Cognitive impairment in long-COVID DOI
Julide Tozkir, Çiğdem Turkmen, Barış Topçular

et al.

Ideggyógyászati Szemle, Journal Year: 2024, Volume and Issue: 77(5-6), P. 151 - 159

Published: Jan. 1, 2024

Background – Long Covid is a complex condition characterised by symptoms that persist for weeks and months after the infection, accompanied cognitive im­pairment negatively affects daily life. Understanding this important development of diagnostic therapeutic strategies. Purpose This article aims to provide comprehensive overview impairment in long-COVID, including its definition, symptoms, pathophysiology, risk factors, assessment tools, imaging abnormalities, potential biomarkers, management strategies, long-term outcomes, future directions research. Methods The search methodology used review aimed include wide range research on related both COVID-19 long-COVID. Systematic searches PubMed Google Scholar databases were conducted using mixture MeSH terms keywords ‘cognition’, ‘cognitive impairment’, ‘brain fog’, ‘COVID-19’ ‘long-COVID’. was restricted studies published English between 1 January 2019 11 February 2024, which presented findings neurological manifestations human participants. Results Long-COVID characterized persistent following with being prominent feature. Symptoms brain fog, difficulties concentration, memory issues, executive function deficits. Pathophysiological mechanisms involve viral persistence, immune responses, vascular damage. Risk factors age, pre-existing conditions, disease severity. Cognitive tools such as Montreal Assessment (MoCA) are essential diagnosis. Imaging studies, MRI, PET, SPECT, reveal structural functional alterations. Potential biomarkers C-reactive protein, interleukin-6, neuron-specific enolase. Management strategies encompass rehabilitation, occupational therapy, medications, lifestyle modifications. Discussion poses multifaceted challenge, significantly impacts patients’ lives. A multidisciplinary approach, rehabilitation medication when appropriate, effective management. Future should focus validating understanding outcomes. Conclusion global health concern, distressing symptom. While pharmacological interventions have potential, they require careful consideration. Continued crucial improving treatment

Language: Английский

Cognitive impairment after long COVID-19: current evidence and perspectives DOI Creative Commons
Zhitao Li, Zhen Zhang, Zhuoya Zhang

et al.

Frontiers in Neurology, Journal Year: 2023, Volume and Issue: 14

Published: July 31, 2023

COVID-19, caused by the SARS-CoV-2 virus, is a respiratory infectious disease. While most patients recover after treatment, there growing evidence that COVID-19 may result in cognitive impairment. Recent studies reveal some individuals experience deficits, such as diminished memory and attention, well sleep disturbances, suggesting could have long-term effects on function. Research indicates contribute to decline damaging crucial brain regions, including hippocampus anterior cingulate cortex. Additionally, identified active neuroinflammation, mitochondrial dysfunction, microglial activation patients, implying these factors be potential mechanisms leading Given findings, possibility of impairment following treatment warrants careful consideration. Large-scale follow-up are needed investigate impact function offer support clinical rehabilitation practices. In-depth neuropathological biological can elucidate precise provide theoretical basis for prevention, intervention research. Considering risks reinfection, it imperative integrate basic research data optimize preservation patients' quality life. This integration will also valuable insights responding similar public health events future. perspective article synthesizes discussing outlining future directions.

Language: Английский

Citations

38

Psychiatric symptoms in Long-COVID patients: a systematic review DOI Creative Commons
Mattia Marchi,

Pietro Grenzi,

Valentina Serafini

et al.

Frontiers in Psychiatry, Journal Year: 2023, Volume and Issue: 14

Published: June 21, 2023

People who have been infected by COVID-19 showing persistent symptoms after 4 weeks from recovery are thought to suffer Long-COVID syndrome (LC). There is uncertainty on the clinical manifestations of LC. We undertook a systematic review summarize available evidence about main psychiatric LC.PubMed (Medline), Scopus, CINHAL, PsycINFO, and EMBASE were searched until May 2022. Studies reporting estimation emerging and/or diagnoses among adult people with LC included. Pooled prevalence for each condition was calculated in absence control groups compare with.Thirty-three reports included final selection, corresponding 282,711 participants After infection recovery, reported following symptoms: depression, anxiety, post-traumatic (PTS), cognitive sleeping disturbances (i.e., insomnia or hypersomnia). The most common manifestation resulted be sleep disturbances, followed PTS, impairment attention memory deficits). However, some estimates affected important outlier effect played one study. If study weight not considered, anxiety.LC may non-specific manifestations. More research needed better define differentiate it other post-infectious post-hospitalization syndromes.PROSPERO (CRD42022299408).

Language: Английский

Citations

30

COVID-19 and Long COVID: Disruption of the Neurovascular Unit, Blood-Brain Barrier, and Tight Junctions DOI
Duraisamy Kempuraj, Kristina Aenlle, Jessica R. Cohen

et al.

