Frontiers in Immunology,
Год журнала:
2025,
Номер
16
Опубликована: Фев. 14, 2025
Porphyromonas
gingivalis
(
P.
)
is
a
gram-negative
bacterium
and
the
main
causative
agent
of
periodontitis,
disease
closely
associated
with
development
periodontal
disease.
The
progression
chronic
infectious
disease,
intricately
linked
to
inflammatory
immune
response.
Inflammatory
cytokines
act
on
tissues
via
immunomodulation,
resulting
in
destruction
tissue.
Recent
studies
have
established
connections
between
periodontitis
various
systemic
diseases,
including
cardiovascular
tumors,
neurodegenerative
diseases.
Neurodegenerative
diseases
are
neurological
disorders
caused
by
system
dysfunction,
Alzheimer’s
Parkinson’s
One
characteristics
an
impaired
response,
which
mediates
neuroinflammation
through
microglial
activation.
Some
shown
association
as
primary
culprit.
can
cross
blood-brain
barrier
(BBB)
or
mediate
injury
variety
pathways,
gut-brain
axis,
thereby
affecting
neuronal
growth
survival
participating
onset
However,
comprehensive
systematic
summaries
origin
lacking.
This
article
reviews
summarizes
relationship
its
possible
regulatory
mechanisms.
review
offers
new
perspectives
into
understanding
highlights
innovative
approaches
for
investigating
developing
tailored
medications
treating
conditions,
particularly
from
viewpoint
their
.
Frontiers in Immunology,
Год журнала:
2023,
Номер
14
Опубликована: Фев. 22, 2023
Alzheimer’s
disease
(AD)
is
defined
as
a
severe
chronic
degenerative
neurological
in
human.
The
pathogenic
mechanism
of
AD
has
been
convincingly
elucidated
by
the
“amyloid
cascade
hypothesis”
with
main
focus
pathological
accretion
β-amyloid
(Aβ)
peptides
outside
cell.
However,
increasing
evidence
suggests
that
this
hypothesis
weak
explaining
pathogenesis
AD.
Neuroinflammation
crucial
development
AD,
which
proven
elevated
levels
inflammatory
markers
and
identification
risk
genes
relevant
to
innate
immune
function.
Here,
we
summarize
effects
microglia-mediated
neuroinflammation
on
focusing
temporal
spatial
changes
microglial
phenotype,
interactions
among
microglia,
Aβ,
tau,
neurons,
prospects
recent
advances
diagnostic
therapeutic
target
International Journal of Molecular Sciences,
Год журнала:
2022,
Номер
23(21), С. 12990 - 12990
Опубликована: Окт. 27, 2022
There
is
a
huge
need
for
novel
therapeutic
and
preventative
approaches
to
Alzheimer’s
disease
(AD)
neuroinflammation
seems
be
one
of
the
most
fascinating
solutions.
The
primary
cell
type
that
performs
immunosurveillance
helps
clear
out
unwanted
chemicals
from
brain
microglia.
Microglia
work
reestablish
efficiency
stop
further
degeneration
in
early
stages
AD
but
mainly
fail
illness’s
later
phases.
This
may
caused
by
number
reasons,
e.g.,
protracted
exposure
cytokines
induce
inflammation
an
inappropriate
accumulation
amyloid
beta
(Aβ)
peptide.
Extracellular
and/or
intraneuronal
phosphorylated
tau
can
both
activate
activation
TLRs
scavenger
receptors,
inducing
numerous
inflammatory
pathways,
including
NF-kB,
JAK-STAT,
NLRP3
inflammasome,
facilitates
microglial
phagocytosis
response
these
mediators.
Aβ/tau
are
taken
up
microglia,
their
removal
extracellular
space
also
have
protective
effects,
if
illness
worsens,
environment
constantly
inflamed
overexposed
oxidative
might
encourage
continuous
activation,
which
lead
neuroinflammation,
stress,
iron
overload,
neurotoxicity.
complexity
diversity
roles
microglia
play
health
necessitate
urgent
development
new
biomarkers
identify
activity
different
It
imperative
comprehend
intricate
mechanisms
result
impairment
develop
immunomodulating
therapies
primarily
attempt
recover
physiological
role
allowing
them
carry
core
function
protection.
Frontiers in Immunology,
Год журнала:
2024,
Номер
14
Опубликована: Янв. 8, 2024
The
increasing
life
expectancy
has
led
to
a
higher
incidence
of
age-related
neurodegenerative
conditions.
Within
this
framework,
neuroinflammation
emerges
as
significant
contributing
factor.
It
involves
the
activation
microglia
and
astrocytes,
leading
release
pro-inflammatory
cytokines
chemokines
infiltration
peripheral
leukocytes
into
central
nervous
system
(CNS).
These
instances
result
in
neuronal
damage
neurodegeneration
through
activated
nucleotide-binding
domain
leucine-rich
repeat
containing
(NLR)
family
pyrin
protein
3
(NLRP3)
nuclear
factor
kappa
B
(NF-kB)
pathways
decreased
erythroid
2-related
2
(Nrf2)
activity.
