European Radiology, Год журнала: 2023, Номер 33(12), С. 8540 - 8541
Опубликована: Июль 11, 2023
Язык: Английский
GeroScience, Год журнала: 2025, Номер unknown
Опубликована: Янв. 7, 2025
Abstract Long COVID (also known as post-acute sequelae of SARS-CoV-2 infection [PASC] or post-COVID syndrome) is characterized by persistent symptoms that extend beyond the acute phase infection, affecting approximately 10% to over 30% those infected. It presents a significant clinical challenge, notably due pronounced neurocognitive such brain fog. The mechanisms underlying these effects are multifactorial, with mounting evidence pointing central role cerebromicrovascular dysfunction. This review investigates key pathophysiological contributing cerebrovascular dysfunction in long and their impacts on health. We discuss how endothelial tropism direct vascular trigger dysfunction, impaired neurovascular coupling, blood–brain barrier disruption, resulting compromised cerebral perfusion. Furthermore, appears induce mitochondrial enhancing oxidative stress inflammation within cells. Autoantibody formation following also potentially exacerbates injury, chronic ongoing compromise. These factors collectively contribute emergence white matter hyperintensities, promote amyloid pathology, may accelerate neurodegenerative processes, including Alzheimer’s disease. emphasizes critical advanced imaging techniques assessing health need for targeted interventions address complications. A deeper understanding essential advance treatments mitigate its long-term consequences.
Язык: Английский
Процитировано
4
Frontiers in Neurology, Год журнала: 2023, Номер 14
Опубликована: Июль 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.
Язык: Английский
Процитировано
39
Brain Communications, Год журнала: 2024, Номер 6(2)
Опубликована: Янв. 1, 2024
Abstract Components that comprise our brain parenchymal and cerebrovascular structures provide a homeostatic environment for proper neuronal function to ensure normal cognition. Cerebral insults (e.g. ischaemia, microbleeds infection) alter cellular physiologic processes within the neurovascular unit contribute cognitive dysfunction. COVID-19 has posed significant complications during acute convalescent stages in multiple organ systems, including brain. Cognitive impairment is prevalent complication patients, irrespective of severity SARS-CoV-2 infection. Moreover, overwhelming evidence from vitro, preclinical clinical studies reported SARS-CoV-2-induced pathologies components are associated with impairment. Neurovascular disruption alters coupling response, critical mechanism regulates cerebromicrovascular blood flow meet energetic demands locally active neurons. Normal processing achieved through response involves coordinated action cells (i.e. neurons glia) cell types endothelia, smooth muscle pericytes). However, current work on COVID-19-induced yet investigate as causal factor. Hence, this review, we aim describe SARS-CoV-2's effects how they can impact decline disease. Additionally, explore potential therapeutic interventions mitigate Given great both individuals public health, necessity effort fundamental scientific research application becomes imperative. This integrated endeavour crucial mitigating deficits induced by its subsequent burden especially vulnerable population.
Язык: Английский
Процитировано
13
GeroScience, Год журнала: 2024, Номер unknown
Опубликована: Июнь 14, 2024
Язык: Английский
Процитировано
12
GeroScience, Год журнала: 2024, Номер 46(3), С. 2885 - 2899
Опубликована: Фев. 23, 2024
Abstract The long COVID (coronavirus disease), a multisystemic condition following severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2) infection, is one of the widespread problems. Some its symptoms affect nervous system and resemble Alzheimer’s disease (AD)—a neurodegenerative caused by accumulation amyloid beta hyperphosphorylation tau proteins. Multiple studies have found dependence between these two conditions. Patients with greater risk SARS-CoV-2 infection due to increased levels angiotensin-converting enzyme 2 (ACE2), itself promotes generation which enhances AD. Also, molecular pathways are alike—misregulations in folate-mediated one-carbon metabolism, deficit Cq10, disease-associated microglia. Medical imaging both diseases shows decrease volume gray matter, global brain size reduction, hypometabolism parahippocampal gyrus, thalamus, cingulate cortex. In some studies, similar approach applied medication can be seen, including use amino adamantanes phenolic compounds rosemary. significance connections their possible application medical practice still needs further study but there possibility that they will help better understand COVID.
