Abstract
Under
pathological
conditions,
the
immune-specialized
brain
microenvironment
contains
both
resident
microglia
and
bone
marrow-derived
myeloid
cells
recruited
from
peripheral
circulation.
Due
to
largely
overlapping
phenotypic
similarities
between
these
ontogenically
distinct
populations,
studying
their
individual
functions
in
central
nervous
system
diseases
has
been
challenging.
Recently,
transmembrane
protein
119
(Tmem119)
reported
as
a
marker
for
which
is
not
expressed
by
cells.
However,
several
studies
have
loss
or
reduction
of
Tmem119
expression
pathologically
activated
microglia.
Here,
we
examined
whether
could
be
used
robust
identify
metastasis-associated
In
addition,
also
compared
primary
immortalized
microglia-like
BV2
cell
line
characterized
changes
after
LPS
treatment.
Lastly,
commercially
available
transgenic
mouse
(Tmem119-eGFP)
compare
patterns
traditional
antibody-based
detection
methods.
Our
results
indicate
that
reduced
gene
expression.
Biomedicine & Pharmacotherapy,
Год журнала:
2023,
Номер
165, С. 115218 - 115218
Опубликована: Июль 29, 2023
Alzheimer's
disease
(AD)
is
the
most
common
neurodegenerative
disease,
resulting
in
loss
of
cognitive
ability
and
memory.
However,
there
no
specific
treatment
to
mechanistically
inhibit
progression
drugs
only
provide
symptom
relief
do
not
fundamentally
reverse
AD.
Current
studies
show
that
triggering
receptor
expressed
on
myeloid
cells
2
(TREM2)
predominantly
microglia
central
nervous
system
(CNS)
involved
proliferation,
survival,
migration
phagocytosis.
The
current
academic
view
suggests
TREM2
its
ligands
have
CNS
protective
effects
Specifically,
acts
by
regulating
function
promoting
clearance
neuronal
toxic
substances
abnormal
proteins
microglia.
In
addition,
also
inflammatory
response
cell
signaling
pathways,
affecting
immune
regulatory
role
Although
relationship
between
has
been
extensively
studied,
mechanism
action
fully
understood.
purpose
this
review
a
comprehensive
analysis
research
TREM2,
including
regulation
response,
lipid
metabolism
phagocytosis
AD,
explore
potential
application
prospects
as
well
limitations
targeting
for
Molecules,
Год журнала:
2024,
Номер
29(7), С. 1478 - 1478
Опубликована: Март 26, 2024
Alzheimer’s
disease
(AD)
is
a
complex
degenerative
of
the
central
nervous
system
that
clinically
characterized
by
progressive
decline
in
memory
and
cognitive
function.
The
pathogenesis
AD
intricate
not
yet
fully
understood.
Neuroinflammation,
particularly
microglial
activation-mediated
neuroinflammation,
believed
to
play
crucial
role
increasing
risk,
triggering
onset,
hastening
progression
AD.
Modulating
activation
regulating
energy
metabolic
disorder
are
seen
as
promising
strategies
intervene
application
anti-inflammatory
drugs
targeting
microglia
for
prevention
treatment
has
emerged
new
area
research
interest.
This
article
provides
comprehensive
review
neuroinflammation
regulation
development
AD,
exploring
connection
between
disorder,
development.
Additionally,
advancements
microglia-regulating
therapies
discussed.
Aging and Disease,
Год журнала:
2024,
Номер
15(5), С. 2168 - 2168
Опубликована: Янв. 1, 2024
Alzheimer's
disease
(AD)
is
an
age-dependent
neurodegenerative
characterized
by
extracellular
Amyloid
Aβ
peptide
(Aβ)
deposition
and
intracellular
Tau
protein
aggregation.
Glia,
especially
microglia
astrocytes
are
core
participants
during
the
progression
of
AD
these
cells
mediators
clearance
degradation.
The
microbiota-gut-brain
axis
(MGBA)
a
complex
interactive
network
between
gut
brain
involved
in
neurodegeneration.
MGBA
affects
function
glia
central
nervous
system
(CNS),
microbial
metabolites
regulate
communication
microglia;
however,
whether
such
part
pathophysiology
remains
unknown.
One
potential
links
bilateral
gut-brain
tryptophan
(Trp)
metabolism.
microbiota-originated
Trp
its
enter
CNS
to
control
microglial
activation,
activated
subsequently
affect
astrocyte
functions.
present
review
highlights
role
pathology,
roles
per
se
metabolism
as
microbiota
communications.
We
(i)
discuss
derivatives
microglia-astrocyte
crosstalk
from
bioinformatics
perspective,
(ii)
describe
polarization
(iii)
summarize
therapeutic
target.
Finally,
we
perspective
microglia,
well
crosstalk,
inspire
discovery
novel
therapeutics.
Pharmaceuticals,
Год журнала:
2024,
Номер
17(7), С. 831 - 831
Опубликована: Июнь 25, 2024
Histamine
performs
dual
roles
as
an
immune
regulator
and
a
neurotransmitter
in
the
mammalian
brain.
The
histaminergic
system
plays
vital
role
regulation
of
wakefulness,
cognition,
neuroinflammation,
neurogenesis
that
are
substantially
disrupted
various
neurodegenerative
neurodevelopmental
disorders.
H3
receptor
(H3R)
antagonists
inverse
agonists
potentiate
endogenous
release
brain
histamine
have
been
shown
to
enhance
cognitive
abilities
animal
models
several
Microglial
activation
subsequent
neuroinflammation
implicated
impacting
embryonic
adult
neurogenesis,
contributing
development
Alzheimer's
disease
(AD),
Parkinson's
(PD),
autism
spectrum
disorder
(ASD).
