Frontiers in Neuroscience,
Journal Year:
2023,
Volume and Issue:
17
Published: Jan. 27, 2023
After
an
ischemic
stroke
(IS)
occurs,
immune
cells
begin
traveling
to
the
brain
and
system
from
gut
gastrointestinal
tract,
where
most
of
them
typically
reside.
Because
majority
body’s
macrophages
more
than
70%
total
cell
pool
are
found
within
inflammation
responses
in
organs
require
mobilization
a
large
number
cells.
The
bidirectional
communication
pathway
between
is
often
referred
as
gut-brain
axis.
IS
usually
leads
intestinal
motility
disorders,
dysbiosis
microbiota,
leaky
gut,
which
associated
with
poor
prognosis
patients
IS.
In
recent
years,
several
studies
have
suggested
that
play
key
roles
development
IS,
thus
may
become
potential
therapeutic
targets
can
drive
new
strategies.
However,
research
on
after
remains
its
infancy.
A
better
understanding
be
important
for
developing
effective
therapies.
This
review
discusses
immune-related
mechanisms
axis
compiles
provide
ideas
strategies
future
treatment
Frontiers in Immunology,
Journal Year:
2024,
Volume and Issue:
15
Published: Feb. 21, 2024
The
bidirectional
communication
between
the
gut
and
brain
or
gut-brain
axis
is
regulated
by
several
microbes
microbial
derived
metabolites,
such
as
short-chain
fatty
acids,
trimethylamine
N-oxide,
lipopolysaccharides.
Gut
microbiota
(GM)
produce
neuroactives,
specifically
neurotransmitters
that
modulates
local
central
neuronal
functions.
An
imbalance
intestinal
commensals
pathobionts
leads
to
a
disruption
in
dysbiosis,
which
affects
barrier
integrity
gut-immune
neuroimmune
systems.
Currently,
fecal
transplantation
(FMT)
recommended
for
treatment
of
recurrent
ACS Omega,
Journal Year:
2025,
Volume and Issue:
10(6), P. 5148 - 5171
Published: Feb. 3, 2025
Alzheimer's
disease
(AD)
is
an
aging-related
irreversible
neurodegenerative
affecting
mostly
the
elderly
population.
The
main
pathological
features
of
AD
are
extracellular
Aβ
plaques
generated
by
APP
cleavage
through
amyloidogenic
pathway,
intracellular
neurofibrillary
tangles
(NFT)
resulting
from
hyperphosphorylated
tau
proteins,
and
cholinergic
neurodegeneration.
However,
actual
causes
unknown,
but
several
studies
suggest
hereditary
mutations
in
PSEN1
-2,
APOE4,
APP,
TAU
genes
major
perpetrators.
In
order
to
understand
etiology
pathogenesis
AD,
various
hypotheses
proposed.
These
include
following
hypotheses:
amyloid
accumulation,
tauopathy,
inflammation,
oxidative
stress,
mitochondrial
dysfunction,
glutamate/excitotoxicity,
deficiency,
gut
dysbiosis.
Currently
approved
therapeutic
interventions
donepezil,
galantamine,
rivastigmine,
which
cholinesterase
inhibitors
(ChEIs),
memantine,
N-methyl-d-aspartate
(NMDA)
antagonist.
treatment
strategies
focus
on
only
symptomatic
management
attenuating
symptoms
not
regeneration
neurons
or
clearance
Tau.
This
review
focuses
pathophysiology,
novel
targets,
disease-altering
treatments
such
as
α-secretase
modulators,
active
immunotherapy,
passive
natural
antioxidant
products,
nanomaterials,
antiamyloid
therapy,
aggregation
inhibitors,
transplantation
fecal
microbiota
stem
cells,
microtubule
stabilizers
that
clinical
trials
still
under
investigation.
Nutrients,
Journal Year:
2022,
Volume and Issue:
15(1), P. 108 - 108
Published: Dec. 26, 2022
Beyond
brain
deficits
caused
by
strokes,
the
effectiveness
of
neurorehabilitation
is
strongly
influenced
baseline
clinical
features
stroke
patients,
including
a
patient’s
current
nutritional
status.
Malnutrition,
either
as
pre-stroke
existing
condition
or
occurring
because
ischemic
injury,
predisposes
patients
to
poor
rehabilitation
outcomes.
On
other
hand,
proper
status
compliant
with
specific
needs
required
process
recovery
plays
key
role
in
post-stroke
rehabilitative
outcome
favoring
neuroplasticity
mechanisms.
Oxidative
stress
and
inflammation
play
stroke-associated
malnutrition,
well
cascade
events
area,
where
damage
leads
neuronal
death
infarction,
and,
via
cell-to-cell
signaling,
alteration
processes
underlying
functional
induced
multidisciplinary
treatment.
