Can infection of COVID-19 virus exacerbate Alzheimer's symptoms? Hypothetic possible role of angiotensin-converting enzyme-2/Mas/brain-derived neurotrophic factor axis and Tau hyper-phosphorylation

Kermanshahi, Sareh; Gholami, Mina; Motaghinejad, Majid

doi:10.4103/abr.abr_72_20

Cited by 6 publications

(7 citation statements)

References 16 publications

(17 reference statements)

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“…These reports contribute to a growing body of literature about the role that COVID-19 may play in accelerating neurodegeneration in diseases such as CJD, Alzheimer’s disease14 and Parkinson’s disease15 16 Although the mechanism through which it exerts this effect remains unclear, there is evidence suggesting an overlap in neuropathology between COVID-19 and prion disease 17 18…”

Section: Discussionmentioning

confidence: 88%

“…Indeed, elevated proinflammatory cytokines in the context of concomitant infection have previously been shown to accelerate prion disease progression in studies in both humans and animals22 and proinflammatory states and raised CRP have been linked to linked to reduced cognitive function in other neurodegenerative diseases such as Alzheimer’s and Parkinson’s disease 14–16. It is well known that COVID-19 infection can provoke an extreme proinflammatory response, and many viruses have been implicated in exacerbating neurodegeneration through the initiation and propagation of a ‘cytokine storm’ 18…”

Section: Discussionmentioning

confidence: 99%

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Rapid progression of probable Creutzfeldt-Jakob disease with concomitant COVID-19 infection

McGrath,

Pai,

Clack

2023

BMJ Case Rep

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A previously healthy man in his 80s was admitted to a district general hospital with rapidly progressing dementia, gait abnormalities and myoclonus alongside COVID-19 infection. Investigations showed mild elevation of C-reactive protein and neutrophils, unremarkable CT head and mildly raised protein in cerebrospinal spinal fluid (CSF). Brain MRI revealed bilateral cortical and striatal diffusion restriction and electroencephalogram (EEG) findings showed diffuse activity slowing with high amplitude sharp/slow-wave complexes. He was diagnosed with probable sporadic Creutzfeldt-Jakob disease (CJD) and management prioritised comfort and care. He passed away two weeks following admission and a mere 8 weeks after the first onset of symptoms.We present the first documented case of probable CJD with concomitant COVID-19 infection in the UK. We identified six other cases worldwide identified in our literature review. These cases suggest a role of COVID-19 in the rapid progression of CJD and add to the growing evidence of its neuroinflammatory role in other forms of neurodegenerative diseases.

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Section: Discussionmentioning

confidence: 88%

Section: Discussionmentioning

confidence: 99%

Rapid progression of probable Creutzfeldt-Jakob disease with concomitant COVID-19 infection

McGrath,

Pai,

Clack

2023

BMJ Case Rep

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“…Ab is the main component of amyloid plaques which are the extracellular deposits found in the brains of people with AD, produced by activating secretase family enzymes. It has been reported that the inhibition of secretases and kinases is caused by ACE2-related pathways, and the process of inhibiting these signaling pathways can be caused by the COVID-19 virus resulting in long-term neurological sequels following the activation of AD triggering signaling pathways [115] (shown in Fig. 2).…”

Section: The Possible Interactions Of Coronavirus With Neurodegenerat...mentioning

confidence: 99%

“…In this view, to have more explanation, tau phosphorylation is induced by the activation of several kinases, whose activation is inhibited by ACE2-related pathways. However, the process of inhibiting these signaling pathways can be caused by the COVID-19 virus resulting in tau phosphorylation [113,115] (shown in Fig. 2).…”

Section: Frontotemporal Disordermentioning

confidence: 99%

Molecular mechanisms highlighting the potential role of COVID-19 in the development of neurodegenerative diseases

Rahmani

Ghashghayi

Zendehdel

et al. 2022

PhysInt

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Coronavirus disease 2019 (COVID-19) is a contagious disease caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). In addition to the pulmonary manifestations, COVID-19 patients may present a wide range of neurological disorders as extrapulmonary presentations. In this view, several studies have recently documented the worsening of neurological symptoms within COVID-19 morbidity in patients previously diagnosed with neurodegenerative diseases (NDs). Moreover, several cases have also been reported in which the patients presented parkinsonian features after initial COVID-19 symptoms. These data raise a major concern about the possibility of communication between SARS-CoV-2 infection and the initiation and/or worsening of NDs. In this review, we have collected compelling evidence suggesting SARS-CoV-2, as an environmental factor, may be capable of developing NDs. In this respect, the possible links between SARS-CoV-2 infection and molecular pathways related to most NDs and the pathophysiological mechanisms of the NDs such as Alzheimer's disease, vascular dementia, frontotemporal dementia, Parkinson's disease, and amyotrophic lateral sclerosis will be explained.

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“…BDNF regulates neuronal maintenance, neuronal survival, plasticity, and neurotransmitter regulation. Patients with psychiatric and neurodegenerative disorders often have reduced BDNF concentrations in their bloods and brains that may be secondary to the chronic inflammatory state of the brain in certain disorders [ 136 ], since BDNF is downstream the ACE2-Mas axis [ 137 ].…”

Section: The Need Of Developing Accurate “Theranostics” For Earlymentioning

confidence: 99%

Emerging Neurological and Psychobiological Aspects of COVID-19 Infection

et al. 2020

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The SARS-CoV-2 virus, first reported in December 2019 in China, is the causative agent of the current COVID-19 pandemic that, at the time of writing (1 November 2020) has infected almost 43 million people and caused the death of more than 1 million people. The spectrum of clinical manifestations observed during COVID-19 infection varies from asymptomatic to critical life-threatening clinical conditions. Emerging evidence shows that COVID-19 affects far more organs than just the respiratory system, including the heart, kidneys, blood vessels, liver, as well as the central nervous system (CNS) and the peripheral nervous system (PNS). It is also becoming clear that the neurological and psychological disturbances that occur during the acute phase of the infection may persist well beyond the recovery. The aim of this review is to propel further this emerging and relevant field of research related to the pathophysiology of neurological manifestation of COVID-19 infection (Neuro-COVID). We will summarize the PNS and CNS symptoms experienced by people with COVID-19 both during infection and in the recovery phase. Diagnostic and pharmacological findings in this field of study are strongly warranted to address the neurological and psychological symptoms of COVID-19.

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Can infection of COVID-19 virus exacerbate Alzheimer's symptoms? Hypothetic possible role of angiotensin-converting enzyme-2/Mas/brain-derived neurotrophic factor axis and Tau hyper-phosphorylation

Cited by 6 publications

References 16 publications

Rapid progression of probable Creutzfeldt-Jakob disease with concomitant COVID-19 infection

Rapid progression of probable Creutzfeldt-Jakob disease with concomitant COVID-19 infection

Molecular mechanisms highlighting the potential role of COVID-19 in the development of neurodegenerative diseases

Emerging Neurological and Psychobiological Aspects of COVID-19 Infection

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