Journal of Neurochemistry,
Journal Year:
2020,
Volume and Issue:
157(3), P. 370 - 392
Published: Dec. 11, 2020
Abstract
A
comprehensive
overview
of
the
interplay
between
glucocorticoids
(GCs)
and
adult
hippocampal
neurogenesis
(AHN)
is
presented,
particularly,
in
context
a
diseased
brain.
The
effectors
GCs
dentate
gyrus
neurogenic
niche
are
reviewed,
consequences
GC
signaling
on
generation
integration
new
neurons
discussed.
Recent
findings
demonstrating
how
mediates
impairments
AHN
various
brain
pathologies
overviewed.
GC‐mediated
effects
adult‐born
depend
nature,
severity,
duration
acting
stress
factor.
realize
their
primarily
via
specific
glucocorticoid
mineralocorticoid
receptors.
Disruption
reciprocal
regulation
hypothalamic–pituitary–adrenal
(HPA)
axis
granular
currently
considered
to
be
key
mechanism
implicating
into
pathogenesis
numerous
diseases,
including
those
without
direct
damage.
These
alterations
vary
from
reduced
proliferation
stem
progenitor
cells
increased
cell
death
abnormalities
morphology,
connectivity,
localization
young
neurons.
Although
involvement
mutual
HPA
cognitive
deficits
mood
evident,
several
unresolved
critical
issues
stated.
Understanding
details
mechanisms
involved
could
enable
identification
molecular
targets
for
ameliorating
pathology‐induced
imbalance
axis/AHN
conquer
psychiatric
disturbances.
image
Frontiers in Physiology,
Journal Year:
2018,
Volume and Issue:
9
Published: Aug. 17, 2018
During
pregnancy,
the
mother
must
adapt
her
body
systems
to
support
nutrient
and
oxygen
supply
for
growth
of
baby
in
utero
during
subsequent
lactation.
These
include
changes
cardiovascular,
pulmonary,
immune
metabolic
mother.
Failure
appropriately
adjust
maternal
physiology
pregnant
state
may
result
pregnancy
complications,
including
gestational
diabetes
abnormal
birth
weight,
which
can
further
lead
a
range
medically
significant
complications
baby.
The
placenta,
forms
functional
interface
separating
fetal
circulations,
is
important
mediating
adaptations
physiology.
It
secretes
plethora
hormones
into
circulation
modulate
transfers
nutrients
available
fetus
growth.
Among
these
placental
hormones,
prolactin-growth
hormone
family,
steroids
neuropeptides
play
critical
roles
driving
physiological
pregnancy.
This
review
examines
that
occur
response
significance
production
such
changes.
Frontiers in Pharmacology,
Journal Year:
2018,
Volume and Issue:
9
Published: Sept. 12, 2018
The
steroid
hormones
progestagens,
estrogens,
androgens
and
glucocorticoids
as
well
their
precursor
cholesterol
are
required
for
successful
establishment
maintenance
of
pregnancy
proper
development
the
fetus.
human
placenta
forms
at
interface
maternal
fetal
circulation.
It
participates
in
biosynthesis
metabolism
steroids
regulated
exchange
between
compartment.
This
review
outlines
mechanisms
placental
handling
compounds.
Cholesterol
is
transported
from
mother
to
offspring
involving
lipoprotein
receptors
such
low-density
receptor
(LDLR)
scavenger
class
B
type
I
(SRB1)
ATP-binding
cassette
(ABC)-transporters,
ABCA1
ABCG1.
Additionally,
also
a
progesterone
estrogen
synthesis.
Hormone
synthesis
predominantly
performed
by
members
cytochrome
P-450
(CYP)
enzyme
family
including
CYP11A1
or
CYP19A1
hydroxysteroid
dehydrogenases
(HSD)
3β-HSD
17β-HSD.
Placental
requires
delivery
sulfate-conjugated
molecules
serum.
uptake
these
precursors
mediated
solute
carrier
(SLC)
sodium-dependent
organic
anion
transporter
(SOAT),
4
(OAT4),
transporting
polypeptide
2B1
(OATP2B1).
Maternal-fetal
glucocorticoid
transport
has
be
tightly
order
ensure
healthy
growth
development.
For
that
purpose,
expresses
enzymes
11β-HSD
1
2
ABCB1.
article
summarizes
impact
diverse
compounds
diseases
on
expression
level
activity
involved
transporters,
receptors,
metabolizing
concludes
regulatory
changing
physiological
pathophysiological
state
barely
explored.
structure
cellular
composition
barrier
introduced.
While
production,
syncytiotrophoblast
have
been
explored
decades,
few
information
available
role
placental-fetal
endothelial
cells
processes.
With
regard
function,
significant
differences
exist
species.
To
further
decipher
physiologic
pathways
pathologic
alterations
handling,
model
systems
mandatory.
Brain and Behavior,
Journal Year:
2018,
Volume and Issue:
8(2)
Published: Jan. 24, 2018
Abstract
An
adverse
maternal
hormonal
environment
during
pregnancy
can
be
associated
with
abnormal
brain
growth.
Subtle
changes
in
fetal
development
have
been
observed
even
for
hormone
levels
within
the
currently
accepted
physiologic
ranges.
