Abstract
Neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis, comprise a family of disorders characterized by progressive loss of nervous system function. Neuroinflammation is increasingly recognized to be associated with many neurodegenerative diseases but whether it is a cause or consequence of the disease process is unclear. Of growing interest is the role of microbial infections in inciting degenerative neuroinflammatory responses and genetic factors that may regulate those responses. Microbial infections cause inflammation within the central nervous system through activation of brain-resident immune cells and infiltration of peripheral immune cells. These responses are necessary to protect the brain from lethal infections but may also induce neuropathological changes that lead to neurodegeneration. This review discusses the molecular and cellular mechanisms through which microbial infections may increase susceptibility to neurodegenerative diseases. Elucidating these mechanisms is critical for developing targeted therapeutic approaches that prevent the onset and slow the progression of neurodegenerative diseases.
Highlights
Microbial Infections Are a Risk Factor for Neurodegenerative DiseasesDepartment of Biological Sciences, University of North Carolina at Charlotte, Charlotte, NC, United States Edited by: Fabio Blandini, Neurological Institute Foundation Casimiro Mondino (IRCCS), Italy Specialty section: This article was submitted to Cellular Neuropathology, a section of the journal
Neurodegenerative diseases, such as Alzheimer’s disease (AD), Parkinson’s disease (PD), and amyotrophic lateral sclerosis (ALS), are clinically characterized by the progressive decline of cognitive, motor, and behavioral functions
Several genes with polymorphisms that increase the risk of neurodegenerative diseases, such as CD33 and TREM2 in AD, PRKN, SCNA, LRRK2, and HLA in PD, and C9ORF72 in ALS have been linked to various immune functions including phagocytosis, microglial activation, complement activation, MHC class II expression, and hematopoiesis (McGeer et al, 1988; Griciuc et al, 2013; Guerreiro et al, 2013; Jonsson et al, 2013; Dzamko et al, 2015; Burberry et al, 2016; Jimenez-Ferrer and Swanberg, 2018)
Summary
Department of Biological Sciences, University of North Carolina at Charlotte, Charlotte, NC, United States Edited by: Fabio Blandini, Neurological Institute Foundation Casimiro Mondino (IRCCS), Italy Specialty section: This article was submitted to Cellular Neuropathology, a section of the journal
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