Journal of Food Science,
Journal Year:
2025,
Volume and Issue:
90(3)
Published: March 1, 2025
Abstract
Intermittent
fasting
(IF)
is
an
eating
pattern
that
promotes
health
and
cognitive
improvement
through
periodic
eating.
It
has
been
shown
to
enhance
neuroplasticity
reduce
oxidative
stress
inflammation.
Recent
studies
have
demonstrated
probiotic
supplementation
enhances
performance
by
modulating
gut
microbiota
composition
increasing
short‐chain
fatty
acid
production,
which
in
turn
neurogenesis
synaptic
plasticity.
The
microbiota‐gut‐brain
axis
(MGBA)
the
communication
bridge
between
brain,
influencing
function
immune,
endocrine,
nervous
systems.
combination
of
probiotics
IF
may
exert
complementary
effects
on
function,
with
enhancing
microbial
diversity
metabolic
efficiency,
while
further
modulate
barrier
integrity
neurotransmitter
synthesis.
This
review
critically
examines
interplay
via
MGBA,
identifying
key
mechanisms
potential
therapeutic
strategies
remain
underexplored
current
research.
Frontiers in Aging Neuroscience,
Journal Year:
2022,
Volume and Issue:
14
Published: June 16, 2022
As
inflammation
in
the
brain
contributes
to
several
neurological
and
psychiatric
diseases,
cause
of
neuroinflammation
is
being
widely
studied.
The
causes
can
be
roughly
divided
into
following
domains:
viral
infection,
autoimmune
disease,
from
peripheral
organs,
mental
stress,
metabolic
disorders,
lifestyle.
In
particular,
effects
caused
by
organs
have
yet
unclear
mechanisms.
Many
such
as
gastrointestinal
inflammation,
chronic
obstructive
pulmonary
rheumatoid
arthritis,
dermatitis,
fatigue
syndrome,
or
myalgic
encephalomyelitis
(CFS/ME),
trigger
through
pathways.
mechanisms
action
for
inflammation-induced
include
disruption
blood-brain
barrier,
activation
glial
cells
associated
with
systemic
immune
activation,
on
autonomic
nerves
via
organ-brain
axis.
this
review,
we
consider
previous
studies
relationship
between
neuroinflammation,
focusing
regions
susceptible
inflammation.
Frontiers in Immunology,
Journal Year:
2022,
Volume and Issue:
13
Published: Oct. 6, 2022
Inflammatory
bowel
disease
(IBD),
mainly
including
ulcerative
colitis
(UC)
and
Crohn’s
(CD),
is
an
autoimmune
gastrointestinal
characterized
by
chronic
inflammation
frequent
recurrence.
Accumulating
evidence
has
confirmed
that
psychological
stress
considered
to
trigger
IBD
deterioration
relapse.
Moreover,
studies
have
demonstrated
patients
with
a
higher
risk
of
developing
symptoms
anxiety
depression
than
healthy
individuals.
However,
the
underlying
mechanism
link
between
remains
poorly
understood.
This
review
used
psychoneuroimmunology
perspective
assess
possible
neuro-visceral
integration,
immune
modulation,
crucial
intestinal
microbiome
changes
in
IBD.
Furthermore,
bidirectionality
brain–gut
axis
was
emphasized
context,
indicating
pathophysiology
increases
inflammatory
response
central
nervous
system
further
contributes
anxiety-
depression-like
behavioral
comorbidities.
information
will
help
accurately
characterize
activity.
Additionally,
clinical
application
functional
brain
imaging,
microbiota-targeted
treatment,
psychotherapy
antidepressants
should
be
during
treatment
diagnosis
elucidates
significance
more
high-quality
research
combined
large
sample
sizes
multiple
diagnostic
methods
psychotherapy,
which
may
achieve
personalized
therapeutic
strategies
for
based
on
relief.
Journal of Clinical Medicine,
Journal Year:
2025,
Volume and Issue:
14(2), P. 386 - 386
Published: Jan. 9, 2025
The
blood-brain
barrier
(BBB)
is
a
crucial
structure
that
maintains
brain
homeostasis
by
regulating
the
entry
of
molecules
and
cells
from
bloodstream
into
central
nervous
system
(CNS).
Neurodegenerative
diseases
such
as
Alzheimer's
Parkinson's
disease,
well
ischemic
stroke,
compromise
integrity
BBB.
This
leads
to
increased
permeability
infiltration
harmful
substances,
thereby
accelerating
neurodegeneration.
In
this
review,
we
explore
mechanisms
underlying
BBB
disruption,
including
oxidative
stress,
neuroinflammation,
vascular
dysfunction,
loss
tight
junction
integrity,
in
patients
with
neurodegenerative
diseases.
We
discuss
how
breakdown
contributes
neurotoxicity,
abnormal
accumulation
pathological
proteins,
all
which
exacerbate
neuronal
damage
facilitate
disease
progression.
Furthermore,
potential
therapeutic
strategies
aimed
at
preserving
or
restoring
function,
anti-inflammatory
treatments,
antioxidant
therapies,
approaches
enhance
integrity.