Due
limited
effectiveness
regarding
inhibition
neuroinflammatory
targets
using
conventional
drugs,
there
is
challenging
growth
search
for
innovative
therapies
alleviating
CNS
diseases
or
even
before
their
onset.
Our
results
indicate
that
interventions
focusing
on
Interleukin-Driven
Immunomodulation,
Chemokine
(CXC)
Receptor
Signaling
Expression,
Cold
Exposure,
Fibrin-Targeted
strategies
significantly
promise
mitigate
processes.
approaches
demonstrate
potential
anti-neuroinflammatory
effects,
addressing
conditions
such
Multiple
Sclerosis,
Experimental
autoimmune
encephalomyelitis,
Parkinson’s
Disease,
Alzheimer’s
Disease.
While
findings
are
promising,
immunomodulatory
often
face
limitations
due
Immune-Related
Adverse
Events.
Therefore,
conduction
randomized
clinical
trials
matter
mandatory,
will
pave
way
promising
future
development
new
medicines
with
specific
therapeutic
targets.
Acta Pharmaceutica Sinica B,
Год журнала:
2024,
Номер
15(1), С. 15 - 34
Опубликована: Окт. 16, 2024
Neuroprotection
is
a
proactive
approach
to
safeguarding
the
nervous
system,
including
brain,
spinal
cord,
and
peripheral
nerves,
by
preventing
or
limiting
damage
nerve
cells
other
components.
It
primarily
defends
central
system
against
injury
from
acute
progressive
neurodegenerative
disorders.
Oxidative
stress,
an
imbalance
between
body's
natural
defense
mechanisms
generation
of
reactive
oxygen
species,
crucial
in
developing
neurological
Due
its
high
metabolic
rate
consumption,
brain
particularly
vulnerable
oxidative
stress.
Excessive
ROS
damages
essential
biomolecules,
leading
cellular
malfunction
neurodegeneration.
Several
disorders,
Alzheimer's,
Parkinson's,
Amyotrophic
lateral
sclerosis,
multiple
ischemic
stroke,
are
associated
with
Understanding
impact
stress
these
conditions
for
new
treatment
methods.
Researchers
exploring
using
antioxidants
molecules
mitigate
aiming
prevent
slow
down
progression
diseases.
By
understanding
intricate
interplay
scientists
hope
pave
way
innovative
therapeutic
preventive
approaches,
ultimately
improving
individuals'
living
standards.
Neuroinflammation
is
a
complex
and
multifaceted
process
that
involves
dynamic
interactions
among
various
cellular
molecular
components.
This
sophisticated
interplay
supports
both
environmental
adaptability
system
resilience
in
the
central
nervous
(CNS)
but
may
be
disrupted
during
neuroinflammation.
In
this
article,
we
first
characterize
key
players
neuroimmune
interactions,
including
microglia,
astrocytes,
neurons,
immune
cells,
essential
signaling
molecules
such
as
cytokines,
neurotransmitters,
extracellular
matrix
(ECM)
components,
neurotrophic
factors.
Under
homeostatic
conditions,
these
elements
promote
cooperation
stability,
whereas
neuroinflammatory
states,
they
drive
adaptive
responses
become
pathological
if
dysregulated.
We
examine
how
mediated
through
actors
pathways,
create
networks
regulate
CNS
functionality
respond
to
injury
or
inflammation.
To
further
elucidate
dynamics,
provide
insights
using
multilayer
network
(MLN)
approach,
highlighting
interconnected
nature
of
under
inflammatory
conditions.
perspective
aims
enhance
our
understanding
communication
mechanisms
underlying
shifts
from
homeostasis
Applying
an
MLN
approach
offers
more
integrative
view
adaptability,
helping
clarify
processes
identify
novel
intervention
points
within
layered
landscape
responses.
Frontiers in Cellular Neuroscience,
Год журнала:
2022,
Номер
16
Опубликована: Авг. 16, 2022
Stroke
remains
a
major
cause
of
long-term
disability
and
mortality
worldwide.
The
immune
system
plays
an
important
role
in
determining
the
condition
brain
following
stroke.
As
resident
innate
cells
central
nervous
system,
microglia
are
primary
responders
defense
network
covering
entire
parenchyma,
exert
various
functions
depending
on
dynamic
communications
with
neurons,
astrocytes,
other
neighboring
under
both
physiological
or
pathological
conditions.
Microglia
activation
polarization
is
crucial
for
damage
repair
ischemic
stroke,
considered
double-edged
sword
neurological
recovery.
can
exist
pro-inflammatory
states
promote
secondary
damage,
but
they
also
secrete
anti-inflammatory
cytokines
neurotrophic
factors
facilitate
recovery
In
this
review,
we
focus
mechanisms
microglia-mediated
neuroinflammation
neuroplasticity
after
ischemia
relevant
potential
microglia-based
interventions
stroke
therapy.
