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The role of microbial amyloid in neurodegeneration.

Abstract It has become apparent that the intestinal microbiota orchestrates important aspects of our metabolism, immunity, and development. Recent work has demonstrated that the microbiota also influences brain function in healthy and diseased individuals. Of great interest are reports that intestinal bacteria play a role in the pathogenic cascade of both Parkinson and Alzheimer diseases. These neurodegenerative disorders both involve misfolding of endogenous proteins that spreads from one region of the body to another in a manner analogous to prions. The mechanisms of how the microbiota influences or is correlated with disease require elaboration. Microbial proteins or metabolites may influence neurodegeneration through the promotion of amyloid formation by human proteins or by enhancing inflammatory responses to endogenous neuronal amyloids. We review the current knowledge concerning bacterial amyloids and their potential to influence cerebral amyloid aggregation and neuroinflammation. We propose the term "mapranosis" to describe the process of microbiota-associated proteopathy and neuroinflammation. The study of amyloid proteins made by the microbiota and their influence on health and disease is in its infancy. This is a promising area for therapeutic intervention because there are many ways to alter our microbial partners and their products, including amyloid proteins.
PMID
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Authors

Mayor MeshTerms
Keywords
Journal Title plos pathogens
Publication Year Start




PMID- 29267402
OWN - NLM
STAT- In-Data-Review
LR  - 20171221
IS  - 1553-7374 (Electronic)
IS  - 1553-7366 (Linking)
VI  - 13
IP  - 12
DP  - 2017 Dec
TI  - The role of microbial amyloid in neurodegeneration.
PG  - e1006654
LID - 10.1371/journal.ppat.1006654 [doi]
AB  - It has become apparent that the intestinal microbiota orchestrates important
      aspects of our metabolism, immunity, and development. Recent work has
      demonstrated that the microbiota also influences brain function in healthy and
      diseased individuals. Of great interest are reports that intestinal bacteria play
      a role in the pathogenic cascade of both Parkinson and Alzheimer diseases. These 
      neurodegenerative disorders both involve misfolding of endogenous proteins that
      spreads from one region of the body to another in a manner analogous to prions.
      The mechanisms of how the microbiota influences or is correlated with disease
      require elaboration. Microbial proteins or metabolites may influence
      neurodegeneration through the promotion of amyloid formation by human proteins or
      by enhancing inflammatory responses to endogenous neuronal amyloids. We review
      the current knowledge concerning bacterial amyloids and their potential to
      influence cerebral amyloid aggregation and neuroinflammation. We propose the term
      "mapranosis" to describe the process of microbiota-associated proteopathy and
      neuroinflammation. The study of amyloid proteins made by the microbiota and their
      influence on health and disease is in its infancy. This is a promising area for
      therapeutic intervention because there are many ways to alter our microbial
      partners and their products, including amyloid proteins.
FAU - Friedland, Robert P
AU  - Friedland RP
AUID- ORCID: http://orcid.org/0000-0001-5721-1843
AD  - Department of Neurology, University of Louisville, Louisville, Kentucky, United
      States of America.
FAU - Chapman, Matthew R
AU  - Chapman MR
AUID- ORCID: http://orcid.org/0000-0002-2645-1294
AD  - Department of Molecular, Cellular, and Developmental Biology, University of
      Michigan, Ann Arbor, Michigan, United States of America.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20171221
PL  - United States
TA  - PLoS Pathog
JT  - PLoS pathogens
JID - 101238921
EDAT- 2017/12/22 06:00
MHDA- 2017/12/22 06:00
CRDT- 2017/12/22 06:00
PHST- 2017/12/22 06:00 [entrez]
PHST- 2017/12/22 06:00 [pubmed]
PHST- 2017/12/22 06:00 [medline]
AID - 10.1371/journal.ppat.1006654 [doi]
AID - PPATHOGENS-D-17-01644 [pii]
PST - epublish
SO  - PLoS Pathog. 2017 Dec 21;13(12):e1006654. doi: 10.1371/journal.ppat.1006654.
      eCollection 2017 Dec.