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Long COVID - Dopamine  Apr 02, 2023  10 months, 2 weeks, 5 days, 21 hours, 48 minutes ago

Study Proposes That SARS-CoV-2 Induced Neuroinflammation Causes Dopamine Dysfunction and Transmission Imbalance, Contributing To Long COVID

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Study Proposes That SARS-CoV-2 Induced Neuroinflammation Causes Dopamine Dysfunction and Transmission Imbalance, Contributing To Long COVID
Long COVID - Dopamine  Apr 02, 2023  10 months, 2 weeks, 5 days, 21 hours, 48 minutes ago
A new study by researchers from University of Pavia-Italy, IRCCS Mondino Foundation-Italy, University of Rome-Italy, IRCCS Maugeri Pavia-Italy and the University of Milan-Italy proposes that dopamine transmission imbalance due to neuroinflammation along with the induced cytokines causing dopamine dysfunction could contribute to Long COVID.

Dopamine (DA) is a crucial neurotransmitter in the basal ganglia, playing a significant role in the control of movement and motivation. Alteration of DA levels is central in Parkinson's disease (PD), a common neurodegenerative disorder characterized by motor and non-motor manifestations and the deposition of alpha-synuclein (α-syn) aggregates.
There has been speculation about a link between PD and viral infections, including COVID-19.
The study reviews the role of proinflammatory molecules in modulating DA homeostasis and the possible mechanistic interplay between SARS-CoV-2-mediated neuroinflammation, nigrostriatal DAergic impairment, and aberrant α-syn metabolism.
Mechanisms of SARS-CoV-2 Invasion and Associated Immune Responses
SARS-CoV-2 is an enveloped, positive-sense, single-stranded RNA virus. It enters the cell and replicates itself using the host's RNA and protein synthesis machinery. The virus activates immune cells, including macrophages, monocytes, T cells, neutrophils, and natural killer cells, which release proinflammatory cytokines and chemokines to combat the virus. SARS-CoV-2 can invade the central nervous system (CNS) and infect neurons, causing the secretion of cytokines from glial cells, astrocytes, and microglia. This disrupts their homeostatic conditions and indirectly impacts neuronal activities.
In the substantia nigra, SARS-CoV-2 has an affinity for dopaminergic neurons, as evidenced by in vitro studies and the expression of ACE2 receptor in human and mouse brains. Other mechanisms for SARS-CoV-2 access to the brain have been identified, such as Neuropilin-1 (NRP1), BASIGIN (BSG), Cathepsin L (CTSL), furin, and CD147, which facilitate the virus entry into the CNS and its spread.
These proteins, expressed at higher levels in the human brain compared to ACE2, facilitate the virus's access and spread within the CNS. The virus can induce a robust inflammatory response, characterized by massive cytokine production, persistent microglia activation, and abnormal α-synuclein levels, leading to alterations in DA neurotransmission and release during or after acute infection.
Cytokine-Induced Dopamine Dysregulation
Cytokines, such as interleukin (IL)-1, IL-2, and interferons (IFNs), have been shown to affect DA signaling in response to various inflammatory stimuli. These cytokines can either increase or decrease DA levels in different brain regions, depending on the experimental conditions and dosage. Chemokines, such as SDF-1α (CXCL12) and CCL2, also modulate DA release, affecting neuron excitability and related locomotor activities.
The overall DA response during immune stress, such as that induced by SARS-CoV-2 infection, involves a complex interplay between various cytokines and chemokines, with significant implications for DA-dependent behaviors.
ng>Neuroinflammation, Dopamine, and Long COVID
The chronic inflammatory state induced by SARS-CoV-2 infection has been shown to disturb DA signaling and DA-dependent phenomena. For example, studies have reported that IFN-α administration can lead to behavioral abnormalities reminiscent of PD, such as reduced locomotor activity and effort-based sucrose consumption. It has been hypothesized that SARS-CoV-2-induced inflammation might unmask latent neurodegenerative processes, contributing to the onset of Long COVID or PD.
However, more research is needed to confirm this hypothesis and establish a causal link between COVID-19-associated inflammation and PD or Long COVID.
Although the exact mechanisms underlying SARS-CoV-2-induced DA dysregulation are yet to be fully elucidated, it is evident that the virus can trigger a robust immune response marked by cytokine storms and neuroinflammation. This immune response can, in turn, affect DA neurotransmission, potentially contributing to the development of Long COVID or PD. Further research is needed to better understand the interplay between SARS-CoV-2 infection, inflammation, and DA dysregulation, and how this knowledge can be leveraged for the development of novel therapeutic strategies to combat the long-term neurological
The study findings were published in the peer reviewed International Journal of Molecular Sciences
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