COVID-19 and Alzheimer's Disease: A Review of Mechanisms and Pathophysiology

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KHANIZADEH ALI MOHAMMAD; KARIMZADEH FARIBA

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Journal Paper

Paper Information

Journal: Neuroscience Journal of Shefaye Khatam Year:2021 | Volume:9 | Issue:2 Page(s): 151-159

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Information Journal Paper

Title

COVID-19 and Alzheimer's Disease: A Review of Mechanisms and Pathophysiology

Author(s)

KHANIZADEH ALI MOHAMMAD | KARIMZADEH FARIBA | Issue Writer Certificate

Keywords

Alzheimer Disease

Memory

Oxidative Stress

Abstract

Introduction: SARSCoV2 virus, which has emerged as a worldwide epidemic, is accompanied by sys temic symptoms, such as fever, cough, shortness of breath, and body aches. The virus enters the central nervous sys tem in various ways and causes symptoms, such as dizziness, headache, and loss of consciousness, encephalitis, demyelination, neuropathy, s troke, seizure, and Memory loss. Infection of the virus into the nervous sys tem, particularly the hippocampus, can cause Memory impairment. On the other hand, hypoxia due to lung infection may have a role in the development or progression of Alzheimer’ s disease (AD). An increase of beta-amyloid production, as well as autophagy following hypoxia, causes nerve damage. Furthermore, chronic hypoxia reduces the expression of beta-amyloid-degrading enzymes by increasing the expression of the beta-secretase enzyme. On the other hand, peripheral proinflammatory cytokines produced by microglia are involved in increasing beta-amyloid levels and tau hyperphosphorylation. Other possible mechanisms involved in the development of AD following the SARSCoV2 virus infection include mitochondrial disorders and increased oxidative s tress, which play an important role in the pathophysiology of AD. Oxidative s tress increases beta-amyloid production by reducing alpha-secretase activity. Conclusion: The SARSCoV2 virus may exacerbate the symptoms of AD by entering directly into the central nervous sys tem and damaging vital areas in-Memory s torage or the consequences of chronic hypoxia, oxidative s tress, or increased production of peripheral proinflammatory cytokines.

Cites

Investigation of the Profile of Psychosomatic Disorders and Psychological Problems in Women Recovered from COVID-19

References

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APA: Copy

KHANIZADEH, ALI MOHAMMAD, & KARIMZADEH, FARIBA. (2021). COVID-19 and Alzheimer's Disease: A Review of Mechanisms and Pathophysiology. NEUROSCIENCE JOURNAL OF SHEFAYE KHATAM, 9(2 ), 151-159. SID. https://sid.ir/paper/950480/en

Vancouver: Copy

KHANIZADEH ALI MOHAMMAD, KARIMZADEH FARIBA. COVID-19 and Alzheimer's Disease: A Review of Mechanisms and Pathophysiology. NEUROSCIENCE JOURNAL OF SHEFAYE KHATAM[Internet]. 2021;9(2 ):151-159. Available from: https://sid.ir/paper/950480/en

IEEE: Copy

ALI MOHAMMAD KHANIZADEH, and FARIBA KARIMZADEH, “COVID-19 and Alzheimer's Disease: A Review of Mechanisms and Pathophysiology,” NEUROSCIENCE JOURNAL OF SHEFAYE KHATAM, vol. 9, no. 2 , pp. 151–159, 2021, [Online]. Available: https://sid.ir/paper/950480/en

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