In
this
review,
we
provide
an
update
of
research
data
on
impact
neurodevelopment,
giving
particular
emphasis
to
thyroid
hormones
and
glucocorticoids.
Thyroid
are
required
normal
development.
Despite
serum
TSH
appearing
most
accurate
indicator
function
pregnancy,
free
T4
first
trimester
major
determinant
postnatal
psychomotor
Even
a
transient
period
hypothyroxinemia
at
beginning
neurogenesis
confer
higher
risk
expressive
language
nonverbal
cognitive
delays
offspring.
Nevertheless,
recent
clinical
guidelines
advocate
targeted
high‐risk
case
finding
despite
universal
screening.
Corticosteroids
suppressing
cell
proliferation
stimulating
terminal
differentiation,
fundamental
switch
maturation
organs.
Not
surprisingly,
intrauterine
exposure
stress
or
high
glucocorticoids,
endogenous
synthetic,
has
molecular
structural
appears
impair
cognition
increase
anxiety
reactivity
stress.
Limbic
regions,
such
as
hippocampus
amygdala,
particularly
sensitive.
Repeated
doses
prenatal
corticosteroids
seem
short‐term
benefits
less
respiratory
distress
fewer
serious
health
problems
neurodevelopmental
growth
later
childhood
adulthood
needs
further
clarification.
Future
studies
should
address
relevance
monitoring
level
stratification
impaired
neurodevelopment.
Frontiers in Behavioral Neuroscience,
Journal Year:
2018,
Volume and Issue:
12
Published: Oct. 5, 2018
The
earliest
stages
of
development
are
critically
sensitive
to
environmental
insults.
An
unfortunately
timed
stress
on
the
developing
brain
can
have
dramatic
consequences
for
neurodevelopment
and
future
mental
health
individual.
In
particular,
infection
mother
during
pregnancy
has
been
correlated
with
increased
risk
psychiatric
neurodevelopmental
disorders.
Evidence
suggests
that
maternal
immune
activation,
independently
from
itself,
be
responsible
outcome
in
offspring.
This
recognition
resulted
expanding
study
designs
epidemiologic
correlations
search
a
causal
relationship
between
activation
system
cognitive
However,
this
causality
analysis
remained
limited
humans
until
recent
work
longitudinally
linked
specific
markers
inflammation
alterations
newborn
toddlers.
focused
narrative
review
compares
discusses
results
these
studies
places
them
into
broader
landscape
literature.
New
data
point,
association
levels
interleukin
6
(IL-6)
modifications
offspring's
salience
network
subsequent
impairments.
article
further
emphasizes
need
carefully
control
potential
confounders
studying
effects
neonatal
as
well
under-investigated
intra-partum
fever
offspring
neurodevelopment.
Proceedings of the National Academy of Sciences,
Journal Year:
2018,
Volume and Issue:
115(40), P. 9851 - 9858
Published: Oct. 1, 2018
Attention
deficit
hyperactivity
disorder
(ADHD)
is
now
among
the
most
commonly
diagnosed
chronic
psychological
dysfunctions
of
childhood.
By
varying
estimates,
it
has
increased
by
30%
in
past
20
years.
Environmental
factors
that
might
explain
this
increase
have
been
explored.
One
such
factor
may
be
audiovisual
media
exposure
during
early
Observational
studies
humans
linked
to
fast-paced
television
first
3
years
life
with
subsequent
attentional
deficits
later
Although
longitudinal
and
well
controlled,
observational
nature
these
precludes
definitive
conclusions
regarding
a
causal
relationship.
As
experimental
are
neither
ethical
nor
practical,
mouse
models
excessive
sensory
stimulation
(ESS)
childhood,
akin
enrichment
previously
shown
benefits
rodents,
developed.
Experimental
using
model
corroborated
ESS
leads
cognitive
behavioral
deficits,
some
which
potentially
detrimental.
Given
ubiquity
findings
humansand
rodents
perhaps
important
implications
for
public
health.
Particle and Fibre Toxicology,
Journal Year:
2020,
Volume and Issue:
17(1)
Published: July 11, 2020
Abstract
Background
Epidemiological
and
animal
studies
provide
compelling
indications
that
environmental
engineered
nanomaterials
(NMs)
pose
a
risk
for
pregnancy,
fetal
development
offspring
health
later
in
life.
Understanding
the
origin
mechanisms
underlying
NM-induced
developmental
toxicity
will
be
cornerstone
protection
of
sensitive
populations
design
safe
sustainable
nanotechnology
applications.
Main
body
Direct
originating
from
NMs
crossing
placental
barrier
is
frequently
assumed
to
key
pathway
toxicity.
However,
transfer
particles
often
highly
limited,
evidence
growing
can
also
indirectly
interfere
with
development.
Here,
we
outline
current
knowledge
on
potential
indirect
NMs.
Short
conclusion
Until
now,
research
has
mainly
focused
biodistribution
translocation
fetus
delineate
processes.
Systematic
addressing
NM
impact
maternal
tissues
as
contributors
mechanistic
pathways
only
slowly
gathering
momentum.
So
far,
oxidative
stress
inflammation,
activation
toll-like
receptors
(TLRs),
impairment
growth
secretion
hormones,
vascular
factors
have
been
suggested
mediate
Therefore,
effects
tissue
function
ought
comprehensively
evaluated
addition
future
assessment
exposure
during
pregnancy.