Reader response: Neurologic complications of coronavirus infections
Pedro JesusSerrano-Castro, Neurologist, Regional Universitary Hospital of Malaga, Biomedical Research Institute of Malaga (IBIMA)
Submitted April 17, 2020
I read the editorial by Dr. Nath with interest.1 One aspect of Central Nervous System (CNS) involvement in SARS-CoV2 infection that has attracted little interest so far is the medium or long-term consequences on patients with neurodegenerative diseases (NDD). It is known that chronic neuroinflammation has been associated with the neuropathophysiology of some NDDs such as multiple sclerosis, Parkinson disease, Alzheimer disease (AD), and others.2 In the case of AD, in presence of proinflammatory cytokines/chemokines, the microglia loses ability to phagocytize the Aβ protein, favoring the pathogenic deposits.3 Similar evidence exists in other NDD.4 The cytokine storm of SARS-CoV2 infection involves the activation of a neuroinflammatory cascade similar to that described in NDD.5 Furthermore, the possibility that this molecular movement may be persistent over time after acute infection is eliminated, in a similar way to what occurs in the so-called "Persistent Inflammation-immunosuppression and Catabolism Syndrome."5 Finally, we do not know whether SARS-CoV2 may have the ability to remain latent in the CNS in a similar way as other coronaviruses do,6 increasing the possibility of sustained neuroinflammation. The repercussion on the population vulnerable to NDD is unknown but will force us to be attentive to the future of our patients.
Disclosures
The author reports no relevant disclosures. Contact [email protected] for full disclosures.
References
Nath A. Neurologic complications of coronavirus infections. Neurology 2020 Epub Mar 30.
Frank-Cannon TC, Alto LT, McAlpine FE, Tansey MG. Does neuroinflammation fan the flame in neurodegenerative diseases? Mol Neurodegener 2009;4:47.
Koenigsknecht-Talboo J, Landreth GE. Microglial phagocytosis induced by fibrillar beta-amyloid and IgGs are differentially regulated by proinflammatory cytokines. J Neurosci 2005;25:8240–8249.
McGeer PL, Itagaki S, Boyes BE, McGeer EG: Reactive microglia are positive for HLA-DR in the substantia nigra of Parkinson's and Alzheimer's disease brains. Neurology 1988;38:1285–1291.
Hawkins RB, Raymond SL, Stortz JA, et al. Chronic Critical Illness and the Persistent Inflammation, Immunosuppression, and Catabolism Syndrome. Front Immunol 2018;9:1511.
Jacomy H, Fragoso G, Almazan G, Mushynsi WE, Talbot PJ. Human coronavirus OC43 infection induces chronic encephalitis leading to disabilities in BALB/C mice. Virology 2006;349:335–346.
I read the editorial by Dr. Nath with interest.1 One aspect of Central Nervous System (CNS) involvement in SARS-CoV2 infection that has attracted little interest so far is the medium or long-term consequences on patients with neurodegenerative diseases (NDD). It is known that chronic neuroinflammation has been associated with the neuropathophysiology of some NDDs such as multiple sclerosis, Parkinson disease, Alzheimer disease (AD), and others.2 In the case of AD, in presence of proinflammatory cytokines/chemokines, the microglia loses ability to phagocytize the Aβ protein, favoring the pathogenic deposits.3 Similar evidence exists in other NDD.4 The cytokine storm of SARS-CoV2 infection involves the activation of a neuroinflammatory cascade similar to that described in NDD.5 Furthermore, the possibility that this molecular movement may be persistent over time after acute infection is eliminated, in a similar way to what occurs in the so-called "Persistent Inflammation-immunosuppression and Catabolism Syndrome."5 Finally, we do not know whether SARS-CoV2 may have the ability to remain latent in the CNS in a similar way as other coronaviruses do,6 increasing the possibility of sustained neuroinflammation. The repercussion on the population vulnerable to NDD is unknown but will force us to be attentive to the future of our patients.
Disclosures
The author reports no relevant disclosures. Contact [email protected] for full disclosures.
References