The Neuroscientist, Journal Year: 2023, Volume and Issue: 30(4), P. 421 - 439

Published: Sept. 11, 2023

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of disease 2019 (COVID-19), could affect brain structure and function. SARS-CoV-2 can enter through different routes, including olfactory, trigeminal, vagus nerves, blood immunocytes. may also from peripheral a disrupted blood-brain barrier (BBB). The neurovascular unit in brain, composed neurons, astrocytes, endothelial cells, pericytes, protects parenchyma by regulating entry substances blood. astrocytes highly express angiotensin converting enzyme (ACE2), indicating that BBB be disturbed lead to derangements tight junction adherens proteins. This leads increased permeability, leakage components, movement immune cells into parenchyma. cross microvascular an ACE2 receptor–associated pathway. exact mechanism dysregulation COVID-19/neuro-COVID is not clearly known, nor development long COVID. Various biomarkers indicate severity neurologic complications COVID-19 help objectively diagnose those developing review highlights importance disruption, as well some potentially useful COVID-19, COVID/neuro-COVID.

Language: Английский

Citations

29

Unraveling Links between Chronic Inflammation and Long COVID: Workshop Report DOI Open Access
Pushpa Tandon, Natalie Abrams, Leela Rani Avula

et al.

The Journal of Immunology, Journal Year: 2024, Volume and Issue: 212(4), P. 505 - 512

Published: Feb. 5, 2024

As COVID-19 continues, an increasing number of patients develop long COVID symptoms varying in severity that last for weeks, months, or longer. Symptoms commonly include lingering loss smell and taste, hearing loss, extreme fatigue, "brain fog." Still, persistent cardiovascular respiratory problems, muscle weakness, neurologic issues have also been documented. A major problem is the lack clear guidelines diagnosing COVID. Although some studies suggest due to prolonged inflammation after SARS-CoV-2 infection, underlying mechanisms remain unclear. The broad range COVID-19's bodily effects responses initial viral infection are poorly understood. This workshop brought together multidisciplinary experts showcase discuss latest research on chronic might be associated with sequelae following infection.

Language: Английский

Citations

11

Flavonoids derived from medicinal plants as a COVID‐19 treatment DOI Creative Commons
Mentor Sopjani, Francesca Falco, Federica Impellitteri

et al.

Phytotherapy Research, Journal Year: 2024, Volume and Issue: 38(3), P. 1589 - 1609

Published: Jan. 29, 2024

Abstract The severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) causes COVID‐19 disease. Through its viral spike (S) protein, the virus enters and infects epithelial cells by utilizing angiotensin‐converting enzyme as a host cell's receptor protein. pandemic had profound impact on global public health economies. Although various effective vaccinations medications are now available to prevent treat COVID‐19, natural compounds derived from medicinal plants, particularly flavonoids, demonstrated therapeutic potential Flavonoids exhibit dual antiviral mechanisms: direct interference with invasion inhibition of replication. Specifically, they target key molecules, proteases, involved in infection. These showcase significant immunomodulatory anti‐inflammatory properties, effectively inhibiting inflammatory cytokines. Additionally, emerging evidence supports flavonoids mitigate progression individuals obesity positively influencing lipid metabolism. This review aims elucidate molecular structure SARS‐CoV‐2 underlying mechanism action virus. study evaluates anti‐SARS‐CoV‐2 properties exhibited flavonoid compounds, specific interest their mechanisms action, applications for prevention treatment COVID‐19. Nevertheless, portion existing knowledge is based theoretical frameworks findings vitro investigations. Further research required better assess effectiveness combating SARS‐CoV‐2, particular emphasis vivo clinical

Language: Английский

Citations

8

Possible Role of Fibrinaloid Microclots in Postural Orthostatic Tachycardia Syndrome (POTS): Focus on Long COVID DOI Open Access
Douglas B. Kell, Asad Khan,

Binita Kane

et al.

Journal of Personalized Medicine, Journal Year: 2024, Volume and Issue: 14(2), P. 170 - 170

Published: Jan. 31, 2024

Postural orthostatic tachycardia syndrome (POTS) is a common accompaniment of variety chronic, inflammatory diseases, including long COVID, as are small, insoluble, 'fibrinaloid' microclots. We here develop the argument, with accompanying evidence, that fibrinaloid microclots, through their ability to block flow blood microcapillaries and thus cause tissue hypoxia, not simply correlated but in fact, by preceding it, may be chief intermediary POTS, which body's exaggerated 'physiological' response hypoxia. Similar reasoning accounts for symptoms bundled under term 'fatigue'. Amyloids known membrane disruptors, when targets nerve membranes, this can explain neurotoxicity hence autonomic nervous system dysfunction contributes POTS. Taken together view, we indicate microclots serve link POTS fatigue COVID manner at once both mechanistic explanatory. This has clear implications treatment such diseases.

