South African General Practitioner, Год журнала: 2022, Номер 3(3), С. 74 - 76
Опубликована: Июнь 1, 2022
Язык: Английский
Nature Reviews Microbiology, Год журнала: 2023, Номер 21(3), С. 133 - 146
Опубликована: Янв. 13, 2023
Язык: Английский
Процитировано
2751
Journal of Internal Medicine, Год журнала: 2023, Номер 294(5), С. 563 - 581
Опубликована: Сен. 27, 2023
Abstract The long‐term effects of COVID‐19 on cognitive function have become an area increasing concern. This paper provides overview characteristics, risk factors, possible mechanisms, and management strategies for dysfunction in post‐COVID‐19 condition (PCC). Prolonged is one the most common impairments PCC, affecting between 17% 28% individuals more than 12 weeks after infection persisting some cases several years. Cognitive dysfunctions can be manifested as a wide range symptoms including memory impairment, attention deficit, executive dysfunction, reduced processing speed. Risk factors developing with or without impairments, include advanced age, preexisting medical conditions, severity acute illness. underlying mechanisms remain unclear, but proposed contributors neuroinflammation, hypoxia, vascular damage, latent virus reactivation not excluding possibility direct viral invasion central nervous system, illustrating complex pathology. As individual variation large, neuropsychological examination person‐centered multidimensional approach are required. According to World Health Organization, limited evidence COVID‐19‐related necessitates implementing rehabilitation interventions from established practices similar conditions. Psychoeducation compensatory skills training recommended. Assistive products environmental modifications adapted needs might helpful. In specific attention‐ working dysfunctions, training—carefully monitored intensity—might effective people who do suffer post‐exertional malaise. Further research crucial evidence‐based impairments.
Язык: Английский
Процитировано
38
International Journal of Molecular Sciences, Год журнала: 2023, Номер 24(13), С. 10458 - 10458
Опубликована: Июнь 21, 2023
Long COVID (LC) encompasses a constellation of long-term symptoms experienced by at least 10% people after the initial SARS-CoV-2 infection, and so far it has affected about 65 million people. The etiology LC remains unclear; however, many pathophysiological pathways may be involved, including viral persistence; chronic, low-grade inflammatory response; immune dysregulation defective reactivation latent viruses; autoimmunity; persistent endothelial dysfunction coagulopathy; gut dysbiosis; hormonal metabolic dysregulation; mitochondrial dysfunction; autonomic nervous system dysfunction. There are no specific tests for diagnosis LC, clinical features laboratory findings biomarkers not specifically relate to LC. Therefore, is paramount importance develop validate that can employed prediction, prognosis its therapeutic response, although this effort hampered challenges pertaining non-specific nature majority manifestations in spectrum, small sample sizes relevant studies other methodological issues. Promising candidate found some patients markers systemic inflammation, acute phase proteins, cytokines chemokines; reflecting persistence, herpesviruses endotheliopathy, coagulation fibrinolysis; microbiota alterations; diverse proteins metabolites; biomarkers; cerebrospinal fluid biomarkers. At present, there only two reviews summarizing they do cover entire umbrella current biomarkers, their link etiopathogenetic mechanisms or diagnostic work-up comprehensive manner. Herein, we aim appraise synopsize available evidence on typical classification based pathogenetic main symptomatology frame epidemiological aspects syndrome furthermore assess limitations as well potential implications interventions.
Язык: Английский
Процитировано
32
Scientific Reports, Год журнала: 2023, Номер 13(1)
Опубликована: Ноя. 2, 2023
After Covid-19 infection, 12.5% develops post-Covid-syndrome (PCS). Symptoms indicate numerous affected organ systems. a year, chronic fatigue, dysautonomia and neurological neuropsychiatric complaints predominate. In this study, 95 PCS patients were treated with selective serotonin reuptake inhibitors (SSRIs). This study used an exploratory questionnaire found that two-thirds of had reasonably good to strong response on SSRIs, over quarter moderate response, while 10% reported no response. Overall, experienced substantial improved well-being. Brainfog sensory overload decreased most, followed by fatigue dysautonomia. Outcomes measured three different measures correlated strongly each other. The SSRIs in conditions was explained seven possible neurobiological mechanisms based recent literature integrated already existing knowledge. Important for understanding these is the underlying biochemical interaction between various neurotransmitter systems parts immune system, their dysregulation PCS. main link appears be metabolic kynurenine pathway (KP) which interacts extensively system. KP uses same precursor as serotonin: tryptophan. overactive maintains inflammation causes lack Finally, potential avenues future research advance line clinical are discussed.
