International Journal of Environmental Research and Public Health,
Год журнала:
2022,
Номер
19(21), С. 14045 - 14045
Опубликована: Окт. 28, 2022
Aim:
This
study
aims
to
develop
new
approaches
characterize
brain
networks
potentially
contribute
a
better
understanding
of
mechanisms
involved
in
depression.
Method
and
subjects:
We
recruited
90
49
healthy
controls
(HC)
41
patients
with
major
depressive
episode
(MDE).
All
subjects
underwent
clinical
evaluation
functional
resting-state
MRI.
The
data
were
processed
investigating
connectivity
network
measures
across
the
two
groups
using
Brain
Connectivity
Toolbox.
statistical
inferences
developed
at
level,
false
discovery
rate
method.
Linear
discriminant
analysis
was
used
differentiate
between
groups.
Results
discussion:
Significant
differences
(FC)
depressed
vs.
demonstrated,
regions
including
lingual
gyrus,
cerebellum,
midcingulate
cortex
thalamus
more
prominent
as
compared
depression
where
orbitofrontal
emerged
key
node.
demonstrated
that
full-connectivity
matrices
most
precise
differentiating
health
subjects.
Conclusion:
provides
supportive
evidence
for
impaired
MDE
patients.
Signal Transduction and Targeted Therapy,
Год журнала:
2024,
Номер
9(1)
Опубликована: Фев. 9, 2024
Abstract
Worldwide,
the
incidence
of
major
depressive
disorder
(MDD)
is
increasing
annually,
resulting
in
greater
economic
and
social
burdens.
Moreover,
pathological
mechanisms
MDD
underlying
effects
pharmacological
treatments
for
are
complex
unclear,
additional
diagnostic
therapeutic
strategies
still
needed.
The
currently
widely
accepted
theories
pathogenesis
include
neurotransmitter
receptor
hypothesis,
hypothalamic-pituitary-adrenal
(HPA)
axis
cytokine
neuroplasticity
hypothesis
systemic
influence
but
these
cannot
completely
explain
mechanism
MDD.
Even
it
hard
to
adopt
only
one
reveal
MDD,
thus
recent
years,
great
progress
has
been
made
elucidating
roles
multiple
organ
interactions
identifying
novel
approaches
multitarget
modulatory
strategies,
further
revealing
disease
features
Furthermore,
some
newly
discovered
potential
targets
studied
antidepressants
have
attracted
widespread
attention,
reagents
even
approved
clinical
treatment
methods
such
as
phototherapy
acupuncture
effective
improvement
symptoms.
In
this
work,
we
comprehensively
summarize
latest
research
on
diagnosis
preventive
medicines,
well
related
trials.
Nature Neuroscience,
Год журнала:
2023,
Номер
26(9), С. 1613 - 1629
Опубликована: Авг. 14, 2023
The
substantial
individual
heterogeneity
that
characterizes
people
with
mental
illness
is
often
ignored
by
classical
case-control
research,
which
relies
on
group
mean
comparisons.
Here
we
present
a
comprehensive,
multiscale
characterization
of
the
gray
matter
volume
(GMV)
differences
in
1,294
cases
diagnosed
one
six
conditions
(attention-deficit/hyperactivity
disorder,
autism
spectrum
bipolar
depression,
obsessive-compulsive
disorder
and
schizophrenia)
1,465
matched
controls.
Normative
models
indicated
person-specific
deviations
from
population
expectations
for
regional
GMV
were
highly
heterogeneous,
affecting
same
area
<7%
diagnosis.
However,
these
embedded
within
common
functional
circuits
networks
up
to
56%
cases.
salience-ventral
attention
system
was
implicated
transdiagnostically,
other
systems
selectively
involved
schizophrenia
attention-deficit/hyperactivity
disorder.
Phenotypic
between
assigned
diagnosis
may
thus
arise
heterogeneous
localization
specific
deviations,
whereas
phenotypic
similarities
be
attributable
dysfunction
networks.
American Journal of Psychiatry,
Год журнала:
2022,
Номер
179(7), С. 458 - 469
Опубликована: Июль 1, 2022
Anhedonia—the
loss
of
pleasure
or
lack
reactivity
to
pleasurable
stimuli—remains
a
formidable
treatment
challenge
across
neuropsychiatric
disorders.
In
major
depressive
disorder,
anhedonia
has
been
linked
poor
disease
course,
worse
response
psychological,
pharmacological,
and
neurostimulation
treatments,
increased
suicide
risk.
Moreover,
although
some
neural
abnormalities
normalize
after
successful
treatment,
several
persist—for
example,
blunted
activation
the
ventral
striatum
reward-related
cues
reduced
functional
connectivity
involving
striatum.
Critically,
these
have
also
identified
in
unaffected,
never-depressed
children
parents
with
disorder
found
prospectively
predict
first
onset
depression.
Thus,
may
be
promising
targets
for
prevention.
Despite
appreciation
clinical
importance
its
underlying
mechanisms,
important
gaps
remain.
this
overview,
author
summarizes
extant
knowledge
about
pathophysiology
anhedonia,
which
provide
road
map
toward
novel
prevention
strategies,
then
highlights
priorities
facilitate
clinically
meaningful
breakthroughs.