Language: Английский

Citations

8

Precision nutrition to reset virus-induced human metabolic reprogramming and dysregulation (HMRD) in long-COVID DOI Creative Commons
A. Satyanarayan Naidu, Chin‐Kun Wang, Pingfan Rao

et al.

npj Science of Food, Journal Year: 2024, Volume and Issue: 8(1)

Published: March 30, 2024

Language: Английский

Citations

8

Vascular Dysfunctions Contribute to the Long-Term Cognitive Deficits Following COVID-19 DOI Creative Commons
Zahra Shabani, Jialing Liu, Hua Su

et al.

Biology, Journal Year: 2023, Volume and Issue: 12(8), P. 1106 - 1106

Published: Aug. 9, 2023

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) is a single-stranded RNA virus and member of the corona family, primarily affecting upper system lungs. Like many other viruses, SARS-CoV-2 can spread to organ systems. Apart from causing diarrhea, another very common but debilitating complication caused by neurological symptoms cognitive difficulties, which occur in up two thirds hospitalized COVID-19 patients range shortness concentration overall declined speed executive or memory function impairment. Neuro-cognitive dysfunction “brain fog” are frequently present cases, last several months after infection, leading disruption daily life. Cumulative evidence suggests that affects vasculature extra-pulmonary systems directly indirectly, impairment endothelial even multi-organ damage. The post long-lasting neurocognitive impairments have not been studied fully their underlying mechanism remains elusive. In this review, we summarize current understanding effects on vascular how leads patients.

Language: Английский

Citations

19

Mast cells in the autonomic nervous system and potential role in disorders with dysautonomia and neuroinflammation DOI Creative Commons
Theoharis C. Theoharides,

Assma Twahir,

Duraisamy Kempuraj

et al.

Annals of Allergy Asthma & Immunology, Journal Year: 2023, Volume and Issue: 132(4), P. 440 - 454

Published: Nov. 10, 2023

Mast cells (MC) are ubiquitous in the body, and they critical for not only allergic diseases but also immunity inflammation, including having potential involvement pathophysiology of dysautonomias neuroinflammatory disorders. MC located perivascularly close to nerve endings sites such as carotid bodies, heart, hypothalamus, pineal gland, adrenal gland that would allow them regulate be affected by autonomic nervous system (ANS). stimulated allergens many other triggers some from ANS can affect release neurosensitizing, proinflammatory, vasoactive mediators. Hence, may able homeostatic functions seem dysfunctional conditions, postural orthostatic tachycardia syndrome, autism spectrum disorder, myalgic encephalomyelitis/chronic fatigue Long-COVID syndrome. The evidence indicates there is a possible association between these conditions associated with activation. There no effective treatment any form than minimizing symptoms. Given ways could activated numerous mediators released, it important develop inhibit stimulation ANS-relevant

Language: Английский

Citations

17

Neurovascular unit, neuroinflammation and neurodegeneration markers in brain disorders DOI Creative Commons
Duraisamy Kempuraj,

Kirk D. Dourvetakis,

Jessica R. Cohen

et al.

Frontiers in Cellular Neuroscience, Journal Year: 2024, Volume and Issue: 18

Published: Oct. 25, 2024

Neurovascular unit (NVU) inflammation via activation of glial cells and neuronal damage plays a critical role in neurodegenerative diseases. Though the exact mechanism disease pathogenesis is not understood, certain biomarkers provide valuable insight into pathogenesis, severity, progression therapeutic efficacy. These markers can be used to assess pathophysiological status brain including neurons, astrocytes, microglia, oligodendrocytes, specialized microvascular endothelial cells, pericytes, NVU, blood-brain barrier (BBB) disruption. Damage or derangements tight junction (TJ), adherens (AdJ), gap (GJ) components BBB lead increased permeability neuroinflammation various disorders disorders. Thus, neuroinflammatory evaluated blood, cerebrospinal fluid (CSF), tissues determine neurological progression, responsiveness. Chronic common age-related Alzheimer's (AD), Parkinson's (PD), dementia. Neurotrauma/traumatic injury (TBI) also leads acute chronic responses. The expression some may altered many years even decades before onset In this review, we discuss neuroinflammation, neurodegeneration associated with disorders, especially those neurovascular pathologies. CSF, tissues. Neurofilament light (NfL), ubiquitin C-terminal hydrolase-L1 (UCHL1), fibrillary acidic protein (GFAP), Ionized calcium-binding adaptor molecule 1 (Iba-1), transmembrane 119 (TMEM119), aquaporin, endothelin-1, platelet-derived growth factor receptor beta (PDGFRβ) are important markers. Recent BBB-on-a-chip modeling offers promising potential for providing an in-depth understanding neurotherapeutics. Integration these clinical practice could potentially enhance early diagnosis, monitor improve outcomes.

Language: Английский

Citations

5