Journal of Neuroinflammation,
Год журнала:
2024,
Номер
21(1)
Опубликована: Янв. 23, 2024
Abstract
Parkinson’s
disease
(PD)
and
Alzheimer’s
(AD)
are
neurodegenerative
disorders
caused
by
the
interaction
of
genetic,
environmental,
familial
factors.
These
diseases
have
distinct
pathologies
symptoms
that
linked
to
specific
cell
populations
in
brain.
Notably,
immune
system
has
been
implicated
both
diseases,
with
a
particular
focus
on
dysfunction
microglia,
brain’s
resident
cells,
contributing
neuronal
loss
exacerbating
symptoms.
Researchers
use
models
neuroimmune
gain
deeper
understanding
physiological
biological
aspects
these
how
they
progress.
Several
vitro
vivo
models,
including
2D
cultures
animal
utilized.
Recently,
advancements
made
optimizing
existing
developing
3D
organ-on-a-chip
systems,
holding
tremendous
promise
accurately
mimicking
intricate
intracellular
environment.
As
result,
represent
crucial
breakthrough
transformation
current
treatments
for
PD
AD
offering
potential
conducting
long-term
disease-based
modeling
therapeutic
testing,
reducing
reliance
significantly
improving
viability
compared
conventional
models.
The
application
research
marks
prosperous
step
forward,
providing
more
realistic
representation
complex
interactions
within
system.
Ultimately,
refined
aim
aid
quest
combat
mitigate
impact
debilitating
patients
their
families.
Current Issues in Molecular Biology,
Год журнала:
2024,
Номер
46(3), С. 1851 - 1864
Опубликована: Фев. 28, 2024
Autism
spectrum
disorder
(ASD)
is
thought
to
result
from
susceptibility
genotypes
and
environmental
risk
factors.
The
offspring
of
women
who
experience
pregnancy
infection
have
an
increased
for
autism.
Maternal
immune
activation
(MIA)
in
pregnant
animals
produces
with
autistic
behaviors,
making
MIA
a
useful
model
However,
how
causes
behaviors
not
fully
understood.
Here,
we
show
that
NKCC1
critical
mediating
offspring.
We
confirmed
induced
by
poly(I:C)
during
leads
further
demonstrated
showed
significant
microglia
activation,
excessive
dendritic
spines,
narrow
postsynaptic
density
(PSD)
their
prefrontal
cortex
(PFC).
Then,
discovered
these
abnormalities
may
be
caused
overexpression
offspring’s
PFCs.
Finally,
ameliorated
the
using
PFC
microinjection
inhibitor
bumetanide
(BTN)
Our
findings
shed
new
light
on
pathological
mechanisms
autism
infection.
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(10), С. 5480 - 5480
Опубликована: Май 17, 2024
Maternal
immune
activation
(MIA)
is
a
risk
factor
for
multiple
neurodevelopmental
disorders;
however,
animal
models
developed
to
explore
MIA
mechanisms
are
sensitive
experimental
factors,
which
has
led
complexity
in
previous
reports
of
the
phenotype.
We
sought
characterize
an
protocol
throughout
development
understand
how
prenatal
insult
alters
trajectory
important
processes,
including
microglial
regulation
synaptic
spines
and
complement
signaling.
used
polyinosinic:polycytidylic
acid
(polyI:C)
induce
on
gestational
day
9.5
CD-1
mice,
measured
their
spine
density,
pruning,
protein
expression.
found
reduced
dendritic
density
somatosensory
cortex
starting
at
3-weeks-of-age
with
requisite
increases
pruning
phagocytosis,
suggesting
loss
was
caused
by
increased
pruning.
Additionally,
we
showed
dysregulation
expression
persisting
into
adulthood.
Our
findings
highlight
disruptions
environment
leading
alterations
dynamic
processes
through
postnatal
development.
This
could
potentially
suggest
developmental
time
points
during
be
as
factors
or
targeted
therapeutics
disorders.
Family Medicine and Primary Care Open Access,
Год журнала:
2024,
Номер
8(1)
Опубликована: Май 23, 2024
Motto:
Living
with
ADHD
is
like
being
locked
in
a
room
100
televisions
and
radios
all
playing.
None
of
them
have
power
buttons
so
you
can
turn
off
the
door
from
outside
–
Sarah
Young
[1].
Developmental Neuroscience,
Год журнала:
2023,
Номер
46(3), С. 179 - 187
Опубликована: Сен. 15, 2023
Understanding
the
long-term
functional
implications
of
gut
microbial
communities
during
perinatal
period
is
a
bourgeoning
area
research.
