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
Frontiers in bioscience,
Journal Year:
2020,
Volume and Issue:
25(9), P. 1682 - 1717
Published: Jan. 1, 2020
The
prevalence
rate
of
Autism
Spectrum
Disorder
(ASD)
has
reached
over
1%
world-wide
prompting
governments,
health
providers
and
schools
to
develop
programs
policies
address
this
challenging
disorder.
Here,
we
review
the
cause(s),
as
well
environmental
factors,
genetic
mutations,
neural
pathways
that
are
implicated
in
ASD.
We
also
discuss
criteria
commonly
used
for
diagnosis
ASD
future
clinical
testing
can
aid
Finally,
provide
practical
steps
be
reduce
incidence
severity
ASD,
prognosis
treatment
autism.
Scientific Reports,
Journal Year:
2016,
Volume and Issue:
6(1)
Published: Sept. 14, 2016
Abstract
Fine
particulate
matter
(PM
2.5
)
has
been
implicated
as
a
risk
factor
for
neurodevelopmental
disorders
including
autism
in
children.
However,
the
underlying
biological
mechanism
remains
unclear.
DNA
methylation
is
suggested
to
be
fundamental
neuronal
responses
environmental
cues.
We
prepared
whole
particle
of
PM
),
water-soluble
extracts
(Pw),
organic
(Po)
and
carbon
core
component
(Pc)
characterized
their
chemical
constitutes.
found
that
induced
significant
redox
imbalance,
decreased
levels
intercellular
methyl
donor
S-adenosylmethionine
caused
global
hypomethylation.
Furthermore,
exposure
triggered
gene-specific
promoter
hypo-
or
hypermethylation
abnormal
mRNA
expression
candidate
genes.
-induced
regions
synapse
related
genes
were
associated
with
decreases
protein
expression.
The
inhibiting
effects
antioxidative
reagents,
methylation-supporting
agent
methyltransferase
inhibitor
demonstrated
involvement
redox/methylation
patterns
synaptic
above
generally
followed
sequence
≥
Pwo
>
Po
Pw
Pc.
Our
results
novel
epigenetic
toxicity
air
pollution,
eliminating
components
could
mitigate
neurotoxicity
.
JAMA Pediatrics,
Journal Year:
2021,
Volume and Issue:
175(3), P. e205487 - e205487
Published: Jan. 19, 2021
Maternal
autoimmune
disease
has
been
associated
with
increased
risk
of
neurodevelopmental
disorders
in
offspring,
but
few
studies
have
assessed
the
association
attention-deficit/hyperactivity
disorder
(ADHD).To
examine
between
maternal
and
ADHD
within
a
population-based
cohort
combine
results
subsequent
systematic
review
meta-analysis.A
study
was
conducted
singleton
children
born
at
term
gestation
(37-41
weeks)
New
South
Wales,
Australia,
from
July
1,
2000,
to
December
31,
2010,
followed
up
until
end
2014;
evaluated
articles
MEDLINE,
Embase,
Web
Science
databases
identify
all
published
before
November
20,
2019.
A
total
12
610
exposed
were
propensity
score
matched
(1:4)
50
440
unexposed
children,
for
63
050.
child
considered
if
they
had
(1)
an
authorization
or
filled
prescription
stimulant
treatment
(2)
hospital
diagnosis
ADHD.
Children
linked
first
event
3
years
age
excluded.
Data
analyzed
January
13
April
2020.One
more
diagnoses
admission
records
2012.
Thirty-five
conditions
together
individually.The
main
outcome
identified
data
records.
Multivariable
Cox
regression
used
assess
adjusted
sex.
Pooled
hazard
ratios
(HRs)
calculated
using
random-effects
meta-analysis
inverse-variance
weights
each
exposure
reported
by
2
studies.In
analysis,
831
718
singleton,
infants
mothers
(mean
[SD]
age,
29.8
[5.6]
years)
assessed.
Of
767
(1.5%)
who
diagnosis,
control
infants,
050
infants.
In
this
cohort,
any
offspring
(HR,
1.30;
95%
CI
1.15-1.46),
as
type
1
diabetes
2.23;
CI,
1.66-3.00),
psoriasis
1.66;
1.02-2.70),
rheumatic
fever
carditis
1.75;
1.06-2.89).
Five
(including
present
study)
included
meta-analysis.
Any
(2
studies:
HR,
1.20;
1.03-1.38),
(4
1.53;
1.27-1.85),
hyperthyroidism
(3
1.15;
1.06-1.26),
1.31;
1.10-1.56)
ADHD.In
study,
diseases
among
children.
These
findings
suggest
possible
shared
genetic
vulnerability
potential
role
immune
activation
expression
Future
measuring
activity,
modifiers,
medication
use
are
required
better
understand
mechanisms
underlying
association.
Glia,
Journal Year:
2021,
Volume and Issue:
69(12), P. 2771 - 2797
Published: June 11, 2021
The
dynamic
expansions
and
contractions
of
the
microglia
population
in
central
nervous
system
(CNS)
to
achieve
homeostasis
are
likely
vital
for
their
function.
Microglia
respond
injury
or
disease
but
also
help
guide
neurodevelopment,
modulate
neural
circuitry
throughout
life,
direct
regeneration.
Throughout
these
processes,
density
changes,
as
does
volume
area
that
each
surveys.
Given
responsible
sensing
subtle
alterations
environment,
a
change
could
affect
capacity
mobilize
rapidly.
In
this
review,
we
attempt
synthesize
current
literature
on
ligands
conditions
promote
microglial
proliferation
across
development,
adulthood,
neurodegenerative
conditions.
display
an
impressive
proliferative
during
development
diseases
is
almost
completely
absent
at
homeostasis.
However,
appropriate
function
state
critically
dependent
fluctuations
primarily
induced
by
proliferation.
Proliferation
natural
response
insult
often
serves
neuroprotective
functions.
contrast,
inappropriate
proliferation,
whether
too
much
little,
precipitates
undesirable
consequences
health.
Thus,
tightly
regulated
ensure
immune
cells
can
execute
diverse
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
