Journal of Clinical Investigation,
Journal Year:
2024,
Volume and Issue:
134(23)
Published: Dec. 1, 2024
The
transmissible
nature
of
prion
diseases
enables
reproduction
neurodegeneration
in
small
animal
models
that
faithfully
follows
the
disease
process
observed
natural
animals
and
humans.
This
allows
temporal
development
to
be
investigated
correlated
with
pathology
a
complex
brain
environment.
In
this
issue
JCI,
Makarava
et
al.
describe
shift
microglia
morphology
from
an
active
phagocytic
phenotype
passive
association
neuronal
cell
bodies.
Whether
morphological
change
reflects
supportive
action
response
impairment
or
exhaustion
PrPSc-laden
remains
determined.
However,
if
microglial
populations
effectively
contain
PrPSc
propagation
early
infection
process,
as
current
study
suggests,
identifying
ways
maintain
enhance
function
population
could
key
prolonging
patient
survival.
Seminars in Immunopathology,
Journal Year:
2024,
Volume and Issue:
46(1-2)
Published: July 1, 2024
Activation
of
the
maternal
immune
system
during
gestation
has
been
associated
with
an
increased
risk
for
neurodevelopmental
disorders
in
offspring,
particularly
schizophrenia
and
autism
spectrum
disorder.
Microglia,
tissue-resident
macrophages
central
nervous
system,
are
implicated
as
potential
mediators
this
risk.
Early
development,
microglia
start
populating
embryonic
addition
to
their
traditional
role
responders
under
homeostatic
conditions,
also
intricately
involved
various
early
processes.
The
timing
activation
may
interfere
functioning
neurodevelopment,
potentially
leading
long-term
consequences
postnatal
life.
In
review
we
will
discuss
involvement
brain
development
prenatal
stages
life,
while
examining
effects
on
Additionally,
recent
single
cell
RNA-sequencing
studies
focusing
hypothesize
how
life
microglial
priming,
through
epigenetic
reprogramming,
be
related
disorders.
Sensory
experience
during
developmental
critical
periods
has
lifelong
consequences
for
circuit
function
and
behavior,
but
the
molecular
cellular
mechanisms
through
which
causes
these
changes
are
not
well
understood.
The
Drosophila
antennal
lobe
houses
synapses
between
olfactory
sensory
neurons
(OSNs)
downstream
projection
(PNs)
in
stereotyped
glomeruli.
Many
glomeruli
exhibit
structural
plasticity
response
to
early-life
odor
exposure,
indicating
a
general
sensitivity
of
fly
circuitry
early
experience.
We
recently
found
that
glia
shape
development
young
adults,
leading
us
ask
if
also
drive
experience-dependent
this
period.
Here,
we
define
period
functional
OSN-PN
ethyl
butyrate
(EB)-sensitive
glomerulus
VM7.
EB
exposure
first
2
days
post-eclosion
drives
large-scale
reductions
glomerular
volume,
presynapse
number,
post-
synaptic
activity.
Crucially,
pruning
long-term
since
both
synapse
number
spontaneous
activity
PNs
remain
persistently
decreased
following
exposure.
highly
conserved
engulfment
receptor
Draper
is
required
as
ensheathing
upregulate
Draper,
invade
VM7
glomerulus,
phagocytose
OSN
presynaptic
terminals
critical-period
Loss
fully
suppresses
morphological
physiological
arguing
phagocytic
engulf
intact
terminals.
These
data
demonstrate
argue
powerful
model
defining
plasticity.
Sensory
experience
during
developmental
critical
periods
has
lifelong
consequences
for
circuit
function
and
behavior,
but
the
molecular
cellular
mechanisms
through
which
causes
these
changes
are
not
well
understood.
The
Drosophila
antennal
lobe
houses
synapses
between
olfactory
sensory
neurons
(OSNs)
downstream
projection
(PNs)
in
stereotyped
glomeruli.
Many
glomeruli
exhibit
structural
plasticity
response
to
early-life
odor
exposure,
indicating
a
general
sensitivity
of
fly
circuitry
early
experience.
We
recently
found
that
glia
shape
development
young
adults,
leading
us
ask
if
also
drive
experience-dependent
this
period.
Here
we
define
period
functional
OSN-PN
ethyl
butyrate
(EB)-sensitive
glomerulus
VM7.
EB
exposure
first
two
days
post-eclosion
drives
large-scale
reductions
glomerular
volume,
presynapse
number,
post-synaptic
activity.
