Frontiers in Aging Neuroscience,
Journal Year:
2023,
Volume and Issue:
15
Published: June 15, 2023
Alzheimer’s
disease
(AD)
is
a
neurodegenerative
disorder
characterized
by
protein
aggregation
in
the
brain.
Recent
studies
have
revealed
critical
role
of
microglia
AD
pathogenesis.
This
review
provides
comprehensive
summary
current
understanding
microglial
involvement
AD,
focusing
on
genetic
determinants,
phenotypic
state,
phagocytic
capacity,
neuroinflammatory
response,
and
impact
synaptic
plasticity
neuronal
regulation.
Furthermore,
recent
developments
drug
discovery
targeting
are
reviewed,
highlighting
potential
avenues
for
therapeutic
intervention.
emphasizes
essential
insights
into
treatments.
Journal of Neurogastroenterology and Motility,
Journal Year:
2019,
Volume and Issue:
25(1), P. 48 - 60
Published: Jan. 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
International Journal of Molecular Sciences,
Journal Year:
2019,
Volume and Issue:
20(10), P. 2534 - 2534
Published: May 23, 2019
Nowadays,
the
oral
use
of
probiotics
is
widespread.
However,
safety
profile
with
live
still
a
matter
debate.
Main
risks
include:
Cases
systemic
infections
due
to
translocation,
particularly
in
vulnerable
patients
and
pediatric
populations;
acquisition
antibiotic
resistance
genes;
or
interference
gut
colonization
neonates.
To
avoid
these
risks,
there
an
increasing
interest
non-viable
microorganisms
microbial
cell
extracts
be
used
as
probiotics,
mainly
heat-killed
(including
tyndallized)
probiotic
bacteria
(lactic
acid
bifidobacteria).
Heat-treated
cells,
cell-free
supernatants,
purified
key
components
are
able
confer
beneficial
effects,
immunomodulatory
protection
against
enteropathogens,
maintenance
intestinal
barrier
integrity.
At
clinical
level,
products
containing
tyndallized
strains
have
had
role
gastrointestinal
diseases,
including
bloating
infantile
coli—in
combination
mucosal
protectors—and
diarrhea.
Heat-inactivated
could
also
management
dermatological
respiratory
allergic
diseases.
The
reviewed
data
indicate
that
their
fractions
advantages
versus
(mainly
profile),
positioning
them
interesting
strategies
for
common
prevalent
conditions
wide
variety
patients´
characteristics.
Journal of Neuroinflammation,
Journal Year:
2018,
Volume and Issue:
15(1)
Published: Sept. 24, 2018
Alzheimer’s
disease
(AD)
is
a
neurodegenerative
disorder,
most
cases
of
which
lack
clear
causative
event.
This
has
made
the
difficult
to
characterize
and,
thus,
diagnose.
Although
some
are
genetically
linked,
there
many
diseases
and
lifestyle
factors
that
can
lead
an
increased
risk
developing
AD,
including
traumatic
brain
injury,
diabetes,
hypertension,
obesity,
other
metabolic
syndromes,
in
addition
aging.
Identifying
common
trends
between
these
conditions
could
enhance
our
understanding
AD
development
more
effective
treatments.
immune
system
one
body’s
key
defense
mechanisms,
chronic
inflammation
been
increasingly
linked
with
several
age-related
diseases.
Moreover,
it
now
well
accepted
important
role
onset
progression
AD.
In
this
review,
different
inflammatory
signals
associated
its
will
be
outlined
demonstrate
how
may
influencing
individual
susceptibility
Our
goal
bring
attention
potential
shared
presented
by
during
successful
International Journal of Molecular Sciences,
Journal Year:
2019,
Volume and Issue:
20(9), P. 2293 - 2293
Published: May 9, 2019
A
large
body
of
experimental
evidence
suggests
that
neuroinflammation
is
a
key
pathological
event
triggering
and
perpetuating
the
neurodegenerative
process
associated
with
many
neurological
diseases.
Therefore,
different
stimuli,
such
as
lipopolysaccharide
(LPS),
are
used
to
model
neurodegeneration.
By
acting
at
its
receptors,
LPS
activates
various
intracellular
molecules,
which
alter
expression
plethora
inflammatory
mediators.
These
factors,
in
turn,
initiate
or
contribute
development
processes.
an
important
tool
for
study
However,
serotype,
route
administration,
number
injections
this
toxin
induce
varied
responses.
Thus,
here,
we
review
use
models
neurodegeneration
well
discuss
neuroinflammatory
mechanisms
induced
by
could
underpin
events
linked
process.
Journal of Neuroinflammation,
Journal Year:
2019,
Volume and Issue:
16(1)
Published: Sept. 13, 2019
The
endotoxin
hypothesis
of
neurodegeneration
is
the
that
causes
or
contributes
to
neurodegeneration.
