OWN - NLM
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.