Long COVID and long chain fatty acids (LCFAs): Psychoneuroimmunity implication of omega-3 LCFAs in delayed consequences of COVID-19

Yang, Chun‐Pai; Chang, Ching-Ter; Yang, Cheng-Chia; Pariante, Carmine; Su, Kuan‐Pin

doi:10.1016/j.bbi.2022.04.001

Cited by 30 publications

(28 citation statements)

References 99 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The neuropsychiatric sequelae of long COVID are multifactorial. The development of depression and other psychiatric symptoms of long COVID may involve several different mechanisms, including direct brain infection and neuro-injury by SARS-CoV-2, unresolved systemic inflammation and ensuing increased inflammation in the brain through compromised blood-brain barrier (BBB), and oxidative stress [ 7 , 35 , 37 , 38 ]. They may operate alone or together, leading to the development of depression, cognitive impairments, and other psychiatric sequelae (sleep disturbances, fatigue) in COVID-19 survivors.…”

Section: Could the Inflammation Theory Of Depression Apply To Long Co...mentioning

confidence: 99%

“…Long-chain omega-3 polyunsaturated fatty acids (omega-3 PUFAs) are a promising choice with solid empirical evidence established for their effects on improving major depressive disorder, anxiety, and antenatal and postnatal depression [ 63 - 67 ]. In addition, there is emerging evidence on the effect of omega-3 PUFAs in addressing immune dysregulation induced by SARS-CoV- 2 infection as well as post-COVID depression, anxiety, and other psychological distress [ 38 , 68 ]. Further research is needed using an experimental design (randomized controlled trial) to test the effect of nutrition interventions with omega-3 PUFAs on post-COVID depression as well as to test decreased inflammation as the mediating mechanism of the intervention effect.…”

Section: Addressing Inflammation As a Treatment Target For Post-covid...mentioning

confidence: 99%

See 1 more Smart Citation

The Clinical Observation of Inflammation Theory for Depression: The Initiative of the Formosa Long COVID Multicenter Study (FOCuS)

Liu

Lin

Chang

et al. 2023

Clin Psychopharmacol Neurosci

Self Cite

View full text Add to dashboard Cite

There is growing evidence that the coronavirus disease 2019 (COVID-19) caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is associated with increased risks of psychiatric sequelae. Depression, anxiety, cognitive impairments, sleep disturbance, and fatigue during and after the acute phase of COVID-19 are prevalent, long-lasting, and exerting negative consequences on well-being and imposing a huge burden on healthcare systems and society. This current review presented timely updates of clinical research findings, particularly focusing on the pathogenetic mechanisms underlying the neuropsychiatric sequelae, and identified potential key targets for developing effective treatment strategies for long COVID. In addition, we introduced the Formosa Long COVID Multicenter Study (FOCuS), which aims to apply the inflammation theory to the pathogenesis and the psychosocial and nutrition treatments of post-COVID depression and anxiety.

show abstract

Section: Could the Inflammation Theory Of Depression Apply To Long Co...mentioning

confidence: 99%

Section: Addressing Inflammation As a Treatment Target For Post-covid...mentioning

confidence: 99%

The Clinical Observation of Inflammation Theory for Depression: The Initiative of the Formosa Long COVID Multicenter Study (FOCuS)

Liu

Lin

Chang

et al. 2023

Clin Psychopharmacol Neurosci

Self Cite

View full text Add to dashboard Cite

show abstract

“…Earlier reports have suggested a role for peroxisome injury in COVID-19. 65 Our studies point to a general reduction in peroxisome biogenesis factor expression in the CNS during COVID-19. In the brainstem of COVID-19 patients, we observed suppression of critical peroxisome genes, including PEX11B and PEX3, suppression of peroxisomal proteins PEX14 and PMP70 and decreased PEX3 immunoreactivity.…”

