Journal of Neuroinflammation,
Год журнала:
2021,
Номер
18(1)
Опубликована: Ноя. 4, 2021
Chronic
unpredictable
mild
stress
(CUMS)
can
not
only
lead
to
depression-like
behavior
but
also
change
the
composition
of
gut
microbiome.
Regulating
microbiome
have
an
antidepressant
effect,
mechanism
by
which
it
improves
depressive
symptoms
is
clear.
Short-chain
fatty
acids
(SCFAs)
are
small
molecular
compounds
produced
fermentation
non-digestible
carbohydrates.
SFCAs
ubiquitous
in
intestinal
endocrine
and
immune
cells,
making
them
important
mediators
microbiome-regulated
body
functions.
The
balance
between
pro-
anti-inflammatory
microglia
plays
role
occurrence
treatment
depression
caused
chronic
stress.
Non-absorbable
antibiotic
rifaximin
regulate
structure
We
hypothesized
that
protects
against
stress-induced
inflammation
behaviors
regulating
abundance
fecal
microbial
metabolites
microglial
functions.We
administered
150
mg/kg
intragastrically
rats
exposed
CUMS
for
4
weeks
investigated
microbiome,
content
short-chain
serum
brain,
functional
profiles
hippocampal
neurogenesis.Our
results
show
ameliorated
depressive-like
induced
CUMS,
as
reflected
sucrose
preference,
open
field
test
Morris
water
maze.
Rifaximin
increased
relative
Ruminococcaceae
Lachnospiraceae,
were
significantly
positively
correlated
with
high
level
butyrate
brain.
factors
released
microglia,
prevented
neurogenic
abnormalities
CUMS.These
suggest
inflammatory
function
play
a
protective
pubertal
neurodevelopment
during
acids.
Microorganisms,
Год журнала:
2020,
Номер
8(4), С. 573 - 573
Опубликована: Апрель 15, 2020
The
complex
polymicrobial
composition
of
human
gut
microbiota
plays
a
key
role
in
health
and
disease.
Lachnospiraceae
belong
to
the
core
microbiota,
colonizing
intestinal
lumen
from
birth
increasing,
terms
species
richness
their
relative
abundances
during
host's
life.
Although,
members
are
among
main
producers
short-chain
fatty
acids,
different
taxa
also
associated
with
intra-
extraintestinal
diseases.
Their
impact
on
host
physiology
is
often
inconsistent
across
studies.
Here,
we
discuss
changes
according
With
aim
harnessing
promote
health,
analyze
how
nutrients
diet
can
influence
growth
metabolites
can,
turn,
physiology.
Frontiers in Neuroscience,
Год журнала:
2018,
Номер
12
Опубликована: Фев. 7, 2018
The
microbiota,
the
gut,
and
brain
communicate
through
microbiota-gut-brain
axis
in
a
bidirectional
way
that
involves
autonomic
nervous
system.
vagus
nerve
(VN),
principal
component
of
parasympathetic
system,
is
mixed
composed
80%
afferent
20%
efferent
fibers.
VN,
because
its
role
interoceptive
awareness,
able
to
sense
microbiota
metabolites
afferents,
transfer
this
gut
information
central
system
where
it
integrated
network,
then
generate
an
adapted
or
inappropriate
response.
A
cholinergic
anti-inflammatory
pathway
has
been
described
VN's
fibers,
which
dampen
peripheral
inflammation
decrease
intestinal
permeability,
thus
very
probably
modulating
composition.
Stress
inhibits
VN
deleterious
effects
on
gastrointestinal
tract
involved
pathophysiology
disorders
such
as
irritable
bowel
syndrome
(IBS)
inflammatory
disease
(IBD)
are
both
characterized
by
dysbiosis.
low
vagal
tone
IBD
IBS
patients
favoring
inflammation.
Targeting
for
example
stimulation
properties,
would
be
interest
restore
homeostasis
axis.
Immunology,
Год журнала:
2018,
Номер
154(2), С. 204 - 219
Опубликована: Март 7, 2018
Neurodegenerative
diseases,
the
leading
cause
of
morbidity
and
disability,
are
gaining
increased
attention
as
they
impose
a
considerable
socioeconomic
impact,
due
in
part
to
ageing
community.
