Journal of clinical practice,
Год журнала:
2023,
Номер
14(3), С. 36 - 49
Опубликована: Окт. 19, 2023
Ischemic
stroke
is
a
global
medical
problem
and
one
of
the
leading
causes
death
or
disability
worldwide.
The
main
approach
ischemic
therapy
in
most
acute
period,
which
can
prevent
minimize
development
neurological
deficit,
restoration
blood
flow
brain
tissue
using
enzymatic
thrombolysis
endovascular
thromboextraction.
When
therapeutic
window
missed,
modulation
inflammatory
response
may
play
an
important
role
determining
fate
neurons
penumbra.
key
players
this
process
are
T-regulatory
cells
(Tregs)
immunosuppressive
population
CD4+
T-cells
with
CD4+,
CD25+
CD127low,
FoxP3+
phenotype.
Despite
existing
reports
that
Tregs
(or
certain
Treg
subpopulations)
exacerbate
microcirculatory
disorders
tissue,
many
stadies
convincingly
suggest
positive
stroke.
Resident
CD69+
found
normal
mammalian
have
neuroprotective
activity,
produce
IL-10
other
anti-inflammatory
cytokines,
control
astrogliosis,
downregulate
cytotoxic
subpopulations
T
microglia.
Systemic
administration
accompained
by
decrease
volume
cerebral
infarction
decreased
levels
secondary
neuronal
death.
Thus,
methods
allowing
activation
expansion
ex
vivo
open
up
several
new
avenues
for
immunocorrection
not
only
systemic
autoimmune
diseases,
but,
potentially,
relationship
between
Treg,
inflammation,
cerebrovascular
pathology
particular
interest
case
COVID-19
as
comorbidity.
It
has
been
demonstrated
inflammation
caused
SARS-CoV-2
infection
leads
to
significant
suppression
accompanied
increased
risk
complications.
Overall,
information
summarized
herein
about
possible
potential
be
practical
researchers,
but
also
clinicians.
Biology,
Год журнала:
2024,
Номер
13(11), С. 917 - 917
Опубликована: Ноя. 12, 2024
Hemorrhagic
stroke
is
the
deadliest
type
of
stroke.
Cellular
and
molecular
biomarkers
are
important
for
understanding
pathophysiology
Microglia
among
most
promising
biological
markers.
However,
morphological
physiological
characteristics
microglia,
as
well
structural
functional
aspects
their
interactions
with
neurons
other
cells,
largely
unknown.
Due
to
large
number
different
phenotypes
very
limited
information
on
microglial
changes
in
subarachnoid
hemorrhage
(SAH),
we
performed
this
study
aimed
at
identifying
features
distribution
various
layers
cerebral
cortex
hyperacute
phase
non-traumatic
SAH.
We
studied
SAH
non-survivors
a
control
group
(coronary
heart
disease
sudden
cardiac
death
were
underlying
causes
death).
An
immunohistochemical
using
antibodies
iba-1
(a
marker
microglia)
revealed
microglia
after
hemorrhage.
Significant
differences
between
groups
indicate
rapid
response
injury.
The
findings
that
there
quantitative
phenotypic
during
early
human
cortex.
Aging and Disease,
Год журнала:
2024,
Номер
unknown, С. 0 - 0
Опубликована: Янв. 1, 2024
Stroke
is
a
serious
disease
that
can
lead
to
local
neurological
dysfunction
and
cause
great
harm
the
patient's
health
due
blood
cerebral
circulation
disorder.
Synaptic
pruning
critical
for
normal
development
of
human
brain,
which
makes
synaptic
circuit
completer
more
efficient
by
removing
redundant
synapses.
The
complement
system
considered
key
player
in
loss
cognitive
impairment
neurodegenerative
disease.
After
stroke,
over-activated,
proteins
be
labeled
on
Microglia
astrocytes
recognize
engulf
synapses
through
corresponding
receptors.
Complement-mediated
excessive
post-stroke
(PSCI)
secondary
brain
damage.
This
review
summarizes
latest
progress
complement-mediated
after
stroke
potential
mechanisms.
Targeting
may
essential
exploring
therapeutic
strategies
injury
(SBI)
stroke.
Folia Medica Indonesiana,
Год журнала:
2024,
Номер
60(2), С. 167 - 181
Опубликована: Июнь 10, 2024
Highlights:1.
As
minocycline
plays
an
important
role
in
stroke
microglia
activation
and
iron
chelation,
it
is
to
further
analyze
its
effects
on
treatment.2.
This
meta-analysis
revealed
a
significant
effect
of
therapy,
as
evidenced
by
improved
functional
outcomes
inhibited
matrix
metalloproteinase-9
(MMP-9)
activity.
Abstract
Stroke
the
most
common
devastating
cerebrovascular
disease.
Many
neuroprotective
medications,
such
scale
minocycline,
have
been
developed
help
nervous
system
recover
or
regenerate
after
stroke.
However,
remains
unclear
whether
provides
beneficial
We
conducted
this
systematic
review
synthesize
treatment.
