible pathways of brain invasion, either blood-borne or through retrograde axonal transport (olfactory route) [ 2 , 3 ]. Brain tissue may be exposed to injury as a result of COVID-19-related hypercoagulable states, hypoxia, inflammation and immune response (cytokine storm), or dyselectrolytemia as well [ 2 , 3 ].…”

“…There are two possible pathways of brain invasion, either blood-borne or through retrograde axonal transport (olfactory route) [ 2 , 3 ]. Brain tissue may be exposed to injury as a result of COVID-19-related hypercoagulable states, hypoxia, inflammation and immune response (cytokine storm), or dyselectrolytemia as well [ 2 , 3 ]. It is these events that are currently thought to play the major role in the cerebral pathology reported during infection, as mounting evidence shows negligibly low levels of both viral RNA and proteins in the brains of affected patients, making the direct pathomechanism of viral damage an unlikely cause of all the neurological symptoms [ 4 , 5 ].…”

“…Nonetheless, the interplay between SARS-CoV-2 and abundant ACE2 receptors gives solid grounds to discuss the role of COVID-19 in neurodegenerative conditions. Recent studies indicate that there may exist (not yet elucidated) a molecular link between the infection and the pathogenesis of Alzheimer’s disease, multiple sclerosis, and Parkinson’s disease (PD)/parkinsonism [ 1 , 3 , 6 , 7 , 8 , 9 ].…”