The disorder of the iron metabolism as a possible mechanism for the development of neurodegeneration after new coronavirus infection of SARS-CoV-2

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Abstract

The involvement of the nervous system in the pathological process that occurs when COVID-19 is infected is becoming more and more obvious. The question of the possibility of the debut or progression of the already developed Parkinsonism syndrome in patients who have undergone COVID-19 is regularly raised. A large number of hypotheses are put forward to explain this relationship. It is assumed that a violation of iron metabolism in the brain may underlie the development and progression of neurodegenerative diseases, including after the new coronavirus infection SARS-CoV-2. The analysis of stu dies on the possible influence of iron metabolism disorders on the occurrence and mechanism of development of neurodegenerative diseases after infection with SARS-CoV-2 has been carried out. The processes of physiological maintenance of iron homeostasis, as well as the influence of physiological aging on the accumulation of iron in the central nervous system are described. The relationship between hyperferritinemia occurring in COVID-19 and ferroptosis as the basis of the neurodegenerative process in Parkinson’s disease and Alzheimer’s disease is discussed. The main molecular mechanisms involved in ferroptosis are described. Examples of involvement of metal homeostasis disorders in the process of altering the structure of α-synuclein, synthesis of β-amyloid, hyperphosphorylated tau- protein are given. The causes of excessive iron accumulation in certain brain structures are discussed. The question of the possibility of using the assessment of changes in iron metabolism as a new biomarker of the progression of Parkinson’s disease is analyzed. (1 figure, bibliography: 62 refs)

About the authors

Igor V. Litvinenko

S.M. Kirov Military Medical Academy

Email: litvinenkoiv@rambler.ru
ORCID iD: 0000-0001-8988-3011
SPIN-code: 6112-2792
Scopus Author ID: 57202361039
ResearcherId: F-9120-2013

D.Sc. (Medicine), Professor

Russian Federation, Saint Petersburg

Igor V. Krasakov

Nikiforov Russian Center of Emergency and Radiation Medicine

Author for correspondence.
Email: ikrasakov@gmail.com
ORCID iD: 0000-0001-6092-0659
SPIN-code: 9891-8300
Scopus Author ID: 26642102200
ResearcherId: I-8865-2016

Ph.D. (Medicine)

Russian Federation, Saint Petersburg

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2. Fig. 1. The main molecular mechanisms involved in ferroptosis (adapted from [29]). CP - ceruloplasmin; Tf - transferrin; TfR — transferrin receptor; DMT-1 - divalent metal transporter; ROS - reactive oxygen species

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