Endotoxin
a
lipopolysaccharide
(LPS),
constituting
much
outer
membrane
gram-negative
bacteria,
present
at
high
concentrations
in
gut,
gums
and
skin
other
tissue
during
bacterial
infection.
Blood
plasma
levels
are
normally
low,
but
elevated
infections,
gut
inflammation,
gum
disease
neurodegenerative
disease.
Adding
such
blood
healthy
humans
induces
systemic
inflammation
brain
microglial
activation.
body
rodents
activation,
priming
and/or
tolerance,
memory
deficits
loss
synapses
neurons.
promotes
amyloid
β
tau
aggregation
neuropathology,
suggesting
possibility
synergises
with
different
aggregable
proteins
give
diseases.
Alzheimer's
disease,
which
accelerated
by
including
binds
directly
APOE,
APOE4
variant
both
sensitises
predisposes
Intestinal
permeability
increases
early
Parkinson's
injection
into
mice
α-synuclein
production
aggregation,
as
well
dopaminergic
neurons
substantia
nigra.
microbiome
changes
changing
endotoxin-producing
species
can
affect
patients
mouse
models.
amyotrophic
lateral
sclerosis,
TDP-43
neuropathology.
Peripheral
diseases
elevate
endotoxin,
sepsis,
AIDS
liver
failure,
also
result
indirectly
activates
microglia
damage
via
nitric
oxide,
oxidants
cytokines,
phagocytosis
unproven,
if
correct,
then
may
be
reduced
decreasing
endotoxin-induced
neuroinflammation.
Journal of Neuroinflammation,
Journal Year:
2019,
Volume and Issue:
16(1)
Published: May 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.
Molecular Neurobiology,
Journal Year:
2020,
Volume and Issue:
57(12), P. 5026 - 5043
Published: Aug. 22, 2020
Understanding
how
gut
flora
influences
gut-brain
communications
has
been
the
subject
of
significant
research
over
past
decade.
The
broadening
term
"microbiota-gut-brain
axis"
from
"gut-brain
underscores
a
bidirectional
communication
system
between
and
brain.
microbiota-gut-brain
axis
involves
metabolic,
endocrine,
neural,
immune
pathways
which
are
crucial
for
maintenance
brain
homeostasis.
Alterations
in
composition
microbiota
associated
with
multiple
neuropsychiatric
disorders.
Although
causal
relationship
dysbiosis
neural
dysfunction
remains
elusive,
emerging
evidence
indicates
that
may
promote
amyloid-beta
aggregation,
neuroinflammation,
oxidative
stress,
insulin
resistance
pathogenesis
Alzheimer's
disease
(AD).
Illustration
mechanisms
underlying
regulation
by
pave
way
developing
novel
therapeutic
strategies
AD.
In
this
narrative
review,
we
provide
an
overview
their
dysregulation
Novel
insights
into
modification
as
preventive
or
approach
AD
highlighted.
Frontiers in Cellular and Infection Microbiology,
Journal Year:
2020,
Volume and Issue:
10
Published: March 24, 2020
Background
Several
studies
suggested
an
important
role
of
the
gut
microbiota
in
pathophysiology
neurological
disorders,
implying
that
alteration
might
serve
as
a
treatment
strategy.
Fecal
transplantation
(FMT)
is
currently
most
effective
intervention
and
accepted
for
recurrent
Clostridioioides
difficile
infections.
To
evaluate
indications
FMT
patients
with
we
summarized
available
literature
on
FMT.
In
addition,
provide
suggestions
future
directions.
Methods
July
2019,
five
main
databases
were
searched
case
descriptions
disorders
humans
or
animal
models.
ClinicalTrials.gov
website
was
consulted
registered
planned
ongoing
trials.
Results
Of
541
identified
studies,
34
included
analysis.
Clinical
trials
have
been
performed
autism
spectrum
disorder
showed
beneficial
effects
symptoms.
For
multiple
sclerosis
Parkinson's
disease,
several
positive
effect
FMT,
supported
by
some
reports
humans.
epilepsy,
Tourette
syndrome,
diabetic
neuropathy
but
evidence
restricted
to
limited
numbers
studies.
stroke,
Alzheimer's
disease
Guillain-Barré
syndrome
only
models
identified.
These
potential
healthy
donor
contrast,
one
study
model
stroke
increased
mortality
after
Whether
findings
from
can
be
confirmed
human
diseases
awaits
seen.
above
mentioned
are
ongoing,
well
amyotrophic
lateral
sclerosis.
Conclusions
Preliminary
suggests
may
promising
option
disorders.
However,
still
scanty
contrasting
results
observed.
Limited
while
experiments
conducted.
Large
double-blinded
randomized
controlled
needed
further
elucidate