Язык: Английский
Процитировано
26
Frontiers in Aging Neuroscience, Год журнала: 2022, Номер 14
Опубликована: Дек. 9, 2022
Many people with coronavirus disease 2019 (COVID-19) report varying degrees of memory impairment. Neuroimaging techniques such as MRI and PET have been utilized to shed light on how COVID-19 affects brain function in humans, including dysfunction. In this PRISMA-based systematic review, we compared summarized the current literature looking at relationship between COVID-19-induced neuropathological changes by neuroimaging scans symptoms experienced patients who recovered from COVID-19. Overall, review suggests a correlational trend structural abnormalities (e.g., cortical atrophy white matter hyperintensities) or functional hypometabolism) wide range regions (particularly frontal, parietal temporal regions) impairments survivors, although causal them remains elusive absence sufficient caution. Further longitudinal investigations, particularly controlled studies combined analyses, are needed provide additional evidence.
Язык: Английский
Процитировано
33
Progress in molecular biology and translational science, Год журнала: 2024, Номер unknown
Опубликована: Янв. 1, 2024
Язык: Английский
Процитировано
7
Neurology International, Год журнала: 2023, Номер 15(2), С. 725 - 742
Опубликована: Май 31, 2023
Sustained cognitive deficits are a common and debilitating feature of “long COVID”, but currently there no FDA-approved treatments. The functions the dorsolateral prefrontal cortex (dlPFC) most consistently afflicted by long COVID, including in working memory, motivation, executive functioning. COVID-19 infection greatly increases kynurenic acid (KYNA) glutamate carboxypeptidase II (GCPII) brain, both which can be particularly deleterious to PFC function. KYNA blocks NMDA nicotinic-alpha-7 receptors, two receptors required for dlPFC neurotransmission, GCPII reduces mGluR3 regulation cAMP-calcium-potassium channel signaling, weakens network connectivity neuronal firing. Two agents approved other indications may helpful restoring physiology: antioxidant N-acetyl cysteine inhibits production KYNA, α2A-adrenoceptor agonist guanfacine regulates signaling is also anti-inflammatory. Thus, these treating symptoms COVID.
Язык: Английский
Процитировано
15
Journal of Neurology, Год журнала: 2023, Номер 270(10), С. 4640 - 4646
Опубликована: Авг. 9, 2023
Язык: Английский
Процитировано
12
Molecular Psychiatry, Год журнала: 2023, Номер 28(11), С. 4540 - 4552
Опубликована: Апрель 7, 2023
Abstract Neuroinflammatory disorders preferentially impair the higher cognitive and executive functions of prefrontal cortex (PFC). This includes such challenging as delirium, perioperative neurocognitive disorder, sustained deficits from “long-COVID” or traumatic brain injury. There are no FDA-approved treatments for these symptoms; thus, understanding their etiology is important generating therapeutic strategies. The current review describes molecular rationale why PFC circuits especially vulnerable to inflammation, how α2A-adrenoceptor (α2A-AR) actions throughout nervous immune systems can benefit in needed cognition. layer III dorsolateral (dlPFC) that generate sustain mental representations cognition have unusual neurotransmission neuromodulation. They wholly dependent on NMDAR neurotransmission, with little AMPAR contribution, thus kynurenic acid inflammatory signaling which blocks NMDAR. Layer dlPFC spines also neuromodulation, cAMP magnification calcium spines, opens nearby potassium channels rapidly weaken connectivity reduce neuronal firing. process must be tightly regulated, e.g. by mGluR3 α2A-AR prevent loss However, production GCPII reduces markedly diminishes network Both basic clinical studies show agonists guanfacine restore firing function, through direct dlPFC, but reducing activity stress-related circuits, locus coeruleus amygdala, having anti-inflammatory system. information particularly timely, currently focus large trials treatment open label long-COVID.
Язык: Английский
Процитировано
11
European Archives of Psychiatry and Clinical Neuroscience, Год журнала: 2024, Номер 274(8), С. 1829 - 1845
Опубликована: Янв. 3, 2024
Abstract Post-acute sequelae of COVID-19 can present as multi-organ pathology, with neuropsychiatric symptoms being the most common symptom complex, characterizing long COVID a syndrome significant disease burden for affected individuals. Several typical COVID, such fatigue, depressive and cognitive impairment, are also key features other psychiatric disorders myalgic encephalomyelitis/chronic fatigue (ME/CFS) major disorder (MDD). However, clinically successful treatment strategies still lacking often inspired by options diseases similar clinical presentations, ME/CFS. Acetylcarnitine, shortest metabolite class fatty acid metabolites called acylcarnitines one abundant blood in humans be used dietary/nutritional supplement proven efficacy MDD, ME/CFS disorders. Basic research recent decades has established general, acetylcarnitine particular, important regulators indicators mitochondrial function physiological processes neuroinflammation energy production pathways. In this review, we will compare basis fatigue-associated diseases. We review molecular mechanisms associated altered metabolism potential to interfere these therapeutic agent. Finally, current evidence propose future investigate option COVID.
Язык: Английский
Процитировано
4