Given
role
neurodegeneration,
maintaining
its
represents
promising
approach
slow
prevent
progression
International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(2), P. 1470 - 1470
Published: Jan. 12, 2023
The
intestinal
barrier,
with
its
multiple
layers,
is
the
first
line
of
defense
between
outside
world
and
intestine.
Its
disruption,
resulting
in
increased
permeability,
a
recognized
pathogenic
factor
extra-intestinal
diseases.
identification
gut-vascular
barrier
(GVB),
consisting
structured
endothelium
below
epithelial
layer,
has
led
to
new
evidence
on
etiology
management
diseases
gut-liver
axis
gut-brain
axis,
recent
implications
oncology
as
well.
involved
several
neuroinflammatory
processes.
In
particular,
description
choroid
plexus
vascular
regulating
brain
permeability
under
conditions
gut
inflammation
identifies
key
regulator
maintaining
tissue
homeostasis
health.
Journal of Neuroinflammation,
Journal Year:
2023,
Volume and Issue:
20(1)
Published: March 27, 2023
Abstract
Depression
is
a
common
mental
illness,
which
related
to
monoamine
neurotransmitters
and
the
dysfunction
of
cholinergic,
immune,
glutamatergic,
neuroendocrine
systems.
The
hypothesis
one
commonly
recognized
pathogenic
mechanisms
depression;
however,
drugs
designed
based
on
this
have
not
achieved
good
clinical
results.
A
recent
study
demonstrated
that
depression
inflammation
were
strongly
correlated,
activation
alpha7
nicotinic
acetylcholine
receptor
(α7
nAChR)-mediated
cholinergic
anti-inflammatory
pathway
(CAP)
in
system
exhibited
therapeutic
effects
against
depression.
Therefore,
anti-inflammation
might
be
potential
direction
for
treatment
Moreover,
it
also
necessary
further
reveal
key
role
α7
nAChR
pathogenesis
This
review
focused
correlations
between
as
well-discussed
crucial
CAP.
Brain Behavior and Immunity,
Journal Year:
2024,
Volume and Issue:
117, P. 473 - 492
Published: Feb. 8, 2024
The
gut
and
brain
are
increasingly
linked
in
human
disease,
with
neuropsychiatric
conditions
classically
attributed
to
the
showing
an
involvement
of
intestine
inflammatory
bowel
diseases
(IBDs)
displaying
ever-expanding
list
neurological
comorbidities.
To
identify
molecular
systems
that
underpin
this
gut-brain
connection
thus
discover
therapeutic
targets,
experimental
models
dysfunction
must
be
evaluated
for
effects.
In
present
study,
we
examine
disturbances
along
axis
a
widely
used
murine
model
colitis,
dextran
sodium
sulfate
(DSS)
model,
using
high-throughput
transcriptomics
unbiased
network
analysis
strategy
coupled
standard
biochemical
outcome
measures
achieve
comprehensive
approach
key
disease
processes
both
colon
brain.
We
reproducibility
colitis
induction
its
resulting
genetic
programs
during
different
phases
finding
DSS-induced
is
largely
reproducible
few
site-specific
features.
focus
on
circulating
immune
system
as
intermediary
between
brain,
which
exhibits
activation
pro-inflammatory
innate
immunity
colitis.
Our
provides
supporting
evidence
suggests
myelination
may
process
vulnerable
increased
intestinal
permeability,
identifies
possible
role
oxidative
stress
oxygenation.
Overall,
provide
evaluation
multiple
prevalent
will
inform
future
studies
others,
assist
identification
druggable
targets
axis,
contribute
our
understanding
concomitance
dysfunction.
International Journal of Molecular Sciences,
Journal Year:
2022,
Volume and Issue:
23(19), P. 11111 - 11111
Published: Sept. 21, 2022
Inflammatory
bowel
disease
(IBD)
comprises
Crohn's
(CD)
and
ulcerative
colitis
(UC)
is
associated
with
neuropsychiatric
symptoms
like
anxiety
depression.
Both
conditions
strongly
worsen
IBD
burden.
In
the
present
review,
we
summarize
current
understanding
of
pathogenesis
depression
in
IBD.
We
a
stepwise
cascade
along
gut-immune-brain
axis
initiated
by
evasion
chronic
intestinal
inflammation
to
pass
epithelial
vascular
barrier
gut
cause
systemic
inflammation.
then
different
anatomical
transmission
routes
gut-derived
peripheral
into
central
nervous
system
(CNS)
highlight
knowledge
on
neuroinflammatory
changes
CNS
preclinical
mouse
models
focus
microglia,
brain-resident
macrophages.
Subsequently,
discuss
how
neuroinflammation
can
alter
neuronal
circuitry
trigger
anxiety.
Finally,
role
microbiota
will
be
reviewed.
A
more
comprehensive
interaction
between
gastrointestinal
tract,
immune
accounting
for
similarities
differences
UC
CD
pave
path
improved
prediction
treatment
comorbidities
other
inflammatory
diseases.
