Scientific Reports,
Journal Year:
2023,
Volume and Issue:
13(1)
Published: March 27, 2023
Microglia
are
immune
brain
cells
implicated
in
stress-related
mental
illnesses
including
posttraumatic
stress
disorder
(PTSD).
Their
role
the
pathophysiology
of
PTSD,
and
on
neurobiological
systems
that
regulate
stress,
is
not
completely
understood.
We
tested
hypothesis
microglia
activation,
fronto-limbic
regions
involved
would
be
elevated
participants
with
occupation-related
PTSD.
also
explored
relationship
between
cortisol
activation.
Twenty
PTSD
23
healthy
controls
(HC)
completed
positron
emission
tomography
(PET)
scanning
18-kDa
translocator
protein
(TSPO),
a
putative
biomarker
activation
using
probe
[18F]FEPPA,
blood
samples
for
measurement
cortisol.
[18F]FEPPA
VT
was
non-significantly
(6.5-30%)
participants.
significantly
higher
reporting
frequent
cannabis
use
compared
to
non-users
(44%,
p
=
0.047).
Male
(21%,
0.094)
history
early
childhood
trauma
(33%,
0.116)
had
VT.
Average
positively
related
(r
0.530,
0.028)
group
only.
Although
we
did
find
significant
abnormality
TSPO
binding
findings
suggest
microglial
might
have
occurred
subgroup
who
reported
use.
The
suggests
potential
link
hypothalamic-pituitary-adrenal-axis
dysregulation
central
response
which
warrants
further
study.
Neuroglia,
Journal Year:
2024,
Volume and Issue:
5(4), P. 410 - 444
Published: Oct. 21, 2024
Microglia,
the
unique
and
motile
immune
cells
of
central
nervous
system
(CNS),
function
as
a
security
guard
in
maintaining
CNS
homeostasis,
primarily
through
calcium
signaling.
The
dynamics
microglia
control
important
functions
such
phagocytosis,
cytokine
release,
migration.
Calcium
dysregulation
has
been
linked
to
several
disorders,
like
Alzheimer’s
disease
(AD),
Parkinson’s
(PD),
multiple
sclerosis
(MS),
ischemic
stroke
(IS).
entering
channels
voltage-gated
(VGCCs),
store-operated
entry
(SOCE),
transient
receptor
potential
(TRP)
is
essential
for
microglial
activation
pro-inflammatory
responses.
Under
pathological
conditions,
formation
amyloid-β
plaques
AD,
aggregation
α-synuclein
PD,
oxidative
stress
MS,
exacerbates
neuroinflammation,
mitochondrial
dysfunction,
neurodegeneration.
Therapeutic
strategies
targeting
signaling
pathways,
using
channel
blockers
antioxidant
interventions,
show
promise
alleviating
slowing
down
progression.
This
review
summarizes
underlying
mechanisms
therapeutic
benefits
restoring
balance
disorders.
International Journal of Molecular Sciences,
Journal Year:
2025,
Volume and Issue:
26(1), P. 310 - 310
Published: Jan. 1, 2025
Schizophrenia
(SZ),
a
complex
psychiatric
disorder
of
neurodevelopment,
is
characterised
by
range
symptoms,
including
hallucinations,
delusions,
social
isolation
and
cognitive
deterioration.
One
the
hypotheses
that
underlie
SZ
related
to
inflammatory
events
which
could
be
partly
responsible
for
symptoms.
However,
it
unknown
how
molecules
can
contribute
decline
in
SZ.
This
review
summarises
exposes
possible
contribution
imbalance
between
pro-inflammatory
anti-inflammatory
interleukins
like
IL-1beta,
IL-4
TNFalfa
among
others
on
impairment.
We
discuss
this
affects
microglia
astrocytes
inducing
disruption
blood–brain
barrier
(BBB)
SZ,
impact
prefrontal
cortex
or
associative
areas
involved
executive
functions
such
as
planning
working
tasks.
also
highlight
generated
intestinal
microbiota
alterations,
due
dysfunctional
microbial
colonisers
use
some
anti-psychotics,
central
nervous
system.
Finally,
question
arises
whether
modulate
correct
characterises
if
an
immunomodulatory
strategy
incorporated
into
conventional
clinical
treatments,
either
alone
complement,
applied
specific
phases,
prodromal
first-episode
psychosis.
Frontiers in Aging,
Journal Year:
2023,
Volume and Issue:
4
Published: Aug. 15, 2023
Neuroinflammation
is
a
universal
characteristic
of
brain
aging
and
neurological
disorders,
irrespective
the
disease
state.
Glial
inflammation
mediates
this
signaling,
through
astrocyte
microglial
polarization
from
neuroprotective
to
neurotoxic
phenotypes.
reactivity
results
in
loss
homeostasis,
as
these
cells
no
longer
provide
support
neurons,
addition
production
chronically
toxic
pro-inflammatory
mediators.
These
glial
changes
initiate
an
inflammatory
state
that
injures
central
nervous
system
(CNS)
over
time.
As
ages,
glia
are
altered,
including
increased
cell
numbers,
morphological
changes,
either
pre-disposition
or
inability
become
reactive.
alterations
induce
age-related
neuropathologies,
ultimately
leading
neuronal
degradation
irreversible
damage
associated
with
disorders
aged
brain,
Alzheimer’s
Disease
(AD)
other
related
diseases.
While
complex
interactions
well
studied,
role
additional
stressors,
such
infectious
agents,
play
on
neuropathology
has
not
been
fully
elucidated.