Section: Discussionmentioning

confidence: 60%

COVID‐19 Induces Neuroinflammation and Suppresses Peroxisomes in the Brain

Roczkowsky¹,

Limonta²,

Fernandes³

et al. 2023

Annals of Neurology

View full text Add to dashboard Cite

ObjectivePeroxisome injury occurs in the central nervous system (CNS) during multiple virus infections that result in neurological disabilities. We investigated host neuroimmune responses and peroxisome biogenesis factors during severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) infection using a multiplatform strategy.MethodsBrain tissues from coronavirus disease 2019 (COVID‐19) (n = 12) and other disease control (ODC) (n = 12) patients, as well as primary human neural cells and Syrian hamsters, infected with a clinical variant of SARS‐CoV‐2, were investigated by droplet digital polymerase chain reaction (ddPCR), quantitative reverse transcriptase PCR (RT‐qPCR), and immunodetection methods.ResultsSARS‐CoV‐2 RNA was detected in the CNS of 4 patients with COVID‐19 with viral protein (NSP3 and spike) immunodetection in the brainstem. Olfactory bulb, brainstem, and cerebrum from patients with COVID‐19 showed induction of pro‐inflammatory transcripts (IL8, IL18, CXCL10, NOD2) and cytokines (GM‐CSF and IL‐18) compared to CNS tissues from ODC patients (p < 0.05). Peroxisome biogenesis factor transcripts (PEX3, PEX5L, PEX11β, and PEX14) and proteins (PEX3, PEX14, PMP70) were suppressed in the CNS of COVID‐19 compared to ODC patients (p < 0.05). SARS‐CoV‐2 infection of hamsters revealed viral RNA detection in the olfactory bulb at days 4 and 7 post‐infection while inflammatory gene expression was upregulated in the cerebrum of infected animals by day 14 post‐infection (p < 0.05). Pex3 transcript levels together with catalase and PMP70 immunoreactivity were suppressed in the cerebrum of SARS‐CoV‐2 infected animals (p < 0.05).InterpretationCOVID‐19 induced sustained neuroinflammatory responses with peroxisome biogenesis factor suppression despite limited brainstem SARS‐CoV‐2 neurotropism in humans. These observations offer insights into developing biomarkers and therapies, while also implicating persistent peroxisome dysfunction as a contributor to the neurological post‐acute sequelae of COVID‐19. ANN NEUROL 2023

show abstract

“…Putative pathophysiological mechanisms involved in newly diagnosed neuropsychiatric manifestations in patients without a history of mental illness following the acute phase of COVID-19 are multifactorial, resulting either from long-term damage to the brain as a consequence of direct viral effects, persistent systemic inflammation or the psychosocial negative impact of the pandemic, including social isolation, financial instability, fear of infection, lockdowns and lack of family support (Fig. 1) (33)(34)(35)(36).…”

Section: Pathophysiological Mechanisms and 'Long-covid' Neuropsychiat...mentioning

confidence: 99%

New‑onset neuropsychiatric sequelae and ‘long‑COVID’ syndrome (Review)

et al. 2022

View full text Add to dashboard Cite

The ongoing coronavirus disease 2019 (COVID-19) pandemic has had a widespread impact on individuals' mental health through indirect psychological and social mechanisms, related to factors such as fear of infection or death, social isolation, lack of social support and financial instability. The severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection has also been associated with the development or recurrence of neuropsychiatric symptoms, both during the acute phase, as well as during the post-acute 'long-COVID' phase. In addition to the COVID-19 survivors with a mental health history that are at a high risk of experiencing a range of neuropsychiatric symptoms following resolution of acute COVID-19, there is accumulating evidence that a diagnosis of COVID-19 may also be associated with new-onset neuropsychiatric morbidity among survivors without pre-existing mental health disorders. In particular, studies investigating the incidence of post-acute neuropsychiatric sequelae, based mostly on retrospective cohort study designs and data from national health registries, have reported the development of new-onset manifestations, including depression, anxiety, psychotic symptoms, sleep disturbances and fatigue. Nevertheless, when COVID-19 survivors were compared with SARS-CoV-2-negative controls and especially survivors of other disorders (such as influenza), the findings regarding the risk of incident neuropsychiatric manifestations varied among studies. While there is evidence of an association between SARS-CoV-2 infection and the subsequent occurrence of new-onset neuropsychiatric symptoms, especially among patients with increased disease severity, further research using methodological approaches less susceptible to confounding bias is required to establish causal relationships. Contents 1. Introduction 2. New-onset neuropsychiatric sequelae in COVID-19 survivors 3. Pathophysiological mechanisms and 'long-COVID' neuropsychiatric symptoms 4. Conclusions

show abstract

Long COVID and long chain fatty acids (LCFAs): Psychoneuroimmunity implication of omega-3 LCFAs in delayed consequences of COVID-19

Cited by 30 publications

References 99 publications

The Clinical Observation of Inflammation Theory for Depression: The Initiative of the Formosa Long COVID Multicenter Study (FOCuS)

The Clinical Observation of Inflammation Theory for Depression: The Initiative of the Formosa Long COVID Multicenter Study (FOCuS)

COVID‐19 Induces Neuroinflammation and Suppresses Peroxisomes in the Brain

New‑onset neuropsychiatric sequelae and ‘long‑COVID’ syndrome (Review)

Contact Info

Product

Resources

About