The
was
registered
International
Prospective
Register
Systematic
Reviews
(PROSPERO),
with
registration
number
CRD42023485168.
quality
eligible
studies
assessed
using
Jadad
scale.
included
three
ischemic
trials,
seven
intracerebral
hemorrhage
one
study
acute
There
association
between
intervention
severity
according
National
Institute
Health
Scale
(NIHSS),
pooled
mean
difference
(MD)
-1.92,
95%
confidence
interval
(CI)
-3.39
-0.45,
value
p=0.01.
In
subgroup
stroke,
modified
Rankin
(mRS)
significantly
lower
treatment
group
compared
control
(MD=-0.89,
CI=-1.54
-0.25,
p=0.007).
Additionally,
levels
for
were
(MD=-19.93,
CI=-36.9
-2.96,
p=0.02).
analysis
that
not
associated
hematoma
volume,
mortality,
recurrence.
Our
findings
indicate
supplementation
potential
strategy
treating
hemorrhage.
Translational Stroke Research,
Год журнала:
2024,
Номер
unknown
Опубликована: Авг. 5, 2024
The
direct
interplay
between
the
immune
and
nervous
systems
is
now
well
established.
Within
brain,
these
interactions
take
place
neurons
resident
glial
cells,
i.e.,
microglia
astrocytes,
or
infiltrating
influenced
by
systemic
factors.
A
special
form
of
physical
cell-cell
so-called
"neuroimmunological
(NI)
synapse."
There
compelling
evidence
that
same
signaling
pathways
regulate
inflammatory
responses
to
injury
ischemia
also
play
potent
roles
in
brain
development,
plasticity,
function.
Proper
synaptic
wiring
as
important
during
development
it
disease
states,
necessary
for
activity-dependent
refinement
neuronal
circuits.
Since
process
forming
connections
highly
dynamic,
with
constant
changes
strength
connectivity,
component
perfectly
suited
regulatory
task
turnover.
Many
cellular
molecular
players
this
interaction
remain
be
uncovered,
especially
pathological
states.
In
review,
we
discuss
propose
possible
communication
hubs
components
adaptive
innate
element
ischemic
stroke
pathology.
Research Square (Research Square),
Год журнала:
2024,
Номер
unknown
Опубликована: Дек. 5, 2024
Abstract
Neuroinflammation
significantly
contributes
to
the
progression
of
traumatic
brain
injury
(TBI),
in
which
microglial
activation
playing
a
crucial
role.
This
study
explores
impact
Deltex
E3
ubiquitin
ligase
1
(DTX1)
on
polarization
and
neuroinflammation
post-TBI.
We
investigated
DTX1
expression
rat
TBI
model.
Through
gain-
loss-of-function
approaches,
we
elucidated
DTX1’s
role
modulating
inflammatory
cytokine
production
by
reverse
transcription
PCR,
Western
blot,
enzyme-linked
immunosorbent
assay
(ELISA).
was
up-regulated
LPS-stimulated
microglia
post-TBI
brains.
Overexpression
promoted
proinflammatory
cytokines
induced
an
M1
phenotype,
marked
elevated
inducible
nitric
oxide
synthase
(iNOS)
reduced
Arginase-1
(Arg1).
Conversely,
silencing
exhibited
anti-inflammatory
effects.
In
model,
overexpression
exacerbated
cognitive
impairments,
while
its
knockdown
ameliorated
these
Our
findings
suggested
that
is
key
regulator
neuroinflammation,
herald
promising
therapeutic
target
for
treatment.
Journal of clinical practice,
Год журнала:
2023,
Номер
14(3), С. 36 - 49
Опубликована: Окт. 19, 2023
Ischemic
stroke
is
a
global
medical
problem
and
one
of
the
leading
causes
death
or
disability
worldwide.
The
main
approach
ischemic
therapy
in
most
acute
period,
which
can
prevent
minimize
development
neurological
deficit,
restoration
blood
flow
brain
tissue
using
enzymatic
thrombolysis
endovascular
thromboextraction.
When
therapeutic
window
missed,
modulation
inflammatory
response
may
play
an
important
role
determining
fate
neurons
penumbra.
key
players
this
process
are
T-regulatory
cells
(Tregs)
immunosuppressive
population
CD4+
T-cells
with
CD4+,
CD25+
CD127low,
FoxP3+
phenotype.
Despite
existing
reports
that
Tregs
(or
certain
Treg
subpopulations)
exacerbate
microcirculatory
disorders
tissue,
many
stadies
convincingly
suggest
positive
stroke.
Resident
CD69+
found
normal
mammalian
have
neuroprotective
activity,
produce
IL-10
other
anti-inflammatory
cytokines,
control
astrogliosis,
downregulate
cytotoxic
subpopulations
T
microglia.
Systemic
administration
accompained
by
decrease
volume
cerebral
infarction
decreased
levels
secondary
neuronal
death.
Thus,
methods
allowing
activation
expansion
ex
vivo
open
up
several
new
avenues
for
immunocorrection
not
only
systemic
autoimmune
diseases,
but,
potentially,
relationship
between
Treg,
inflammation,
cerebrovascular
pathology
particular
interest
case
COVID-19
as
comorbidity.
It
has
been
demonstrated
inflammation
caused
SARS-CoV-2
infection
leads
to
significant
suppression
accompanied
increased
risk
complications.
Overall,
information
summarized
herein
about
possible
potential
be
practical
researchers,
but
also
clinicians.