Nutrition
strategies
based
on
food
components
oxidative
anti-inflammatory
properties
may
help
reverse
stop
malnutrition
be
prerequisite
for
supporting
ability
plasticity
result
satisfactory
patients.
To
expand
recommendations
recovery,
studies
considering
evolution
changes
over
time
are
required.
The
assessment
must
included
routine
tool
settings
integrated
care
stroke-patients.
Journal of Neuroinflammation,
Journal Year:
2022,
Volume and Issue:
19(1)
Published: Oct. 4, 2022
Abstract
Background
and
purpose
Stroke
is
associated
with
high
disability
mortality
rates
increases
the
incidence
of
organ-related
complications.
Research
has
revealed
that
outcomes
prognosis
stroke
are
regulated
by
state
intestinal
microbiota.
However,
possibility
manipulation
microbiota
can
alter
sex-related
remain
unknown.
Methods
To
verify
different
effects
from
sexes
on
outcomes,
we
performed
mouse
fecal
transplantation
(FMT)
established
a
model
ischemic
stroke.
Male
female
mice
received
either
male
or
through
FMT.
Ischemic
was
triggered
MCAO
(middle
cerebral
artery
occlusion),
sham
surgery
served
as
control.
Over
next
few
weeks,
underwent
neurological
evaluation
metabolite
inflammatory
level
detection,
collected
samples
for
16S
ribosomal
RNA
analysis.
Results
We
found
when
were
not
treated
FMT,
(especially
Firmicutes-to-Bacteroidetes
ratio)
levels
three
main
metabolites
tended
to
resemble
those
after
experimental
stroke,
indicating
induce
an
ecological
imbalance
in
biological
community.
Through
intragastric
administration,
gut
altered
other
sex.
In
general,
MCAO,
survival
rate
increased,
infarct
area
reduced,
behavioral
test
performance
improved,
release
beneficial
promoted
inflammation
mitigated.
contrast,
much
more
hampered
terms
protection
against
brain
damage
recovery
function.
Conclusion
A
female-like
community
reduces
systemic
proinflammatory
cytokines
Poor
be
positively
modulated
following
supplementation
Current Issues in Molecular Biology,
Journal Year:
2023,
Volume and Issue:
45(11), P. 9132 - 9148
Published: Nov. 15, 2023
Metabolic-associated
liver
disease
(MAFLD)
affects
up
to
70%
of
overweight
and
more
than
90%
morbidly
obese
people,
its
pathogenesis
is
rather
complex
multifactorial.
The
criteria
for
MAFLD
include
the
presence
hepatic
steatosis
in
addition
one
following
three
criteria:
or
obesity,
type
2
diabetes
mellitus
(T2DM),
evidence
metabolic
dysregulation.
If
specific
are
present,
diagnosis
can
be
made
regardless
alcohol
consumption
previous
disease.
pathophysiological
mechanisms
MAFLD,
including
inflammation,
lipotoxicity,
mitochondrial
disfunction,
oxidative
stress,
as
well
impact
intestinal
gut
microbiota,
constantly
being
elucidated.
Treatment
strategies
that
continually
emerging
based
on
different
key
points
pathogenesis.
Yet,
ideal
therapeutic
option
has
still
not
been
found
future
research
great
importance,
represents
a
multisystemic
with
numerous
complications.
Neurobiology of Disease,
Journal Year:
2024,
Volume and Issue:
192, P. 106423 - 106423
Published: Jan. 28, 2024
Trimethylamine-N-oxide
(TMAO)
is
a
gut
microbiota-derived
metabolite
produced
by
the
action
of
microbiota
and
hepatic
enzyme
Flavin
Mono‑oxygenase
3
(FMO3).
TMAO
level
has
positive
correlation
with
risk
cardiovascular
events,
including
stroke,
their
influenced
mainly
dietary
choice
liver
FMO3.
plays
role
in
development
atherosclerosis
plaque,
which
one
causative
factors
stroke
event.
Preclinical
clinical
investigations
on
associated
risk,
severity,
outcomes
are
summarised
this
review.
In
addition,
mechanisms
TMAO-driven
vascular
dysfunction
also
discussed,
such
as
inflammation,
oxidative
stress,
thrombus
foam
cell
formation,
altered
cholesterol
bile
acid
metabolism,
etc.
Post-stroke
inflammatory
cascades
involving
activation
immune
cells,
i.e.,
microglia
astrocytes,
result
Blood-brain-barrier
(BBB)
disruption,
allowing
to
infiltrate
brain
further
aggravate
inflammation.
This
event
occurs
NOD-like
receptor
family
pyrin
domain
containing
(NLRP3)
inflammasome
pathway
through
release
cytokines
chemokines
that
BBB
initiate
recruitment
cells
brain.
Thus,
it's
likely
maintaining
levels
could
be
promising
approach
for
treating
improving
complications.