International journal for autism challenges & solution.,
Journal Year:
2024,
Volume and Issue:
1(1), P. 39 - 50
Published: April 19, 2024
This
review
examines
the
intricate
association
between
maternal
immune
activation
(MIA)
and
autism
spectrum
disorder
(ASD),
emphasizing
impact
of
infections
during
pregnancy.
Epidemiological
studies
link
viral
bacterial
to
an
elevated
risk
ASD,
revealing
complex
interplay
environmental
factors
neurodevelopmental
outcomes.
Immunological
mechanisms,
including
cytokine
dysregulation
neuroinflammation,
involve
key
players
such
as
interleukin-6
tumor
necrosis
factor-alpha,
influencing
fetal
brain
development
ASD
risk.
Genetic
interactions
contribute
individual
susceptibility,
with
specific
variants
MIA's
on
Epigenetic
modifications
provide
a
molecular
exposures,
MIA,
enduring
changes.
Recognizing
critical
periods
neurodevelopment
susceptible
MIA
is
crucial.
Long-term
highlight
consequences
behavior
cognition
into
childhood
adolescence.
Exploring
potential
therapeutic
interventions,
immunomodulatory
strategies
pregnancy,
offers
hope
for
mitigating
Despite
progress,
knowledge
gaps
persist,
motivating
future
research
guided
by
emerging
technologies
interdisciplinary
approaches
unravel
MIA-ASD
relationship.
Translational Psychiatry,
Journal Year:
2024,
Volume and Issue:
14(1)
Published: Feb. 2, 2024
Abstract
Prenatal
exposure
to
heightened
maternal
inflammation
has
been
associated
with
adverse
neurodevelopmental
outcomes,
including
atypical
brain
maturation
and
psychiatric
illness.
In
mothers
experiencing
socioeconomic
disadvantage,
immune
activation
can
be
a
product
of
the
chronic
stress
inherent
such
environmental
hardship.
While
growing
preclinical
clinical
evidence
shown
links
between
altered
neonatal
development
increased
inflammatory
states
in
utero,
potential
mechanism
by
which
disadvantage
differentially
impacts
neural-immune
crosstalk
remains
unclear.
current
study,
we
investigated
associations
gestational
inflammation,
white
matter
microstructure
320
mother-infant
dyads
over-sampled
for
poverty.
We
analyzed
serum
levels
four
cytokines
(IL-6,
IL-8,
IL-10,
TNF-α)
over
course
pregnancy
relation
offspring
disadvantage.
Higher
average
IL-6
was
very
low
status
(SES;
INR
<
200%
poverty
line)
lower
corticospinal
fractional
anisotropy
(FA)
uncinate
axial
diffusivity
(AD).
No
other
cytokine
SES.
IL-10
FA
higher
radial
(RD)
corpus
callosum
tracts,
optic
radiation
RD,
AD,
inferior
fronto-occipital
fasciculus
anterior
limb
internal
capsule
tracts.
SES
moderated
relationship
TNF-α
during
gestation
diffusivity.
When
these
interactions
were
decomposed,
patterns
indicated
that
this
association
significant
positive
among
neonates,
whereby
inversely
significantly
cingulum
AD.
By
contrast,
more
advantaged
neonates
(lower-to-higher
[INR
≥
line]),
positively
superior
Taken
together,
findings
suggest
prenatal
differs
as
function
These
are
consistent
scenario
where
inflammation’s
effects
on
diverge
depending
availability
foundational
resources
utero.
Oxford Open Neuroscience,
Journal Year:
2024,
Volume and Issue:
3
Published: Jan. 1, 2024
Autism
spectrum
disorder
(ASD)
affects
1
in
36
people
and
is
more
often
diagnosed
males
than
females.
Core
features
of
ASD
are
impaired
social
interactions,
repetitive
behaviors
deficits
verbal
communication.
a
highly
heterogeneous
heritable
disorder,
yet
its
underlying
genetic
causes
account
only
for
up
to
80%
the
cases.
