Complex Interaction between Resident Microbiota and Misfolded Proteins: Role in Neuroinflammation and Neurodegeneration
Autor: | Sebastian Aguayo, Carola Muñoz-Montesino, Juliana González-Sanmiguel, Pamina Contreras-Kallens, Christina M.A.P. Schuh, Luis G. Aguayo |
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Jazyk: | angličtina |
Rok vydání: | 2020 |
Předmět: |
Parkinson's disease
Membrane permeability animal diseases microbiome Review Biology neuroinflammation chemistry.chemical_compound Alzheimer Disease medicine Dementia Humans Microbiome lcsh:QH301-705.5 Neuroinflammation Alpha-synuclein Amyloid beta-Peptides Microbiota Neurodegeneration Brain Parkinson Disease General Medicine medicine.disease Creutzfeldt-Jakob disease nervous system diseases chemistry lcsh:Biology (General) membrane permeability Parkinson’s disease alpha-Synuclein biofilms Dysbiosis Neuroscience Alzheimer’s disease periodontal diseases |
Zdroj: | Cells Cells, Vol 9, Iss 2476, p 2476 (2020) |
ISSN: | 2073-4409 |
Popis: | Neurodegenerative diseases such as Alzheimer’s disease (AD), Parkinson’s disease (PD) and Creutzfeldt–Jakob disease (CJD) are brain conditions affecting millions of people worldwide. These diseases are associated with the presence of amyloid-β (Aβ), alpha synuclein (α-Syn) and prion protein (PrP) depositions in the brain, respectively, which lead to synaptic disconnection and subsequent progressive neuronal death. Although considerable progress has been made in elucidating the pathogenesis of these diseases, the specific mechanisms of their origins remain largely unknown. A body of research suggests a potential association between host microbiota, neuroinflammation and dementia, either directly due to bacterial brain invasion because of barrier leakage and production of toxins and inflammation, or indirectly by modulating the immune response. In the present review, we focus on the emerging topics of neuroinflammation and the association between components of the human microbiota and the deposition of Aβ, α-Syn and PrP in the brain. Special focus is given to gut and oral bacteria and biofilms and to the potential mechanisms associating microbiome dysbiosis and toxin production with neurodegeneration. The roles of neuroinflammation, protein misfolding and cellular mediators in membrane damage and increased permeability are also discussed. |
Databáze: | OpenAIRE |
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