The
developing
adolescent
brain
is
highly
susceptible
to
social
experiences
and
environmental
insults,
influencing
how
personality
traits
emerge.We
previously
found
that
stress
leads
long-lasting
behavioral
changes
excitatory/inhibitory
(E/I)
balance
dysregulation
in
the
ventral
hippocampus
(vHip)
associated
with
neurodevelopmental
disorders,
such
as
schizophrenia
bipolar
disorder.The
neurobiological
mechanisms
of
psychiatric
disorders
have
been
linked
oxidative
damage
reduced
antioxidant
capacity
brain.However,
impact
severe
stressors
during
adolescence,
a
critical
period,
on
mitochondrial
function,
redox
balance,
their
functional
consequences
are
not
completely
understood.We
hypothesized
respiratory
function
homeostasis
vHip
affected
by
stress,
leading
electrophysiological
neuropsychiatric
disorders.First,
we
performed
characterization
late
adolescence
(postnatal
day,
PND
47
-50),
including
naïve
animals
exposed
from
31
until
40
(10
days
footshock
3
restraint
sessions)
assessing
sociability
(social
interaction
test)
cognition
(novel-object
recognition
test).Then,
uncovered
E/I
analyzing
activity
glutamate
pyramidal
neurons,
number
parvalbumin
(PV)-containing
GABAergic
interneurons
possible
association
stress.To
address
dynamic
homeostasis,
high-resolution
respirometry,
DHE
staining,
MitoSox™
AmplexRed
®
assays
one
(PND
41)
ten
51)
after
protocol.Also,
evaluated
glutathione
(GSH)
disulfide
(GSSG)
levels
at
51.Finally,
assess
genome-wide
transcriptomic
signature
stressed
performing
bulk
RNAsequencing
following
tests.One
week
adolescent-stressed
exhibited:
(1)
loss
cognitive
impairment;
(2)
enhanced
neuron
activity;
(3)
reduction
PV-positive
cells
perineuronal
nets.These
were
an
increased
marker
vHip,
which
was
co-localized
PV
interneurons.By
respirometry
analysis,
impacted
uncoupled
efficiency
phosphorylation
51).In
addition,
displayed
revealed
molecular
analysis.GSSG
serum
negatively
correlated
performance,
indicating
GSH
oxidized
ROS
conditions,
may
affect
phenotype.In
another
cohort
animals,
identified
three
cluster
subgroups
principal
component
analysis
assessment:
higher-behavioral
z-score
(HBZ),
lower-behavioral
(LBZ),
animals.Genes
encoding
subunits
complexes
significantly
down-regulated
both
LBZ
(Cox7c)
(Coa5),
while
Txnip
gene
encoded
thioredoxin-interacting
protein
up-regulated
performance.Our
results
identify
genes
distinct
phenotypes
highlight
negative
regulation,
partially
imbalance
abnormalities.
Journal of Neurochemistry,
Journal Year:
2024,
Volume and Issue:
unknown
Published: May 21, 2024
Recent
studies
have
highlighted
the
potential
involvement
of
reactive
oxygen
species
(ROS)
and
microglia,
a
major
source
ROS,
in
pathophysiology
schizophrenia.
In
our
study,
we
explored
how
second-generation
antipsychotic
risperidone
(RIS)
affects
ROS
regulation
microglial
activation
hippocampus
using
mouse
ketamine
(KET)
model
KET
administration
resulted
schizophrenia-like
behaviors
male
C57BL/6J
mice,
such
as
impaired
prepulse
inhibition
(PPI)
acoustic
startle
response
hyper-locomotion.
These
were
mitigated
by
RIS.
We
found
that
gene
expression
level
an
enzyme
responsible
for
production
(Nox2),
which
is
primarily
associated
with
activated
was
lower
KET/RIS-treated
mice
than
KET-treated
mice.
Conversely,
levels
antioxidant
enzymes
(Ho-1
Gclc)
higher
The
density
increased
counteracted
Hierarchical
cluster
analysis
revealed
three
morphological
subtypes
microglia.
control
most
microglia
resting-ramified
(type
I,
89.7%).
shifted
composition
to
moderately
ramified
II,
44.4%)
hyper-ramified
III,
25.0%).
type
II
decreased
32.0%,
while
III
34.0%.
An
vitro
assay
showed
dissociated
hippocampal
this
effect
Furthermore,
discovered
NOX2
inhibitor
could
counteract
KET-induced
behavioral
deficits.
findings
suggest
pharmacological
RIS
may
play
crucial
role
ameliorating
schizophrenia-related
symptoms.
Moreover,
modulating
regulate
has
emerged
novel
avenue
developing
innovative
treatments
Frontiers in Molecular Neuroscience,
Journal Year:
2024,
Volume and Issue:
17
Published: Sept. 11, 2024
Disturbances
in
pro/antioxidant
balance
emerge
as
a
crucial
element
bipolar
disorder
(BD).
