The Journal of Perinatal & Neonatal Nursing,
Journal Year:
2020,
Volume and Issue:
34(2), P. 134 - 145
Published: April 1, 2020
Offspring
born
preterm
(ie,
before
37
weeks
of
gestation)
are
more
likely
to
die
or
experience
long-standing
illness
than
full-term
offspring.
Maternal
genetic
variants
heritable,
stable
variations
in
the
code)
and
epigenetic
modifications
chemical
code
that
can
affect
which
genes
turned
on
off)
response
stress
have
been
implicated
birth.
Fetal
linked
birth
though
role
offspring
epigenetics
remains
understudied.
This
systematic
review
synthesizes
literature
examining
associations
among
during
pregnancy
DNA,
with
25
reports
identified.
Ten
examined
DNA
methylation
addition/removal
methyl
groups
to/from
DNA)
across
epigenome.
The
remainder
near
interest,
primarily
hypothalamic-pituitary-adrenal
axis
function
(
NR3C1
,
FKBP51
),
growth/immune
IGF2
socioemotional
regulation
SLC6A4,
OXTR
).
majority
noted
methylation,
when
perceived
stress,
anxiety,
depression
served
as
predictor.
Findings
suggest
differences
patterns
may
play
a
stress-associated
serve
targets
for
novel
interventions.
Dialogues in Clinical Neuroscience,
Journal Year:
2019,
Volume and Issue:
21(4), P. 397 - 405
Published: Dec. 31, 2019
The
risk
for
major
depression
is
both
genetically
and
environmentally
determined.
It
has
been
proposed
that
epigenetic
mechanisms
could
mediate
the
lasting
increases
in
following
exposure
to
adverse
life
events
provide
a
mechanistic
framework
within
which
genetic
environmental
factors
can
be
integrated.
Epigenetics
refers
processes
affecting
gene
expression
translation
do
not
involve
changes
DNA
sequence
include
methylation
(DNAm)
microRNAs
(miRNAs)
as
well
histone
modifications.
Here
we
review
evidence
role
of
epigenetics
pathogenesis
from
studies
investigating
DNAm,
miRNAs,
modifications
using
different
tissues
various
experimental
designs.
From
these
studies,
model
emerges
where
underlying
factors,
interactions
between
two,
drive
aberrant
targeting
stress
response
pathways,
neuronal
plasticity,
other
behaviorally
relevant
pathways
have
implicated
depression.
International Journal of Molecular Sciences,
Journal Year:
2022,
Volume and Issue:
23(23), P. 15114 - 15114
Published: Dec. 1, 2022
Post-stroke
depression
(PSD)
is
a
biopsychosocial
disorder
that
affects
individuals
who
have
suffered
stroke
at
any
point.
PSD
has
20
to
60
percent
reported
prevalence
among
survivors.
Its
effects
are
usually
adverse,
can
lead
disability,
and
may
increase
mortality
if
not
managed
or
treated
early.
linked
several
other
medical
conditions,
including
anxiety,
hyper-locomotor
activity,
poor
functional
recovery.
Despite
significant
awareness
of
its
adverse
impacts,
understanding
the
pathogenesis
proved
challenging.
The
exact
pathophysiology
unknown,
yet
complexity
been
definitively
shown,
involving
mechanisms
such
as
dysfunction
monoamine,
glutamatergic
systems,
gut-brain
axis,
neuroinflammation.
current
effectiveness
treatment
about
30–40
all
cases.
In
this
review,
we
examined
different
pathophysiological
pharmacological
non-pharmacological
approaches
for
PSD.
Ageing Research Reviews,
Journal Year:
2022,
Volume and Issue:
83, P. 101805 - 101805
Published: Nov. 21, 2022
Major
depressive
disorder
(MDD)
is
characterized
by
psychological
and
physiological
manifestations
contributing
to
the
disease
severity
outcome.
In
recent
years,
several
lines
of
evidence
have
suggested
that
individuals
with
MDD
an
elevated
risk
age-related
adverse
outcomes
across
lifespan.
This
review
provided
a
significant
overlap
between
biological
abnormalities
in
changes
commonly
observed
during
aging
process
(i.e.,
hallmarks
aging).
Based
on
such
evidence,
we
formulate
mechanistic
model
showing
how
can
be
common
denominator
mediate
health
MDD.
Finally,
proposed
roadmap
for
novel
studies
investigate
intersection
biology
MDD,
including
use
geroscience-guided
interventions,
as
senolytics,
delay
or
improve
major
depression
targeting
aging.