Both
biological
agents
periphery,
bacterial
infections,
CNS,
viral
infections
like
SARS-CoV-2,
push
into
neuroinflammatory
phenotypes
can
exacerbate
pathology
within
brain.
release
pattern
molecular
patterns
(PAMPs)
bind
recognition
receptors
(PRRs)
cells,
beginning
cascade.
In
review,
we
will
summarize
evidence
reactive
glia,
which
worsens
neuropathology.
bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2025,
Volume and Issue:
unknown
Published: Jan. 16, 2025
Abstract
While
CNS
microglia
have
well-established
roles
in
synapse
pruning
during
neurodevelopment,
only
a
few
studies
identified
for
formation.
These
focused
on
the
cortex
and
primary
sensory
circuits
restricted
developmental
time
periods,
leaving
substantial
gaps
our
understanding
of
early
functions
microglia.
Here
we
investigated
how
absence
impacts
synaptic
development
nucleus
accumbens
(NAc),
region
critical
emotional
regulation
motivated
behaviors
where
dysfunction
is
implicated
psychiatric
disorders
that
arise
life.
Using
genetically
modified
mouse
lacks
(
Csf1r
ΔFIRE/ΔFIRE
),
found
blunted
excitatory
formation
NAc.
This
effect
was
most
prominent
second
third
postnatal
weeks,
when
previously
to
be
overproduced,
accompanied
by
an
increase
presynaptic
release
probability
alterations
postsynaptic
kinetics.
Tissue-level
NAc
proteomics
confirmed
microglial
impacted
numerous
proteins
involved
structure,
trans-synaptic
signaling,
pre-synaptic
function.
However,
did
not
perturb
levels
astrocyte-derived
cues
adhesive
promote
synaptogenesis,
suggesting
reduced
number
may
caused
microglial-derived
synaptogenic
cue.
Although
observed
electrophysiological
changes
were
largely
normalized
adulthood,
lasting
effects
threat
avoidance
behavior,
these
behavioral
directly
associated
with
neuronal
activity.
Together,
results
indicate
role
regulating
landscape
developing
establishing
functional
underlying
adult
repertoires.
Antioxidants,
Journal Year:
2024,
Volume and Issue:
13(7), P. 855 - 855
Published: July 16, 2024
Chronic
obstructive
pulmonary
disease
(COPD)
is
the
third
leading
cause
of
death
globally
and
primarily
caused
by
cigarette
smoking
(CS).
Neurocognitive
comorbidities
such
as
anxiety
cognitive
impairments
are
common
among
people
with
COPD.
CS-induced
lung
inflammation
oxidative
stress
may
“spill-over”
into
systemic
circulation,
driving
onset
these
comorbidities.
We
investigated
whether
a
prophylactic
treatment
NADPH
Oxidase
2
(NOX2)
inhibitor,
apocynin,
could
prevent
neurocognitive
impairments.
Adult
male
BALB/c
mice
were
exposed
to
CS
(9
cigarettes/day,
5
days/week)
or
room
air
(sham)
for
8
weeks
co-administration
apocynin
(5
mg/kg,
intraperitoneal
injection
once
daily)
vehicle
(0.01%
DMSO
in
saline).
Following
7
exposure,
underwent
behavioral
testing
assess
recognition
spatial
memory
(novel
object
Y
maze,
respectively)
anxiety-like
behaviors
(open
field
elevated
plus
maze).
Mice
then
euthanized,
blood,
lungs,
brains
collected.
Apocynin
partially
improved
neutrophilia
reversed
(C-reactive
protein)
(malondialdehyde).
exerted
an
anxiolytic
effect
CS-exposed
mice,
which
was
associated
restored
microglial
profiles
within
amygdala
hippocampus.
Thus,
targeting
using
can
alleviate
represent
novel
strategy
managing
COPD-related
disorders.
Journal of Neuroscience Research,
Journal Year:
2024,
Volume and Issue:
102(10)
Published: Oct. 1, 2024
ABSTRACT
This
study
aims
to
compare
the
efficacy
of
5‐alpha‐reductase
inhibitors
(5ARIs)
on
anxiety
and
depression
between
long‐term
short‐term
treatment
followed
by
withdrawal
in
d
‐galactose
(Dgal)–induced
senescent
male
rats.
Thirty‐two,
8‐week‐old,
Wistar
rats
were
divided
into
two
groups:
control
Dgal‐treated
(150
mg/kg/day;
subcutaneously)
for
18
weeks.
At
week
13,
subdivided
three
subgroups:
(1)
vehicle
(DgV),
(2)
with
5ARIs,
Finasteride
5
mg/kg/day,
per
oral
6
weeks
(DgF),
(3)
2
a
4‐week
period
(DgW).
Anxiety
assessed
using
elevated‐plus
maze
(EPM)
splash
test
(ST).
Blood
was
collected
biochemical
analysis.
After
euthanasia,
brains
removed
examine
brain
inflammation,
oxidative
stress,
neuroactive
steroids,
metabolites,
markers.
We
found
that
DgV
exhibited
metabolic
disturbance
reduced
preference
index
EPM,
grooming
duration
ST.
Increased
neurotoxic
along
increased
inflammation/oxidative
microglia
complexity
observed
Both
therapeutic
approaches
improved
parameters
open
arm
EPM
rats,
while
only
DgF
Our
results
indicate
Fin
reduces
depression‐like
anxiety‐like
behaviors
reducing
senescent.
In
conclusion,
5ARIs
is
more
effective
alleviating
than
Dgal‐induced
early