Chotima Böttcher

Abstract Neurological symptoms, including cognitive impairment and fatigue, can occur in both the acute infection phase of coronavirus disease 2019 (COVID-19) and at later stages, yet the mechanisms that contribute to this remain unclear. Here we profiled single-nucleus transcriptomes and proteomes of brainstem tissue from deceased individuals at various stages of COVID-19. We detected an inflammatory type I interferon response in acute COVID-19 cases, which resolves in the late disease phase.

Abstract The innate immune compartment of the human central nervous system (CNS) is highly diverse and includes several immune-cell populations such as macrophages that are frequent in the brain parenchyma (microglia) and less numerous at the brain interfaces as CNS-associated macrophages (CAMs). Due to their scantiness and particular location, little is known about the presence of temporally and spatially restricted CAM subclasses during development, health and perturbation.

1 Introduction Myelin oligodendrocyte glycoprotein antibody-associated autoimmune disease (MOGAD) is a rare inflammatory demyelinating disease of the central nervous system (CNS), which causes a broad spectrum of atypical, partly multiple sclerosis (MS)-mimicking demyelinating CNS syndromes including (recurrent) optic neuritis (ON), myelitis, aquaporin-4 (AQP4)-seronegative neuromyelitis optica (NMO)-like disease, (brainstem) encephalitis and others (1).