IBRO Neuroscience Reports,
Journal Year:
2022,
Volume and Issue:
14, P. 28 - 37
Published: Dec. 12, 2022
Genome-wide
studies
related
to
neurological
disorders
and
neurodegenerative
diseases
have
pointed
the
role
of
epigenetic
changes
such
as
DNA
methylation,
histone
modification,
noncoding
RNAs.
methylation
machinery
controls
dynamic
regulation
patterns
in
discrete
brain
regions.This
review
aims
describe
inhibiting
progressing
therapeutic
approaches.A
Systematic
search
PubMed,
Web
Science,
Cochrane
Library
was
conducted
for
all
qualified
from
2000
2022.For
current
need
time,
we
focused
on
expression
genes
involved
neurodegeneration
Alzheimer's,
Depression,
Rett
Syndrome.
Finally,
it
appears
that
various
do
not
occur
separately
modification
side
by
affect
each
other.
We
several
associated
with
depression
(NR3C1,
NR3C2,
CRHR1,
SLC6A4,
BDNF,
FKBP5),
syndrome
(MECP2),
(APP,
BACE1,
BIN1
or
ANK1)
Parkinson's
disease
(SNCA),
well
co-occurring
modifications
histones
non-coding
Understanding
these
their
interactions
will
lead
better
treatment
strategies.This
captures
state
understanding
epigenetics
diseases.
With
new
mechanisms
targets
undoubtedly
horizon,
pharmacological
modulation
processes
holds
great
promise
therapy.
Hypertension,
Journal Year:
2020,
Volume and Issue:
75(6), P. 1429 - 1438
Published: April 20, 2020
The
associations
of
maternal
hypertensive
pregnancy
disorders
with
offspring
mental
remain
unclear.
We
examined
whether
and
maximum
blood
pressure
during
predict
childhood
disorders,
the
are
independent
paternal
or
additive
early
overweight/obesity
diabetes
mellitus
mediated
moderated
by
preterm
birth,
small-for-gestational-age
birth
neonatal
intensive
care
unit
admission.
Our
prospective
study
comprised
4743
mother-child
dyads
Prediction
Prevention
Preeclampsia
Intrauterine
Growth
Restriction
study.
Women
were
recruited
to
in
at
Finnish
maternity
hospitals.
Children
born
2006
2010
followed-up
until
December
31,
2016,
ages
6.4
10.8
years.
Hypertensive
identified
from
medical
records,
Medical
Birth
Register,
Care
Register
for
Health
Care.
Systolic
diastolic
measured
antenatal
clinics
hospital
visits.
Mental
disorder
diagnoses
Maternal
gestational
chronic
hypertension,
preeclampsia
its
severity
increased
hazard
any
disorder.
(hazard
ratio=1.66
[95%
CI,
1.14–2.42])
severe
ratio=2.01
1.08–3.73])
all
covariates.
also
additively
disorders.
Preterm
births
admission
partially
effects
on
To
conclude,
carry
adverse
consequences
health.
International Journal of Molecular Sciences,
Journal Year:
2020,
Volume and Issue:
21(3), P. 826 - 826
Published: Jan. 28, 2020
Major
depressive
disorder
(MDD)
is
the
leading
cause
of
disability
worldwide
and
associated
with
high
rates
suicide
medical
comorbidities.
Current
antidepressant
medications
are
suboptimal,
as
most
MDD
patients
fail
to
achieve
complete
remission
from
symptoms.
At
present,
clinicians
unable
predict
which
effective
for
a
particular
patient,
exposing
multiple
medication
trials
side
effects.
Since
MDD’s
etiology
includes
interactions
between
genes
environment,
epigenome
interest
predictive
utility
treatment
monitoring.
Epigenetic
mechanisms
incompletely
understood.
Differences
in
epigenetic
profiles
may
impact
response.
A
systematic
literature
search
yielded
24
studies
reporting
interaction
antidepressants
eight
(BDNF,
MAOA,
SLC6A2,
SLC6A4,
HTR1A,
HTR1B,
IL6,
IL11)
whole
genome
methylation.
Methylation
certain
sites
within
BDNF,
IL11,
was
Comparing
DNA
methylation
during
episodes,
treatment,
remission,
after
cessation
would
help
clarify
influence
on
Individuals’
unique
be
used
clinically
personalization
choice
future.
Psychiatry Investigation,
Journal Year:
2019,
Volume and Issue:
16(9), P. 654 - 661
Published: Aug. 28, 2019
Depression
is
associated
with
various
environmental
risk
factors
such
as
stress,
childhood
maltreatment
experiences,
and
stressful
life
events.