Язык: Английский
Процитировано
9
Academic Radiology, Год журнала: 2025, Номер unknown
Опубликована: Март 1, 2025
Язык: Английский
Процитировано
1
Journal of the Neurological Sciences, Год журнала: 2025, Номер 472, С. 123464 - 123464
Опубликована: Март 12, 2025
Highlights•Multi-b-value diffusion MRI has potential applications in post-COVID assessment.•Post-COVID cerebral microvascular dysfunction is more severe ICU survivors.•Post-COVID may be a result of acute tissue hypoxia.•Objective cognition unaffected by dysfunction.•Subjective complaints are related to dysfunction.AbstractObjectiveCoronavirus disease 2019 (COVID-19) known have adverse effects on the brain's vasculature some patients. After recovery infection, vascular abnormalities persist, but it remains unclear which pathological pathways play role and cognitive contribute complaints.MethodsIn this observational cohort study, 108 previously hospitalized COVID-19 survivors (general ward: n = 53; intensive care unit (ICU): 55) were compared. Cerebral properties cortical gray matter (cGM), normal-appearing white (NAWM), hyperintensities (WMH) assessed using multi-b-value around 9 months post-infection systemic blood markers performance complaints.ResultsA lower perfusion volume fraction (fmv) flow-related measure (fmv·Dmv) found compared general ward patients cGM (p .032; p .021), NAWM .008; .006), WMH .014; .035). No associations between diffusion/perfusion metrics performance, fmv was those with .047). In survivors, higher median lactate levels during admission associated .031) fmv·Dmv .044) NAWM.InterpretationSignificantly widespread survivors. Post-COVID due hypoxia at time infection persisting subjective complaints, even absence objective problems.Graphical abstract
Язык: Английский
Процитировано
1
PLoS ONE, Год журнала: 2023, Номер 18(8), С. e0289508 - e0289508
Опубликована: Авг. 3, 2023
Mild cognitive impairment (MCI) is a prodromal stage to dementia, affecting up 20% of the aging population worldwide. Patients with MCI have an annual conversion rate dementia 15-20%. Thus, conditions that increase from are utmost public health concern. The COVID-19 pandemic poses significant impact on our decline as one leading complications following recovery acute infection. Recent findings suggest increases in older adults. Hence, we aim uncover mechanism for induced and progression pave way future therapeutic targets may mitigate decline.
Язык: Английский
Процитировано
13
Nature and Science of Sleep, Год журнала: 2025, Номер Volume 17, С. 97 - 113
Опубликована: Янв. 1, 2025
COVID-19 has led to reports of fatigue and sleep problems. Brain function changes underlying problems (SP) post-COVID-19 are unclear. This study investigated SP-related brain functional connectivity (FC) alterations. Fifty-five survivors with SP (COVID_SP) 33 without (COVID_NSP), matched for demographics, completed PSQI underwent rs-fMRI at baseline 2-month follow-up. Correlations between FC clinical data were analyzed by Pearson correlation analysis Gaussian random field (GRF) correction. The repeated-measures variance (R-M ANOVA) was explore the interaction time. At baseline, COVID_SP exhibited elevated FC: right precentral gyrus (PrG) left lateral occipital cortex (LOcC)/right PrG, inferior parietal lobule (IPL) superior frontal (SFG), hippocampus (IFG). Higher SFG correlated scores. follow-up, decreased implicated in emotion regulation, executive function, memory; increased semantics, attention, auditory-visual processing. these regions scores PSQI, GAD, PHQ. Repeated-Measures Analysis Variance revealed a significant time effect various scales. Moreover, PrG as well that IPL also discovered effect. provides insight into associated after COVID-19. These may partially explain development SP, they changed over
Язык: Английский
Процитировано
0
Frontiers in Immunology, Год журнала: 2025, Номер 16
Опубликована: Май 26, 2025
Cerebral small vessel disease (CSVD) refers to a group of pathological syndromes that affect the brain’s microcirculation. These conditions involve damage arteries, arterioles, capillaries, venules, and veins. Cerebrovascular risk factors, immunosenescence, inflammatory responses contribute pathogenesis cerebral disease. The global impact Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) has drawn significant attention chronic inflammation caused by infections. Research into mechanisms which infections induce CSVD made continual advancements. It is imperative reassess importance managing phase follows, highlighting their critical role in pathogenesis. Our focus encompasses SARS-CoV-2, Human Immunodeficiency Virus (HIV), Hepatitis C (HCV), Zika Virus(ZIKV), Treponema pallidum, as well microbial communities within gut oral cavity. pathogen can through such neuroinflammation, blood-brain barrier disruption, microthrombosis, endothelial cell damage, thereby promoting occurrence progression This highlights need for detailed mechanistic research on associated with these pathogens. Furthermore, we hope future, will be able devise targeted prevention treatment strategies based unique characteristics pathogenic various
Язык: Английский
Процитировано
0