Neuronal
damage
is
pathological
hallmark
Alzheimer's
Parkinson's
amyotrophic
lateral
sclerosis,
Huntington's
disease,
spinocerebellar
ataxia
multiple
although
such
also
observed
following
neurotropic
viral
infections,
stroke,
genetic
white
matter
diseases
paraneoplastic
disorders.
Despite
different
aetiologies,
for
example,
mutations,
trauma
protein
aggregations,
neuronal
frequently
associated
with
chronic
activation
an
innate
immune
response
CNS.
The
growing
awareness
that
system
inextricably
involved
shaping
brain
during
development
well
mediating
damage,
but
regeneration
repair,
has
stimulated
therapeutic
approaches
modulate
neurodegenerative
diseases.
Here,
we
review
current
understanding
how
astrocytes
microglia,
neurons
oligodendrocytes,
shape
neuroimmune
development,
aberrant
responses
arise
or
environmental
triggers
may
predispose
CNS
We
discuss
known
interactions
between
peripheral
brain,
concepts
on
cells
enter
leave
A
better
disease
will
be
key
further
manipulating
these
effective
therapies
improve
quality
life,
reduce
impact
neuroinflammatory
degenerative
Journal of Neurogastroenterology and Motility,
Год журнала:
2019,
Номер
25(1), С. 48 - 60
Опубликована: Янв. 10, 2019
Disturbances
along
the
brain-gut-microbiota
axis
may
significantly
contribute
to
pathogenesis
of
neurodegenerative
disorders.
Alzheimer's
disease
(AD)
is
most
frequent
cause
dementia
characterized
by
a
progressive
decline
in
cognitive
function
associated
with
formation
amyloid
beta
(Aβ)
plaques
and
neurofibrillary
tangles.
Alterations
gut
microbiota
composition
induce
increased
permeability
barrier
immune
activation
leading
systemic
inflammation,
which
turn
impair
blood-brain
promote
neuroinflammation,
neural
injury,
ultimately
neurodegeneration.
Recently,
Aβ
has
also
been
recognized
as
an
antimicrobial
peptide
participating
innate
response.
However,
dysregulated
state,
reveal
harmful
properties.
Importantly,
bacterial
amyloids
through
molecular
mimicry
elicit
cross-seeding
misfolding
microglial
priming.
The
seeding
propagation
occur
at
different
levels
axis.
potential
mechanisms
spreading
include
neuron-to-neuron
or
distal
neuron
spreading,
direct
crossing
via
other
cells
astrocytes,
fibroblasts,
microglia,
system
cells.
A
growing
body
experimental
clinical
data
confirms
key
role
dysbiosis
microbiota-host
interactions
convergence
gut-derived
inflammatory
response
together
aging
poor
diet
elderly
AD.
Modification
food-based
therapy
probiotic
supplementation
create
new
preventive
therapeutic
options
Translational Neurodegeneration,
Год журнала:
2018,
Номер
7(1)
Опубликована: Янв. 24, 2018
Alzheimer's
disease
(AD)
is
a
progressive
neurodegenerative
disorder
and
the
most
common
cause
for
dementia.
There
are
many
hypotheses
about
AD,
including
abnormal
deposit
of
amyloid
β
(Aβ)
protein
in
extracellular
spaces
neurons,
formation
twisted
fibers
tau
proteins
inside
cholinergic
neuron
damage,
inflammation,
oxidative
stress,
etc.,
anti-AD
drugs
based
on
these
have
been
developed.
In
this
review,
we
will
discuss
existing
emerging
hypothesis
related
therapies.
Molecular Neurobiology,
Год журнала:
2018,
Номер
56(3), С. 1841 - 1851
Опубликована: Июнь 23, 2018
One
of
the
most
important
scientific
discoveries
recent
years
was
disclosure
that
intestinal
microflora
takes
part
in
bidirectional
communication
between
gut
and
brain.
Scientists
suggest
human
may
even
act
as
"second
brain"
be
responsible
for
neurodegenerative
disorders
like
Alzheimer's
disease
(AD).
Although
human-associated
microbial
communities
are
generally
stable,
they
can
altered
by
common
actions
experiences.