Current
approaches
to
assess
the
pathophysiology
of
depression,
epigenetics
gene-environment
(GxE)
interactions,
have
been
widely
leveraged
determine
plausible
markers,
genes,
variants
for
developing
depression.We
focus
on
most
recent
developments
genomic
research
in
GxE
interactions.In
this
review,
we
first
survey
a
variety
association
studies
regarding
depression
consideration
interactions.
We
then
illustrate
evidence
epigenetic
mechanisms
DNA
methylation,
microRNAs,
histone
modifications
influence
terms
animal
models
human
studies.
Finally,
highlight
their
limitations
future
directions.In
light
emerging
technologies
artificial
intelligence
machine
learning,
interactions
promises
achieve
novel
innovations
that
may
lead
disease
prevention
potential
therapeutic
treatments
depression.
Translational Psychiatry,
Journal Year:
2021,
Volume and Issue:
11(1)
Published: Aug. 2, 2021
Abstract
Depression
is
currently
the
leading
cause
of
disability
around
world.
We
conducted
an
epigenome-wide
association
study
(EWAS)
in
a
sample
58
depression
score-discordant
monozygotic
twin
pairs,
aiming
to
detect
specific
epigenetic
variants
potentially
related
and
further
integrate
with
gene
expression
profile
data.
Association
between
methylation
level
each
CpG
site
score
was
tested
by
applying
linear
mixed
effect
model.
Weighted
co-expression
network
analysis
(WGCNA)
performed
for
The
DNA
levels
66
sites
reached
P
<
1
×
10
−4
.
These
top
were
located
at
34
genes,
especially
PTPRN2
,
HES5
GATA2
PRDM7
KCNIP1
Many
ontology
enrichments
highlighted,
including
Notch
signaling
pathway,
Huntington
disease,
p53
pathway
glucose
deprivation,
hedgehog
binding,
nucleic
acid
metabolic
process.
detected
19
differentially
methylated
regions
(DMRs),
some
which
GRIK2
DGKA
NIPA2
While
integrating
data,
HELZ2
ZNF624
expressed.
In
WGCNA,
one
module
positively
correlated
(
r
=
0.62,
0.002).
Some
common
genes
(including
BMP2
)
enrichment
terms
complement
coagulation
cascades
neuron
fate
specification,
glial
cell
differentiation,
thyroid
gland
development)
both
identified
WGCNA.
Our
identifies
variations
are
significantly
involved
regions,
functional
biological
function,
pathways
that
mediate
disorder.
Clinical Epigenetics,
Journal Year:
2022,
Volume and Issue:
14(1)
Published: Feb. 17, 2022
Abstract
Background
DNA
methylation
is
an
epigenetic
mark
that
influenced
by
underlying
genetic
profile,
environment,
and
ageing.
In
addition
to
X-linked
methylation,
sex-specific
patterns
are
widespread
across
autosomal
chromosomes
can
be
present
from
birth
or
arise
over
time.
individuals
where
gender
identity
sex
assigned
at
markedly
incongruent,
as
in
the
case
of
transgender
people,
feminization
masculinization
may
sought
through
gender-affirming
hormone
therapy
(GAHT).
GAHT
a
cornerstone
care,
yet
no
studies
date
have
investigated
its
effect
on
genome-wide
methylation.
We
profiled
blood
women
(
n
=
13)
men
before
during
(6
months
12
into
feminizing
masculinizing
therapy).
Results
identified
several
thousand
differentially
methylated
CpG
sites
(DMPs)
(Δ
β
≥
0.02,
unadjusted
p
value
<
0.05)
regions
(DMRs)
both
people
undergoing
GAHT,
vast
majority
which
were
progressive
changes
X
chromosome
established
early
development
largely
refractory
change
association
with
only
3%
affected
0.05).
The
small
number
DMPs
those
become
lifetime,
known
sex-and-age
DMPs,
including
DMRs
PRR4
VMP1
genes.
GAHT-induced
these
sex-associated
probes
consistently
demonstrated
shift
towards
signature
GAHT-naïve
opposite
sex,
we
observed
enrichment
previously
reported
adolescence-associated
changes.
Conclusion
provide
evidence
for
inducing
unique
people.
This
study
advances
our
understanding
complex
interplay
between
hormones,
chromosomes,
context
immunity.
highlight
need
broaden
field
‘sex-specific’
immunity
beyond
cisgender
males
females,
exhibit
molecular
profile.