Translational Psychiatry, Journal Year: 2024, Volume and Issue: 14(1)
Published: Oct. 26, 2024
Language: Английский
GeroScience, Journal Year: 2025, Volume and Issue: unknown
Published: Jan. 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.
Language: Английский
Citations
2
GeroScience, Journal Year: 2024, Volume and Issue: unknown
Published: June 14, 2024
Language: Английский
Citations
10
Ageing Research Reviews, Journal Year: 2024, Volume and Issue: 101, P. 102448 - 102448
Published: Aug. 8, 2024
Language: Английский
Citations
4
Alzheimer s & Dementia, Journal Year: 2024, Volume and Issue: unknown
Published: Aug. 29, 2024
Many coronavirus disease 2019 (COVID-19) positive individuals exhibit abnormal electroencephalographic (EEG) activity reflecting "brain fog" and mild cognitive impairments even months after the acute phase of infection. Resting-state EEG abnormalities include slowing (reduced alpha rhythm; increased slow waves) epileptiform activity. An expert panel conducted a systematic review to present compelling evidence that deficits due COVID-19 Alzheimer's related dementia (ADRD) are driven by overlapping pathologies neurophysiological abnormalities. seen in patients resemble those observed early stages neurodegenerative diseases, particularly ADRD. It is proposed similar Long COVID ADRD parallel neuroinflammation, astrocyte reactivity, hypoxia, neurovascular injury. These underpinning decline can be detected routine exams. Future research will explore value monitoring for predicting long-term outcomes efficacy therapeutic interventions. HIGHLIGHTS: Abnormal intrinsic electrophysiological brain activity, such as EEG, reduced wave, characteristic findings patients. have potential neural biomarkers identify neurological complications at stage disease, assist clinical assessment, assess risk Similar typically with impairments, Evidence presented supports idea resulting, least part, from neuroinflammatory mechanisms reactivity. Identifying common biological highlight critical underlying disorders decline. elucidates questions regarding impairment not yet been adequately investigated.
Language: Английский
Citations
4
Journal of NeuroVirology, Journal Year: 2025, Volume and Issue: unknown
Published: Feb. 25, 2025
Language: Английский
Citations
0
Cells, Journal Year: 2023, Volume and Issue: 12(22), P. 2601 - 2601
Published: Nov. 10, 2023
A growing body of evidence indicates that a neuropathological cross-talk takes place between the coronavirus disease 2019 (COVID-19) -the pandemic severe pneumonia has had tremendous impact on global economy and health since three years after its outbreak in December 2019- Alzheimer’s Disease (AD), leading cause dementia among human beings, reaching 139 million by year 2050. Even though COVID-19 is primary respiratory disease, causative agent, so-called Severe Acute Respiratory Syndrome 2 (SARS-CoV-2), also endowed with high neuro-invasive potential (Neurocovid). The neurological complications COVID-19, resulting from direct viral entry into Central Nervous System (CNS) and/or indirect systemic inflammation dysregulated activation immune response, encompass memory decline anosmia which are typically associated AD symptomatology. In addition, patients diagnosed more vulnerable to SARS-CoV-2 infection inclined clinical outcomes. present review, we better elucidate intimate connection summarizing involved risk factors/targets underlying biological mechanisms shared these two disorders particular focus Angiotensin-Converting Enzyme (ACE2) receptor, APOlipoprotein E (APOE), aging, neuroinflammation cellular pathways Amyloid Precursor Protein (APP)/Amyloid beta (Aβ) tau neuropathologies. Finally, involvement ophthalmological manifestations, including vitreo-retinal abnormalities visual deficits, both discussed. Understanding common physiopathological aspects linking will pave way novel management diagnostic/therapeutic approaches cope them post-pandemic future.
Language: Английский
Citations
10
Journal of Neurology, Journal Year: 2025, Volume and Issue: 272(6)
Published: May 6, 2025
Abstract Background Neuropathological and clinical studies suggest that infection with SARS-CoV-2 may increase the long-term risk of neurodegeneration. Methods We provide a narrative overview pathological observations justifying implementation surveillance program to monitor changes in incidence neurodegenerative disorders years after COVID-19. Results Autopsy revealed diverse brain, including loss vascular integrity, microthromboses, gliosis, demyelination, neuronal- glial injury cell death, both unvaccinated vaccinated individuals irrespective severity Recent data microglia play an important role sustained COVID-19-related inflammation, which contributes etiology initiating cascade, worsening pre-existing disease or acceleration processes. Histopathological have been supported by neuroimaging, epidemiological also suggested higher for diseases Conclusions Due high prevalence COVID-19 during pandemic, healthcare systems should be aware of, prepared potential upcoming years. Strategies include follow-up well-described cohorts, analyses outcomes COVID-19-registries, nationwide programs using record-linkage ICD-10 diagnoses, comparing post-pandemic periods values pre-pandemic Awareness active are particularly needed, because manifestations due earlier infections no longer quoted as post-COVID-19 symptoms, hence, increasing pathologies at community level remain unnoticed.
Language: Английский
Citations
0
Experimental Neurology, Journal Year: 2024, Volume and Issue: 380, P. 114908 - 114908
Published: July 31, 2024
Language: Английский
Citations
1
bioRxiv (Cold Spring Harbor Laboratory), Journal Year: 2024, Volume and Issue: unknown
Published: April 11, 2024
Abstract The severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2), causing human disease 2019 (COVID-19), not only affects the tract, but also impacts other organs including brain. A considerable number of COVID-19 patients develop neuropsychiatric symptoms that may linger for weeks and months contribute to “long-COVID”. While neurological are well described, cellular mechanisms neurologic disorders attributed infection still enigmatic. Here, we studied effect an with SARS-CoV-2 on structure expression marker proteins astrocytes microglial cells in frontal cortex who died from comparison non-COVID-19 controls. Most had retracted processes rounded enlarged cell bodies both gray white matter, as visualized by anti-Iba1 staining confocal fluorescence microscopy. In addition, matter were frequently labeled intense anti-GFAP staining, whereas controls, most expressed little GFAP. striking difference between controls was found anti-aquaporin-4 (AQP4) staining. patients, a large showed increase AQP4. AQP4 polarity lost covered entire cell, body all processes, while immunostaining mainly detected endfeet around blood vessels did visualize body. summary, our data suggest neuroinflammation upon microgliosis astrogliosis, loss polarity.
Language: Английский
Citations
0
Journal of Neurochemistry, Journal Year: 2024, Volume and Issue: unknown
Published: Aug. 2, 2024
This preface introduces the Special Issue on Neuroimmunology in Journal of Neurochemistry. The basis neuroimmunology is to understand functional interactions between cells immune system and central nervous (CNS). These communicate across systems because they share signaling molecules corresponding receptors. Moreover, this cell allows for dynamic bidirectional communication brain both within CNS proper as well peripheral organs. Because this, intersects with many biological processes including immunity, behavior, endocrinology, metabolism, pathology. Understanding neuroimmune that influence homeostasis especially relevant health disease. special issue comprises 14 articles, representing 9 review articles 5 original covering roles injury, & infections, cancer, Alzheimer's disease, COVID-19. Thus, these highlight different aspects signaling, represent progress understanding consequences inflammation key pathways brains.
Language: Английский
Citations
0