Complex Interaction between Resident Microbiota and Misfolded Proteins: Role in Neuroinflammation and Neurodegeneration

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dc.contributor.authorSebastian Aguayo
dc.date.accessioned2023-05-19T20:46:07Z
dc.date.available2023-05-19T20:46:07Z
dc.date.issued2020
dc.description.abstractNeurodegenerative 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-beta (A beta), alpha synuclein (alpha-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 A beta, alpha-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.
dc.fuente.origenORCID-mayo23
dc.identifier.doi10.3390/cells9112476
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/69707
dc.language.isoen
dc.titleComplex Interaction between Resident Microbiota and Misfolded Proteins: Role in Neuroinflammation and Neurodegenerationes_ES
dc.typeartículo
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