Neurological sequela and disruption of neuron-glia homeostasis in SARS-CoV-2 infection

Savelieff, Masha G.; Feldman, Eva L.; Stino, Amro

doi:10.1016/j.nbd.2022.105715

Cited by 26 publications

(17 citation statements)

References 97 publications

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“…Schizophrenia is a severe mental illness characterized by hallucinations, delusions, disorganized thinking, and cognitive deficits. In both schizophrenia and SARS-CoV-2 infection, a profound breakdown in neuron-glia homeostasis is notable ( Savelieff et al, 2022 ). It has been reported that schizophrenia patients are at higher risk for COVID-19 mortality ( Toubasi et al, 2021 ).…”

Section: Introductionmentioning

confidence: 99%

Severe COVID-19 increases the risk of schizophrenia

Baranova

Cao²,

Zhang³

2022

Psychiatry Research

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Section: Introductionmentioning

confidence: 99%

Severe COVID-19 increases the risk of schizophrenia

Baranova

Cao²,

Zhang³

2022

Psychiatry Research

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“…This may contribute to the elevation of neuroinflammatory markers, the aggravation of neuroinflammation, and result in a more intense and unremitting immune response. In the brain parenchyma, the unrestricted inflammatory reactions are enormously potent to initiate injury cascades, leading to brain tissue damage and functional dysregulation; affecting neurogenesis, synaptic neurotransmission and plasticity, mitochondrial functioning and brain homeostasis [ 51 , 52 ]. Brain tissue injury can also occur as a result of microbleeds caused by SARS-CoV-2-induced endothelial damage.…”

Section: Aged Brain and Neuroinflammationmentioning

confidence: 99%

Aged brain and neuroimmune responses to COVID-19: post-acute sequelae and modulatory effects of behavioral and nutritional interventions

Müller

Benedetto

2023

Immun Ageing

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Advanced age is one of the significant risk determinants for coronavirus disease 2019 (COVID-19)-related mortality and for long COVID complications. The contributing factors may include the age-related dynamical remodeling of the immune system, known as immunosenescence and chronic low-grade systemic inflammation. Both of these factors may induce an inflammatory milieu in the aged brain and drive the changes in the microenvironment of neurons and microglia, which are characterized by a general condition of chronic inflammation, so-called neuroinflammation. Emerging evidence reveals that the immune privilege in the aging brain may be compromised. Resident brain cells, such as astrocytes, neurons, oligodendrocytes and microglia, but also infiltrating immune cells, such as monocytes, T cells and macrophages participate in the complex intercellular networks and multiple reciprocal interactions. Especially changes in microglia playing a regulatory role in inflammation, contribute to disturbing of the brain homeostasis and to impairments of the neuroimmune responses. Neuroinflammation may trigger structural damage, diminish regeneration, induce neuronal cell death, modulate synaptic remodeling and in this manner negatively interfere with the brain functions.In this review article, we give insights into neuroimmune interactions in the aged brain and highlight the impact of COVID-19 on the functional systems already modulated by immunosenescence and neuroinflammation. We discuss the potential ways of these interactions with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and review proposed neuroimmune mechanisms and biological factors that may contribute to the development of persisting long COVID conditions. We summarize the potential mechanisms responsible for long COVID, including inflammation, autoimmunity, direct virus-mediated cytotoxicity, hypercoagulation, mitochondrial failure, dysbiosis, and the reactivation of other persisting viruses, such as the Cytomegalovirus (CMV). Finally, we discuss the effects of various interventional options that can decrease the propagation of biological, physiological, and psychosocial stressors that are responsible for neuroimmune activation and which may inhibit the triggering of unbalanced inflammatory responses. We highlight the modulatory effects of bioactive nutritional compounds along with the multimodal benefits of behavioral interventions and moderate exercise, which can be applied as postinfectious interventions in order to improve brain health.

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“…SARS‐CoV‐2 was detected to infect brain vascular endothelial cells and cause brain damage in K18‐hACE2 transgenic mice and hamster model, indicating that SARS‐CoV‐2 crossed the blood–brain barrier to the brain, and led to neuronal damage and inflammatory response. The activation of microglia and astrogliosis led to chronic encephalitis and ultimately the long‐term neurological dysfunction 26,47,51,52 . In addition, studies have established the relationship between fatigue and mitochondrial dysfunction, and oxidative stress.…”

Section: Manifestations Of Long Covid In Multiple Organsmentioning

confidence: 99%

“…The activation of microglia and astrogliosis led to chronic encephalitis and ultimately the long‐term neurological dysfunction. 26 , 47 , 51 , 52 In addition, studies have established the relationship between fatigue and mitochondrial dysfunction, and oxidative stress. The normal function of central nervous system demands high levels of adenosine triphosphate produced (ATP) by mitochondria.…”

Section: Manifestations Of Long Covid In Multiple Organsmentioning

confidence: 99%

Long COVID: The latest manifestations, mechanisms, and potential therapeutic interventions

Cheng

et al. 2022

MedComm

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COVID‐19 caused by SARS‐CoV‐2 infection affects humans not only during the acute phase of the infection, but also several weeks to 2 years after the recovery. SARS‐CoV‐2 infects a variety of cells in the human body, including lung cells, intestinal cells, vascular endothelial cells, olfactory epithelial cells, etc. The damages caused by the infections of these cells and enduring immune response are the basis of long COVID. Notably, the changes in gene expression caused by viral infection can also indirectly contribute to long COVID. We summarized the occurrences of both common and uncommon long COVID, including damages to lung and respiratory system, olfactory and taste deficiency, damages to myocardial, renal, muscle, and enduring inflammation. Moreover, we provided potential treatments for long COVID symptoms manifested in different organs and systems, which were based on the pathogenesis and the associations between symptoms in different organs. Importantly, we compared the differences in symptoms and frequency of long COVID caused by breakthrough infection after vaccination and infection with different variants of concern, in order to provide a comprehensive understanding of the characteristics of long COVID and propose improvement for tackling COVID‐19.

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Neurological sequela and disruption of neuron-glia homeostasis in SARS-CoV-2 infection

Cited by 26 publications

References 97 publications

Severe COVID-19 increases the risk of schizophrenia

Severe COVID-19 increases the risk of schizophrenia

Aged brain and neuroimmune responses to COVID-19: post-acute sequelae and modulatory effects of behavioral and nutritional interventions

Long COVID: The latest manifestations, mechanisms, and potential therapeutic interventions

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