Molecular Therapy — Nucleic Acids,
Journal Year:
2024,
Volume and Issue:
35(1), P. 102136 - 102136
Published: Feb. 2, 2024
Autism
is
a
widespread
neurodevelopmental
disorder.
Although
the
research
on
autism
spectrum
disorders
has
been
increasing
in
past
decade,
there
still
no
specific
answer
to
its
mechanism
of
action
and
treatment.
As
pro-inflammatory
microRNA,
miR-301a
abnormally
expressed
various
psychiatric
diseases
including
autism.
Here,
we
show
that
deletion
inhibition
exhibited
two
distinct
abnormal
behavioral
phenotypes
mice.
We
observed
mice
impaired
learning/memory,
enhanced
anxiety.
On
contrary,
effectively
reduced
maternal
immune
activation
(MIA)-induced
autism-like
behaviors
further
demonstrated
bound
3′UTR
region
SOCS3,
led
upregulation
SOCS3
hippocampus.
The
last
result
reduction
inflammatory
response
by
inhibiting
phosphorylation
AKT
STAT3,
expression
level
IL-17A
poly(I:C)-induced
features
obtained
data
revealed
as
critical
participant
partial
behavior
phenotypes,
which
may
exhibit
divergent
role
between
gene
knockout
knockdown.
Our
findings
ascertain
negatively
regulates
MIA-induced
could
present
new
therapeutic
target
for
ameliorating
abnormalities
Brain Sciences,
Journal Year:
2024,
Volume and Issue:
14(7), P. 722 - 722
Published: July 18, 2024
Neurodegenerative
disease
is
a
major
global
health
problem
with
150
million
people
predicted
to
have
dementia
by
2050.
Genetic
factors,
environmental
demographics,
and
some
diseases
been
associated
dementia.
In
addition
associations
between
such
as
hypertension
cerebrovascular
dementia,
emerging
findings
associate
psychiatric
disorders
incident
Because
of
the
high
increasing
prevalence
worldwide
disorders,
primary
objective
this
narrative
review
was
evaluate
published
that
association
bipolar
disorder,
depression,
anxiety,
post-traumatic
stress
obsessive–compulsive
attention-deficit/hyperactivity
autism
spectrum
schizophrenia
other
psychosis
syndromes,
personality
traits
Here,
we
highlight
indicating
possible
these
subsequent
suggest
may
be
risk
factors
for
Further
research,
including
more
large
longitudinal
studies
additional
meta-analyses,
however,
needed
better
characterize
identify
mechanisms
putative
associations,
within
predispose
disorder
but
not
others
Additional
important
questions
concern
how
treatment
might
affect
Frontiers in Molecular Neuroscience,
Journal Year:
2023,
Volume and Issue:
16
Published: Sept. 22, 2023
Recent
studies
promote
new
interest
in
the
intersectionality
between
autism
spectrum
disorder
(ASD)
and
Alzheimer’s
Disease.
We
have
reported
high
levels
of
Amyloid-β
Precursor
Protein
(APP)
secreted
APP-alpha
(sAPP
a
)
low
amyloid-beta
(Aβ)
peptides
1–40
1–42
(Aβ40,
Aβ42)
plasma
brain
tissue
from
children
with
ASD.
A
higher
incidence
microcephaly
(head
circumference
less
than
3
rd
percentile)
associates
ASD
compared
to
head
size
individuals
typical
development.
The
role
Aβ
as
contributors
acquired
is
proposed.
may
lead
via
disruption
neurogenesis,
elongation
G1/S
cell
cycle,
arrested
cycle
promoting
apoptosis.
As
APP
gene
exists
on
Chromosome
21,
excess
occur
Trisomy
21-T21
(Down’s
Syndrome).
Microcephaly
some
forms
associate
T21,
therefore
potential
mechanisms
underlying
these
associations
will
be
examined
this
review.
peptides’
other
neurodevelopmental
disorders
that
feature
are
reviewed,
including
dup
15q11.2-q13,
Angelman
Rett
syndrome.
International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(21), P. 15988 - 15988
Published: Nov. 5, 2023
Autism
spectrum
disorder
(ASD)
is
a
neurodevelopmental
disability
and
recent
evidence
suggests
that
autistic
adults
are
more
likely
to
develop
Alzheimer’s
disease
(Alz)
other
dementias
compared
neurotypical
(NT)
adults.