Some
studies
suggest
that
treatment
effects
on
trace
concentration
BD.
This
study
aimed
to
identify
(a)
the
changes
related
oxidative
stress
BD
and
their
relationship
with
elements
engaged
homeostasis;
(b)
biomarkers
using
machine
learning
algorithm
classification
regression
tree
(C&RT)
analysis.
62
individuals
40
healthy
(HC)
were
included
study.
The
of
state
selenium,
zinc,
arsenic
blood
assessed.
We
found
higher
total
antioxidant
capacity,
catalase,
advanced
oxidation
protein
products
lower
4-hydroxynonenal
(4-HNE),
glutathione,
glutathione
peroxidase
(GPx)
compared
HC.
All
examined
group
A
combination
two
variables,
4-HNE
(cut-off:
≤
0.004
uM/mg
protein)
GPx
0.485
U/mg
protein),
was
most
promising
markers
for
separating
from
area
under
receiver
operating
characteristic
curve
values
C&RT
90.5%.
patients
may
be
target
new
therapeutic
or
diagnostic
opportunity
biomarkers.
Neuropsychiatric Disease and Treatment,
Journal Year:
2024,
Volume and Issue:
Volume 20, P. 1757 - 1765
Published: Sept. 1, 2024
Cognitive
domains
are
affected
in
patients
with
schizophrenia.
Mitochondrial
dysfunction
has
been
proposed
as
a
possible
origin
of
these
symptoms.
Cell-free
mitochondrial
DNA
(cf-mtDNA)
is
an
indicator
cellular
stress,
and
it
can
be
identified
individuals
age-associated
disorders,
this
study
aimed
to
explore
the
presence
cf-mtDNA
plasma
schizophrenia
its
association
cognitive
deficit.
Clinical Psychopharmacology and Neuroscience,
Journal Year:
2023,
Volume and Issue:
22(1), P. 139 - 150
Published: Aug. 2, 2023
:
Recent
evidence
suggests
that
oxidative
stress
contributes
to
the
pathophysiology
of
schizophrenia.
This
study
aimed
compare
thiol-disulphide
homeostasis
in
acute
and
stable
phases
schizophrenia
for
first
time.
Schizophrenia
(SZ)
is
a
devastating
psychiatric
disorder
affecting
about
1%
of
the
world’spopulation.
Social-cognitive
impairments
in
SZ
prevent
positive
social
interactions
and
lead
toprogressive
withdrawal.
The
neurobiological
underpinnings
social-cognitive
symptomsremain
poorly
understood,
which
hinders
development
novel
treatments.
At
wholebrainlevel,
an
abnormal
activation
brain
regions
interregional
dysconnectivity
withinsocial-cognitive
networks
have
been
identified
as
major
contributors
to
these
symptoms.
Atthe
cellular
subcellular
levels,
interplay
between
oxidative
stress,
neuroinflammation
andN-methyl-D-aspartate
receptor
hypofunction
thought
underly
pathology.
However,
it
notclear
how
molecular
processes
are
linked
with
genesisof
Here,
we
aim
bridge
gap
macroscale
(connectivityanalyses)
microscale
(molecular
mechanistic)
knowledge
by
proposing
impairedmyelination
disinhibition
local
microcircuits
possible
causative
biological
pathwaysleading
activity
brain.
Furthermore,
recommendelectroencephalography
promising
translational
technique
that
can
foster
pre-clinical
drugdevelopment
discuss
attractive
drug
targets
for
treatment
symptoms
SZ.
Frontiers in Psychology,
Journal Year:
2024,
Volume and Issue:
15
Published: Sept. 26, 2024
Introduction
The
application
of
ketogenic
dietary
interventions
to
mental
health
treatments
is
increasingly
acknowledged
within
medical
and
psychiatric
fields,
yet
its
exploration
in
clinical
psychology
remains
limited.
This
article
discusses
the
potential
implications
diets,
traditionally
utilized
for
neurological
disorders,
broader
practices.
Methods
presents
a
perspective
based
on
existing
diet
research
historical
use,
biological
mechanisms,
therapeutic
benefits.
It
examines
these
diets
treatment
their
relevance
practice.
Results
review
informs
psychologists
benefits
introduces
literature
underlying
mechanisms
involved,
such
as
modulation
neurotransmitters,
reduction
inflammation,
stabilization
brain
energy
metabolism,
demonstrating
biopsychosocial
practice
psychology.
Conclusion
By
considering
metabolic
therapies,
can
broaden
scope
integration
provides
care
model
that
incorporates
knowledge
option
care.
emphasizes
need
further
training
support
effective
implementation
this
psychiatry
intervention.