An overview of the neurological aspects in COVID-19 infection

Singh, Divyanshi; Singh, Ekta

doi:10.1016/j.jchemneu.2022.102101

Cited by 12 publications

(9 citation statements)

References 128 publications

(155 reference statements)

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“…Changes in brain function may be caused not only by the hyperinflammatory environment induced by the virus, but also by direct viral invasion of neurons. SARS-CoV-2 can infect vascular endothelial cells and then may cross into the brain transcellularly through the BBB endothelium [ 37 , 38 , 39 ]. Whether the virus replicates robustly in the vascular endothelium is unresolved with conflicting data [ 40 , 41 ].…”

Section: Mechanisms Underlying Covid-19 Effects On the Brainmentioning

confidence: 99%

Long COVID, the Brain, Nerves, and Cognitive Function

Reiss

Greene

Dayaramani

et al. 2023

Neurology International

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SARS-CoV-2, a single-stranded RNA coronavirus, causes an illness known as coronavirus disease 2019 (COVID-19). Long-term complications are an increasing issue in patients who have been infected with COVID-19 and may be a result of viral-associated systemic and central nervous system inflammation or may arise from a virus-induced hypercoagulable state. COVID-19 may incite changes in brain function with a wide range of lingering symptoms. Patients often experience fatigue and may note brain fog, sensorimotor symptoms, and sleep disturbances. Prolonged neurological and neuropsychiatric symptoms are prevalent and can interfere substantially in everyday life, leading to a massive public health concern. The mechanistic pathways by which SARS-CoV-2 infection causes neurological sequelae are an important subject of ongoing research. Inflammation- induced blood-brain barrier permeability or viral neuro-invasion and direct nerve damage may be involved. Though the mechanisms are uncertain, the resulting symptoms have been documented from numerous patient reports and studies. This review examines the constellation and spectrum of nervous system symptoms seen in long COVID and incorporates information on the prevalence of these symptoms, contributing factors, and typical course. Although treatment options are generally lacking, potential therapeutic approaches for alleviating symptoms and improving quality of life are explored.

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Section: Mechanisms Underlying Covid-19 Effects On the Brainmentioning

confidence: 99%

Long COVID, the Brain, Nerves, and Cognitive Function

Reiss

Greene

Dayaramani

et al. 2023

Neurology International

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“…The virus causes microvascular changes or damage to lung function resulting in impaired flow of oxygen to the brain with subsequent impaired cognitive function. [43][44][45][46] COVID-19 has an additional risk dimension when it comes to Alzheimer's disease (AD), as COVID-19 has been shown to exacerbate the main pathological components of AD, such as beta-amyloid neurotoxicity and pathological tau accumulation. [47][48][49][50][51] It has also been suggested that COVID-19 might impair amyloid processing and mimic cerebrospinal fluid and serum biomarkers of AD, with decreased amyloid beta loads even in cognitively typical patients.…”

Section: Coronavirus Disease 2019 and The Risk Of Dementiamentioning

confidence: 99%

Exploring the Impact of Coronavirus Disease 2019 on Dementia: A Review

Axenhus¹,

Winblad²

2023

US Neurology

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The coronavirus disease 2019 (COVID-19) pandemic has caused significant disruptions to almost every healthcare system worldwide. Older adults have been hit disproportionately hard by the pandemic, with most deaths occurring among people aged 75 or older. Dementia researchers have noted the increased dementia-related mortality among older adults and fewer dementia diagnoses during the pandemic. Questions have therefore been raised regarding the effects of the COVID-19 virus on dementia prevalence and mortality. As a groundbreaking dementia treatment is about to hit the market, proper diagnoses of dementia are now more important than ever. There are also concerns that the COVID-19 virus could precipitate dementia and worsen dementia symptoms. This short review examines the current scientific evidence on the impact of COVID-19 on dementia mortality and prevalence, as well as describing the pathophysiological mechanisms by which COVID-19 might cause dementia and worsen dementia symptoms. Lastly, this review speculates on how dementia epidemiology might change during the next years as a result of the pandemic and provide suggestions for clinicians on how to respond to the coming changes.

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“…The incubation period for COVID-19 is short, about 5–6 days. As the pandemic progressed there is growing evidence that COVID-19 encompasses not only rapid respiratory/gastrointestinal illnesses, but can also lead to myocardial inflammation [24] and neurological and neuropsychiatric impairments [25] . Furthermore, severe COVID-19 is not solely restricted to the aged population as initially reported, children and young adults are also at risk [26] .…”

Section: Clinical Presentation Of Sars-cov-2-induced Pathologymentioning

confidence: 99%