The
ε4-allele
of
the
Apolipoprotein
E
(APOE)
gene
strongest
genetic
risk
factor
for
Alz
negatively
impacts
cognition
in
middle-aged
older
(MA+)
This
study
aimed
determine
impact
APOE
on
verbal
learning
memory
MA+
(ages
40–71
years)
matched
NT
Using
Auditory
Verbal
Learning
Test
(AVLT),
we
found
ε4
carriers
performed
worse
short-term
across
diagnosis
groups,
but
there
was
no
interaction
with
diagnosis.
In
exploratory
analyses
within
sex
only
men
carrying
showed
(p
=
0.02),
who
were
not
carriers.
Finally,
did
significantly
affect
long-term
this
sample.
These
findings
replicate
previous
work
indicating
presents
new
preliminary
may
be
vulnerable
effects
learning.
Future
larger
sample
needed
if
women
also
vulnerable.
Journal of Neurochemistry,
Journal Year:
2024,
Volume and Issue:
unknown
Published: May 29, 2024
Autism
is
a
neurodevelopmental
disorder,
the
prevalence
of
which
has
increased
dramatically
in
United
States
over
past
two
decades.
It
characterized
by
stereotyped
behaviors
and
impairments
social
interaction
communication.
In
this
paper,
we
present
evidence
that
autism
can
be
viewed
as
PIN1
deficiency
syndrome.
Peptidyl-prolyl
cis/trans
isomerase,
NIMA-Interacting
1
(PIN1)
peptidyl-prolyl
it
widespread
influences
biological
organisms.
Broadly
speaking,
linked
to
many
neurodegenerative
diseases,
whereas
over-expression
cancer.
Death-associated
protein
kinase
(DAPK1)
strongly
inhibits
PIN1,
hormone
melatonin
DAPK1.
Melatonin
autism.
recently
been
shown
glyphosate
exposure
rats
synthesis
result
glutamate
release
from
glial
cells
expression
metabotropic
receptors.
Glyphosate's
inhibition
leads
reduction
availability
neurons.
show
explain
unique
morphological
features
autism,
including
dendritic
spine
density,
missing
or
thin
corpus
callosum,
reduced
bone
density.
We
how
disrupts
functioning
powerful
high-level
signaling
molecules,
such
nuclear
factor
erythroid
2-related
2
(NRF2)
p53.
Dysregulation
both
these
proteins
Severe
depletion
glutathione
brain
resulting
chronic
oxidative
stressors
extracellular
oxidation
cysteine
residue
inactivating
further
contributing
deficiency.
Impaired
autophagy
sensitivity
neurons
ferroptosis.
imperative
research
conducted
experimentally
validate
whether
mechanisms
described
here
take
place
response
ultimately
Biomedicines,
Journal Year:
2023,
Volume and Issue:
11(12), P. 3156 - 3156
Published: Nov. 27, 2023
Autism
spectrum
disorder
(ASD)
prevalence
is
emerging
with
an
unclear
etiology,
hindering
effective
therapeutic
interventions.
Recent
studies
suggest
potential
renin-angiotensin
system
(RAS)
alterations
in
different
neurological
pathologies.
However,
its
implications
ASD
are
unexplored.
This
research
fulfills
the
critical
gap
by
investigating
dual
arms
of
RAS
and
their
interplay
Notch
signaling
ASD,
using
a
valproic
acid
(VPA)
model
assessing
astaxanthin's
(AST)
modulatory
impacts.
Experimentally,
male
pups
from
pregnant
rats
receiving
either
saline
or
VPA
on
gestation
day
12.5
were
divided
into
control
groups,
subsequent
AST
treatment
subset
(postnatal
days
34-58).
Behavioral
analyses,
histopathological
investigations,
electron
microscopy
provided
insights
neurobehavioral
structural
changes
induced
AST.
Molecular
investigations
pups'
cortices
revealed
that
outweighs
protective
elements
inhibition
detrimental
arm.
established
neuroprotective
anti-inflammatory
axes
(ACE2/Ang1-7/MasR)
context.
The
results
showed
AST's
normalization
components
underscore
novel
avenue
impacting
neuronal
integrity
behavioral
outcomes.
These
findings
affirm
integral
role
highlight
as
promising
intervention,
inviting
further
implications.