Hence,
subset
cases
could
be
influenced
by
environmental
risk
factors.
Maternal
immune
activation
(MIA)
response
inflammation
during
pregnancy,
which
can
lead
increased
inflammatory
signals
fetus.
Inflammatory
cross
placenta
blood
brain
barriers
affecting
fetal
development.
Epidemiological
animal
studies
suggest
that
MIA
contribute
etiology.
However,
human
mechanistic
have
been
hindered
lack
experimental
systems
replicate
impact
Therefore,
mechanisms
altered
pre-natal
development,
underlie
pathogenesis
largely
understudied.
The
advent
cellular
models
with
induced
pluripotent
stem
cell
(iPSC)
organoid
technology
closing
this
gap
knowledge
providing
both
access
molecular
manipulations
culturing
capability
tissue
would
otherwise
inaccessible.
We
present
an
overview
multiple
levels
evidence
from
clinical,
epidemiological,
provide
potential
link
between
higher
inflammation.
More
importantly,
we
discuss
how
cell-derived
may
constitute
ideal
system
mechanistically
interrogate
effect
early
stages
Nature Communications,
Journal Year:
2024,
Volume and Issue:
15(1)
Published: June 3, 2024
Abstract
The
fetal
development
of
organs
and
functions
is
vulnerable
to
perturbation
by
maternal
inflammation
which
may
increase
susceptibility
disorders
after
birth.
Because
it
not
well
understood
how
the
placenta
fetus
respond
acute
lung-
inflammation,
we
characterize
response
pulmonary
lipopolysaccharide
exposure
across
24
h
in
using
multi-omics,
imaging
integrative
analyses.
Unlike
organs,
mount
strong
inflammatory
immune
responses,
upregulates
immuno-modulatory
genes,
particular
IL-6
signaling
suppressor
Socs3
.
Similarly,
observe
no
liver,
instead
displays
metabolic
changes,
including
increases
lipids
containing
docosahexaenoic
acid,
crucial
for
brain
development.
liver
plasma
display
similar
alterations,
potentially
increasing
bioavailability
acid
mother
fetus.
Thus,
our
integrated
temporal
analysis
shows
that
systemic
leads
a
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(10), P. 5480 - 5480
Published: May 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.
Nutrients,
Journal Year:
2025,
Volume and Issue:
17(6), P. 1033 - 1033
Published: March 15, 2025
Background:
Emerging
evidence
suggests
that
the
maternal
microbiome
plays
a
crucial
role
in
shaping
fetal
neurodevelopment,
immune
programming,
and
metabolic
health.
Dysbiosis
during
pregnancy—whether
gastrointestinal,
oral,
or
vaginal—can
significantly
influence
pregnancy
outcomes
long-term
child
Materials
Methods:
The
search
was
performed
using
databases
such
as
PubMed,
Scopus,
Google
Scholar
including
research
published
from
January
2000
to
2025.
keywords
used
were
“Fetal
Programming”,
“
Maternal
Immune
Activation”,
“Maternal
microbiome”,
“Microbiota–Gut–Brain
Axis”,
“Pregnancy
Dysbiosis”.
Results:
undergoes
substantial
changes
pregnancy,
with
alterations
microbial
diversity
function
linked
conditions
gestational
diabetes,
obesity,
preeclampsia.
Pregnancy-related
dysbiosis
has
been
associated
adverse
neurodevelopmental
outcomes,
an
increased
risk
of
autism
spectrum
disorder
(ASD),
attention-deficit/hyperactivity
(ADHD),
cognitive
impairments
offspring.
Conclusions:
Understanding
intricate
relationship
between
microbiota
health
is
essential
for
developing
targeted
interventions.
Personalized
microbiome-based
strategies,
dietary
modifications
probiotic
supplementation,
hold
promise
optimizing
promoting