Crucially,
pruning
long-term
since
both
synapse
number
spontaneous
activity
PNs
remain
persistently
decreased
following
exposure.
highly
conserved
engulfment
receptor
Draper
is
required
as
ensheathing
upregulate
Draper,
invade
VM7
glomerulus,
phagocytose
OSN
presynaptic
terminals
critical-period
Loss
fully
suppresses
morphological
physiological
arguing
phagocytic
engulf
intact
synaptic
terminals.
These
data
demonstrate
argue
powerful
model
defining
plasticity.
Pharmaceutical Development and Technology,
Journal Year:
2025,
Volume and Issue:
unknown, P. 1 - 30
Published: Feb. 27, 2025
Alzheimer's
disease
(AD)
is
a
neurodegenerative
that
associated
with
neuroinflammation.
Dextromethorphan
(DXM)
exerts
neuroprotective
effects
in
many
central
nervous
system
injuries
and
diseases.
The
cell
wall
of
Saccharomyces
cerevisiae
cell-based
drug
delivery
can
be
suitable
candidate
for
targeted
to
the
site
inflammation.
In
this
study,
nanoparticles
(NPs)
were
prepared
from
walls,
coated
polysorbate-80,
loaded
DXM.
NPs
had
favorable
hemolytic
behavior
particle
size
distribution
187.25
±
73.37
nm
zeta
potential
+4.3
mV.
Pathological
examination
mouse
model
neuroinflammation
showed
ability
reduce
brain
inflammation
adverse
Proceedings of the National Academy of Sciences,
Journal Year:
2025,
Volume and Issue:
122(13)
Published: March 25, 2025
We
investigated
the
role
of
Triggering
Receptor
Expressed
on
Myeloid
cells
2
(TREM2)
in
myelin
regeneration
brain.
TREM2
is
a
receptor
that
activates
microglia,
which
are
crucial
for
clearing
debris
and
promoting
remyelination.
Previous
studies
mouse
model
demyelination
induced
by
copper-chelating
agent
Cuprizone
(CPZ)
have
shown
stimulation
with
monoclonal
antibody
reduces
demyelination,
while
deleting
Trem2
gene
mice
impairs
Here,
we
blocked
function
acutely
an
during
both
remyelination
phases
CPZ
analyzed
impact
treatment
myelination
expression
single
cells.
found
blocking
depleted
distinct
population
microglia
high
transcription
factor
MAFB
The
loss
these
MAFB-high
was
linked
to
impaired
generation
myelinating
oligodendrocytes.
Importantly,
identified
+
acute
acute-chronic
brain
lesions
from
individuals
multiple
sclerosis
(MS),
but
not
inactive
lesions.
conclude
essential
maintaining
associated
repair.
This
finding
has
significant
implications
understanding
demyelinating
diseases
like
MS
suggests
stimulating
could
be
promising
therapeutic
approach
Acta Neuropathologica Communications,
Journal Year:
2025,
Volume and Issue:
13(1)
Published: May 19, 2025
Abstract
Cranial
radiotherapy
and
environmental
radiation
exposure
are
associated
with
increased
risk
of
cognitive
dysfunction,
including
memory
deficits
mood
disorders,
yet
the
underlying
mechanisms
remain
poorly
understood.
In
this
study,
we
demonstrate
that
cranial
irradiation
induces
hypoactivity
in
medial
prefrontal
cortex
(mPFC)
mice,
leading
to
anxiety-like
behaviors
impairments,
which
can
be
prevented
by
optogenetic
activation
mPFC
excitatory
neurons.
Radiaiton
also
causes
a
significant
reduction
microglial
density
within
mPFC,
accompanied
morphological
transcriptional
alterations
remaining
microglia.
Notably,
repopulation,
achieved
through
CSF1R
antagonist-mediated
depletion
prior
subsequent
restores
neuronal
acitivity
reverses
behavioral
deficits.
Integrated
bulk
RNA
sequencing
proteomic
analysis
reveal
repopulation
specifically
modulates
leukotriene-C4
biosynthesis
pathway,
without
changes
canonical
pro-inflammatory
cytokines
or
chemokines.
Importantly,
pharmacological
inhibition
synthase
ameliorates
radiation-induced
anxiety
impairments.
These
findings
identify
signaling
as
critical
mechanism
dysfunction
suggest
targted
represent
potential
therapeutic
strategies
for
mitigating
radiation-associated
disorders.
