Young COVID-19 Patients Show a Higher Degree of Microglial Activation When Compared to Controls

TY - JOUR

T1 - Young COVID-19 Patients Show a Higher Degree of Microglial Activation When Compared to Controls

AU - Matschke, Jakob

AU - Lahann, Henri

AU - Krasemann, Susanne

AU - Altmeppen, Hermann

AU - Pfefferle, Susanne

AU - Galliciotti, Giovanna

AU - Fitzek, Antonia

AU - Sperhake, Jan-Peter

AU - Ondruschka, Benjamin

AU - Busch, Miriam

AU - Rotermund, Natalie

AU - Schulz, Kristina

AU - Lohr, Christian

AU - Dottermusch, Matthias

AU - Glatzel, Markus

N1 - Copyright © 2022 Matschke, Lahann, Krasemann, Altmeppen, Pfefferle, Galliciotti, Fitzek, Sperhake, Ondruschka, Busch, Rotermund, Schulz, Lohr, Dottermusch and Glatzel.

PY - 2022

Y1 - 2022

N2 - The severe acute respiratory syndrome-corona virus type 2 (SARS-CoV-2) is the cause of human coronavirus disease 2019 (COVID-19). Since its identification in late 2019 SARS-CoV-2 has spread rapidly around the world creating a global pandemic. Although considered mainly a respiratory disease, COVID-19 also encompasses a variety of neuropsychiatric symptoms. How infection with SARS-CoV-2 leads to brain damage has remained largely elusive so far. In particular, it has remained unclear, whether signs of immune cell and / or innate immune and reactive astrogliosis are due to direct effects of the virus or may be an expression of a non-specific reaction of the brain to a severe life-threatening disease with a considerable proportion of patients requiring intensive care and invasive ventilation activation. Therefore, we designed a case-control-study of ten patients who died of COVID-19 and ten age-matched non-COVID-19-controls to quantitatively assess microglial and astroglial response. To minimize possible effects of severe systemic inflammation and / or invasive therapeutic measures we included only patients without any clinical or pathomorphological indication of sepsis and who had not been subjected to invasive intensive care treatment. Our results show a significantly higher degree of microglia activation in younger COVID-19 patients, while the difference was less and not significant for older COVID-19 patients. The difference in the degree of reactive gliosis increased with age but was not influenced by COVID-19. These preliminary data warrants further investigation of larger patient cohorts using additional immunohistochemical markers for different microglial phenotypes.

AB - The severe acute respiratory syndrome-corona virus type 2 (SARS-CoV-2) is the cause of human coronavirus disease 2019 (COVID-19). Since its identification in late 2019 SARS-CoV-2 has spread rapidly around the world creating a global pandemic. Although considered mainly a respiratory disease, COVID-19 also encompasses a variety of neuropsychiatric symptoms. How infection with SARS-CoV-2 leads to brain damage has remained largely elusive so far. In particular, it has remained unclear, whether signs of immune cell and / or innate immune and reactive astrogliosis are due to direct effects of the virus or may be an expression of a non-specific reaction of the brain to a severe life-threatening disease with a considerable proportion of patients requiring intensive care and invasive ventilation activation. Therefore, we designed a case-control-study of ten patients who died of COVID-19 and ten age-matched non-COVID-19-controls to quantitatively assess microglial and astroglial response. To minimize possible effects of severe systemic inflammation and / or invasive therapeutic measures we included only patients without any clinical or pathomorphological indication of sepsis and who had not been subjected to invasive intensive care treatment. Our results show a significantly higher degree of microglia activation in younger COVID-19 patients, while the difference was less and not significant for older COVID-19 patients. The difference in the degree of reactive gliosis increased with age but was not influenced by COVID-19. These preliminary data warrants further investigation of larger patient cohorts using additional immunohistochemical markers for different microglial phenotypes.

U2 - 10.3389/fneur.2022.908081

DO - 10.3389/fneur.2022.908081

M3 - SCORING: Journal article

C2 - 35785352

VL - 13

JO - FRONT NEUROL

JF - FRONT NEUROL

SN - 1664-2295

M1 - 908081

ER -