Numerous
studies
have
revealed
existence
“gut-brain
axis”
and
impact
an
alteration
microbiota
composition
in
brain
diseases.
Recent
research
has
highlighted
how
could
affect
development
behavior.
Many
factors
early
life
such
as
mode
delivery
or
preterm
birth
lead
to
disturbance
assembly
maturation
microbiota.
Notably,
global
rates
cesarean
sections
(C-sections)
increased
recent
decades
remain
important
when
considering
premature
delivery.
Both
C-sections
are
associated
with
risk
neurodevelopmental
disorders
autism
spectrum
disorders,
neuroinflammation
major
factor.
In
this
review,
we
explore
links
between
by
C-sections,
alteration,
neuroinflammation.
We
also
highlight
factor
for
developmental
due
alterations
microbiome.
Developmental Neuroscience,
Год журнала:
2023,
Номер
46(4), С. 221 - 236
Опубликована: Сен. 13, 2023
Emerging
studies
have
indicated
that
abnormally
expressed
microRNAs
(miRNAs)
are
related
to
the
pathogenesis
of
cerebral
ischemia.
Nevertheless,
function
miR-26a
in
neuronal
damage
and
microglial
activation
during
infarction
remains
elusive.
It
was
revealed
downregulated
oxygen-glucose
deprivation
(OGD)-treated
microglia
neurons.
Overexpressing
reduced
inflammatory
reaction
BV2
cells
decreased
apoptosis
following
OGD
stimulation.
upregulation
inactivated
TLR4/MyD88/NF-κB
pathway
inhibited
TREM1
expression.
Repressing
NF-κB
phosphorylation
level.
As
supported
by
dual-luciferase
reporter
assay,
directly
targeted
miR-26a.
Furthermore,
a
rat
model
middle
artery
occlusion
(MCAO)
built.
We
discovered
improved
cognitive,
learning,
motor
functions
edema
MCAO
rats.
Mechanistically,
upregulating
inflammation
mitigating
TREM1-TLR4/MyD88/NF-κB
model.
Collectively,
this
study
verified
miR-26a-TREM1-TLR4/MyD88/NF-κB
axis
contributes
modulating
OGD-mediated
injury.
Brain Behavior and Immunity Integrative,
Год журнала:
2024,
Номер
8, С. 100081 - 100081
Опубликована: Авг. 24, 2024
Maternal
immune
activation
(MIA),
a
maternal
stressor,
increases
risk
for
neuropsychiatric
diseases,
such
as
Major
Depressive
Disorder
in
offspring.
MIA
of
toll-like
receptor
7
(TLR7)
initiates
an
response
mother
and
fetuses
sex-selective
manner.
The
paraventricular
nucleus
the
hypothalamus
(PVN),
brain
region
that
is
sexually
dimorphic
regulates
hypothalamic-pituitary-adrenal
(HPA)
stress
responses,
have
been
tied
to
stress-related
behaviors
(i.e.,
depression,
anxiety,
social
impairments).
current
study
characterized
impact
mid-gestational
TLR7
on
PVN
vasculature
adult
offspring
based
prior
excess
prenatal
glucocorticoid
stress.
were
evaluated
determine
if
fetal
impacted
vascular
leakage
brains
mice
with
or
without
restraint
Timed-pregnant
female
administered
agonist
Resiquimod
(RQ)
saline
vehicle
embryonic
day
(E)
12.5.
Basal
stress-induced
corticosterone
was
measured
examine
changes
response.
Mice
perfused
transcardially
fluorescein
isothiocyanate
(FITC)
assess
blood
vessel
integrity.
Sections
FITC-labeled
vessels
through
immunolabeled
Glial
Fibrillary
Acidic
Protein
(GFAP;
astrocytic
end
feet)
IBA-1
(microglia).
RQ
led
elevated
levels
plasma
60-minutes
after
offspring,
suggesting
impairs
negative
feedback.
Blood-brain
barrier
integrity
assessed.
Adult
injected
dams
showed
greater
(greater
males
than
females).
GFAP+
colocalization
lower
from
treated
dams,
potentially
contributing
observed
increased
FITC
leakage.
Microglia
examined
relation
indicator
neuroimmune
Data
show
IBA-1+
cells
size
number
closer
proximity
injection
male-selective
unchanged
females
RQ-treated
but
smaller
restraint.
This
provides
support
influences
antecedents
altered
development
neuroendocrine
function
could
indicate
locus
susceptibility
disorders.