Acknowledging
importance
microglia
both
neurodevelopment,
well
their
by
histamine,
offers
intriguing
therapeutic
target
for
these
inhibition
H3Rs
has
found
facilitate
shift
from
proinflammatory
M1
state
anti-inflammatory
M2
state,
leading
reduction
activity
microglial
cells.
Also,
pharmacological
studies
demonstrated
H3R
showed
positive
effects
reducing
biomarkers,
suggesting
potential
simultaneously
modulating
crucial
neurotransmissions
signaling
cascades
such
PI3K/AKT/GSK-3β
pathway.
In
this
review,
we
highlight
addressing
pathology
decline
disorders,
e.g.,
AD,
PD,
ASD,
with
inflammatory
component.
Cells,
Год журнала:
2025,
Номер
14(3), С. 168 - 168
Опубликована: Янв. 22, 2025
The
recent
approval
of
lecanemab
highlights
that
the
amyloid
beta
(Aβ)
protein
is
an
important
pathological
target
in
Alzheimer’s
disease
(AD)
and
further
emphasizes
significance
neuroinflammatory
pathways
regulating
Aβ
accumulation.
Indeed,
accumulation
triggers
microglia
activation,
which
are
key
mediators
neuroinflammation.
inflammatory
responses
this
process
can
lead
to
neuronal
damage
functional
decline.
Microglia
secrete
proinflammatory
cytokines
accelerate
death
release
anti-inflammatory
growth
factors
contributing
recovery
protection.
Thus,
play
a
dual
role
neurodegeneration
neuroprotection,
complicating
their
function
AD.
Therefore,
elucidating
complex
interactions
between
protein,
microglia,
neuroinflammation
essential
for
developing
new
strategies
treating
This
review
investigates
receptors
involved
activating
aims
enhance
understanding
how
these
processes
impact
AD,
as
well
they
be
regulated.
also
analyzed
studies
reported
existing
literature
ongoing
clinical
trials.
Overall,
will
contribute
regulatory
mechanisms
therapies
slow
progression
Advanced Science,
Год журнала:
2024,
Номер
unknown
Опубликована: Сен. 9, 2024
Abstract
Microglia
are
critically
involved
in
post‐stroke
inflammation
affecting
neurological
outcomes.
Lipid
droplet
(LD)
accumulation
microglia
results
a
dysfunctional
and
pro‐inflammatory
state
the
aged
brain
worsens
outcome
of
neuroinflammatory
neurodegenerative
diseases.
However,
role
LD‐rich
(LDRM)
under
stroke
conditions
is
unknown.
Using
vitro
vivo
models,
herein
patterns
microglial
LD
their
corresponding
inflammatory
signaling
cascades
studied.
Interactions
between
temporal
spatial
dynamics
lipid
profiles
phenotypes
different
regions
found.
Hence,
display
enhanced
levels
elevated
perilipin
2
(PLIN2)
expression
when
exposed
to
hypoxia
or
stroke.
Such
LDRM
exhibit
high
TNF‐α,
IL‐6,
IL‐1β
as
well
phenotype
differentially
expressed
metabolism‐related
genes.
These
post‐ischemic
alterations
result
distinct
with
dynamics,
especially
regard
cholesteryl
ester
triacylglycerol
levels,
further
exacerbating
inflammation.
The
present
study
sheds
new
light
on
dynamic
changes
aggregation
ischemia,
demonstrating
mutual
mechanism
function,
which
contributes
progression
injury.
Journal of Neuropathology & Experimental Neurology,
Год журнала:
2023,
Номер
82(11), С. 894 - 900
Опубликована: Сен. 28, 2023
Abstract
The
morbidity
and
mortality
associated
with
Alzheimer
disease
(AD),
one
of
the
most
common
neurodegenerative
diseases,
are
increasing
each
year.
Although
both
amyloid
β
tau
proteins
known
to
be
involved
in
AD
pathology,
their
detailed
functions
pathogenesis
not
fully
understood.
There
is
evidence
that
neuroinflammation
contributes
development
progression
AD,
astrocytes,
microglia,
cytokines
chemokines
they
secrete
acting
coordinately
these
processes.
Signaling
involving
chemokine
(C-C
motif)
ligand
5
(CCL5)
its
main
receptor
C-C
(CCR5)
plays
an
important
role
normal
physiologic
processes
as
well
pathologic
conditions
such
neurodegeneration.
In
recent
years,
many
studies
have
shown
CCL5/CCR5
axis
a
major
effect
but
there
also
few
contradict
this.
short,
still
intricate.
This
review
summarizes
structure,
distribution,
axis,
progress
understanding
involvement
AD.
Frontiers in Neuroscience,
Год журнала:
2024,
Номер
18
Опубликована: Апрель 11, 2024
Sepsis
is
a
leading
cause
of
death
resulting
from
an
uncontrolled
inflammatory
response
to
infectious
agent.
Multiple
organ
injuries,
including
brain
are
common
in
sepsis.
The
underlying
mechanism
sepsis-associated
encephalopathy
(SAE),
which
associated
with
neuroinflammation,
not
yet
fully
understood.
Recent
studies
suggest
that
the
release
interleukin-1β
(IL-1β)
following
activation
microglial
cells
plays
crucial
role
development
long-lasting
neuroinflammation
after
initial
sepsis
episode.
This
review
provides
comprehensive
analysis
recent
literature
on
molecular
signaling
pathways
involved
cell
and
release.
It
also
explores
physiological
pathophysiological
IL-1β
cognitive
function,
particular
focus
its
contribution
findings
this
may
assist
healthcare
providers
developing
novel
interventions
against
SAE.