Enteric
bacteria,
commensal,
pathogenic
microorganisms,
have
a
major
impact
on
immune
system,
brain
development,
behavior,
able
to
produce
several
neurotransmitters
neuromodulators
serotonin,
kynurenine,
catecholamine,
etc.,
well
amyloids.
However,
destructive
mechanisms,
lead
dementia
AD,
start
with
microbiome
dysbiosis,
development
local
systemic
inflammation,
dysregulation
gut-brain
axis.
Increased
permeability
epithelial
barrier
results
invasion
different
viruses,
their
neuroactive
products
support
neuroinflammatory
reactions
It
seems
that,
inflammatory-infectious
hypothesis
great
role
microbiome,
starts
gently
push
into
shadow
amyloid
cascade
has
dominated
decades.
is
strongly
postulated
AD
begin
gut,
closely
related
imbalance
microbiota.
This
promising
area
therapeutic
intervention.
Modulation
microbiota
through
personalized
diet
or
beneficial
intervention,
alter
partners
including
protein,
will
probably
become
new
treatment
AD.
Journal of Neuroinflammation,
Год журнала:
2019,
Номер
16(1)
Опубликована: Май 22, 2019
Alzheimer's
disease
(AD)
is
a
neurodegenerative
whose
various
pathophysiological
aspects
are
still
being
investigated.
Recently,
it
has
been
hypothesized
that
AD
may
be
associated
with
dysbiosis
of
microbes
in
the
intestine.
In
fact,
intestinal
flora
able
to
influence
activity
brain
and
cause
its
dysfunctions.Given
growing
interest
this
topic,
purpose
review
analyze
role
antibiotics
relation
gut
microbiota
AD.
first
part
review,
we
briefly
theories
supporting
hypothesis
can
pathophysiology.
second
part,
possible
these
events.
Antibiotics
normally
used
remove
or
prevent
bacterial
colonization
human
body,
without
targeting
specific
types
bacteria.
As
result,
broad-spectrum
greatly
affect
composition
microbiota,
reduce
biodiversity,
delay
for
long
period
after
administration.
Thus,
action
could
wide
even
opposite,
depending
on
type
antibiotic
microbiome
pathogenesis.Alteration
induce
changes
activity,
which
raise
possibility
therapeutic
manipulation
other
neurological
disorders.
This
field
research
currently
undergoing
great
development,
but
applications
far
away.
Whether
achieved
using
not
known.
The
future
depends
progresses
We
must
understand
how
when
bacteria
act
promote
Once
well
established,
one
think
modifications
use
pre-,
pro-,
produce
effects.
Alzheimer s & Dementia,
Год журнала:
2019,
Номер
15(10), С. 1357 - 1366
Опубликована: Авг. 18, 2019
Abstract
Objective
Gut
microbiota
changes
before
the
onset
of
Alzheimer's
disease
(AD)
and
alterations
could
be
detected
in
stage
mild
cognitive
impairment
(MCI).
The
findings
might
offer
diagnostic
biomarkers
dementia.
Background
AD
is
most
common
cause
dementia,
MCI
predementia
state.
Recent
studies
suggest
gut
microbial
communities
associated
with
AD,
whereas
dementia
has
not
been
discovered
characterized
humans.
New/Updated
Hypothesis
We
hypothesize
that
dysbiosis
happens
stage.
Patients
have
decreased
diversity,
for
early
detection
AD.
In
our
preliminary
study,
we
identified
differences
between
normal
controls
11
genera
from
feces
blood.
No
difference
was
detected.
Using
model
fecal
samples
all
different
input,
93%
(28
30)
patients
correctly.
Major
Challenges
diagnosis
study
based
on
symptoms
neuroimaging,
should
included
precise
further
validating
studies.
Besides,
as
longitudinally,
their
relationship
progress
needs
to
studied
prospective
Linkage
Other
Theories
Escherichia
observed
increased
at
genus
level
both
blood
MCI.
For
biomarker,
postmortem
brain
tissue
showed
lipopolysaccharides
gram‐negative
coli
fragments
colocalize
amyloid
plaque.
this
way,
pathogenesis
would
triggered
during
by
shifting.
systemic
inflammatory
reactions
caused
compounds
secreted
bacteria
may
impair
blood‐brain
barrier
promote
neuroinflammation
and/or
neurodegeneration.
Furthermore,
abnormal
metabolites
gene
functions
an
impact