| Literature DB >> 34229735 |
Maria C Barbosa-Silva1, Maiara N Lima1, Denise Battaglini2, Chiara Robba2,3, Paolo Pelosi2,3, Patricia R M Rocco4,5,6, Tatiana Maron-Gutierrez7,8,9.
Abstract
Infectious diseases may affect brain function and cause encephalopathy even when the pathogen does not directly infect the central nervous system, known as infectious disease-associated encephalopathy. The systemic inflammatory process may result in neuroinflammation, with glial cell activation and increased levels of cytokines, reduced neurotrophic factors, blood-brain barrier dysfunction, neurotransmitter metabolism imbalances, and neurotoxicity, and behavioral and cognitive impairments often occur in the late course. Even though infectious disease-associated encephalopathies may cause devastating neurologic and cognitive deficits, the concept of infectious disease-associated encephalopathies is still under-investigated; knowledge of the underlying mechanisms, which may be distinct from those of encephalopathies of non-infectious cause, is still limited. In this review, we focus on the pathophysiology of encephalopathies associated with peripheral (sepsis, malaria, influenza, and COVID-19), emerging therapeutic strategies, and the role of neuroinflammation.Entities:
Keywords: COVID-19; Cognition; Encephalopathy; Infection; Influenza; Malaria; Microglial priming; Neuroinflammation; SARS-CoV-2; Sepsis
Year: 2021 PMID: 34229735 DOI: 10.1186/s13054-021-03659-6
Source DB: PubMed Journal: Crit Care ISSN: 1364-8535 Impact factor: 9.097