These
include
need
1)
appropriately
controlled
trials,
especially
those
embracing
an
experimental
therapeutics
approach
probe
target
engagement;
2)
preclinical
models
relevant
stronger
translational
value;
3)
scales
that
incorporate
neuroscientific
advances
our
understanding
anhedonia.
The
concludes
by
highlighting
future
directions,
emphasizing
integrated,
collaborative,
cross-species,
multilevel
tackling
anhedonic
phenotypes.
Neuropharmacology,
Год журнала:
2022,
Номер
226, С. 109398 - 109398
Опубликована: Дек. 27, 2022
This
theoretical
article
revives
a
classical
bridging
construct,
canalization,
to
describe
new
model
of
general
factor
psychopathology.
To
achieve
this,
we
have
distinguished
between
two
types
plasticity,
an
early
one
that
call
'TEMP'
for
'Temperature
or
Entropy
Mediated
Plasticity',
and
another,
'canalization',
which
is
close
Hebbian
plasticity.
These
forms
plasticity
can
be
most
easily
by
their
relationship
'precision'
inverse
variance;
TEMP
relates
increased
variance
decreased
precision,
whereas
the
opposite
true
canalization.
also
subsumes
learning
rate,
(Ising)
temperature
entropy.
Dictionary
definitions
'plasticity'
it
as
property
being
shaped
molded;
better
match
this.
Importantly,
propose
'pathological'
phenotypes
develop
via
mechanisms
canalization
defensive
response
adversity
associated
distress
dysphoria.
Our
states
entrenches
in
psychopathology,
narrowing
phenotypic
state-space
agent
develops
expertise
pathology.
We
suggest
-
combined
with
gently
guiding
psychological
support
counter
address
questions
whether
when
adaptive
versus
maladaptive,
furnish
our
references
basic
human
neuroscience,
offer
concrete
experiments
measures
test
its
main
hypotheses
implications.
part
Special
Issue
on
"National
Institutes
Health
Psilocybin
Research
Speaker
Series".
Translational Psychiatry,
Год журнала:
2023,
Номер
13(1)
Опубликована: Май 9, 2023
Intravenous
ketamine
is
posited
to
rapidly
reverse
depression
by
enhancing
neuroplasticity.
In
human
patients,
we
quantified
gray
matter
microstructural
changes
on
a
rapid
(24-h)
timescale
within
key
regions
where
neuroplasticity
enhancements
post-ketamine
have
been
implicated
in
animal
models.
this
study,
98
unipolar
depressed
adults
who
failed
at
least
one
antidepressant
medication
were
randomized
2:1
single
infusion
of
intravenous
(0.5
mg/kg)
or
vehicle
(saline)
and
completed
diffusion
tensor
imaging
(DTI)
assessments
pre-infusion
baseline
24-h
post-infusion.
DTI
mean
diffusivity
(DTI-MD),
putative
marker
matter,
was
calculated
for
7
interest
(left
right
BA10,
amygdala,
hippocampus;
ventral
Anterior
Cingulate
Cortex)
compared
clinical
response
measured
with
the
Montgomery-Asberg
Depression
Rating
Scale
(MADRS)
Quick
Inventory
Depressive
Symptoms-Self-Report
(QIDS-SR).
Individual
differences
DTI-MD
change
(greater
decrease
from
post-infusion,
indicative
more
enhancement)
associated
larger
improvements
scores
across
several
regions.
left
BA10
these
relationships
driven
primarily
group
(group
*
interaction
effects:
p
=
0.016-0.082).
associations
generalized
both
arms
(p
0.007).
hippocampus,
MADRS
only,
effects
observed
opposite
direction,
such
that
inversely
arm
specifically
0.032-0.06).
The
acute
may
be
mediated,
part,
quantifiable
DTI.
Glia,
Год журнала:
2023,
Номер
72(1), С. 111 - 132
Опубликована: Сен. 7, 2023
Abstract
Chronic
environmental
stress
and
traumatic
social
experiences
induce
maladaptive
behavioral
changes
is
a
risk
factor
for
major
depressive
disorder
(MDD)
various
anxiety‐related
psychiatric
disorders.
Clinical
studies
animal
models
of
chronic
have
reported
that
symptom
severity
correlated
with
innate
immune
responses
upregulation
neuroinflammatory
cytokine
signaling
in
brain
areas
implicated
mood
regulation
(mPFC;
medial
Prefrontal
Cortex).
Despite
increasing
evidence
implicating
impairments
neuroplasticity
synaptic
deficits
into
the
pathophysiology
stress‐related
mental
disorders,
how
microglia
may
modulate
neuronal
homeostasis
response
to
has
not
been
defined.
Here,
using
repeated
defeat
(RSDS)
mouse
model
we
demonstrate
microglial‐induced
inflammatory
are
regulating
plasticity
associated
psychosocial
stress.
Specifically,
show
induces
rapid
activation
proliferation
as
well
macrophage
infiltration
mPFC,
these
processes
spatially
related
activation.
Moreover,
report
significant
association
microglial
susceptibility
or
resilience
In
addition,
find
exposure
exacerbates
phagocytosis
elements
plasticity.
Importantly,
by
utilizing
two
different
CSF1R
inhibitors
(the
penetrant
PLX5622
non‐penetrant
PLX73086)
highlight
crucial
role
(and
secondarily
macrophages)
catalyzing
pathological
manifestations
linked
mPFC
resulting
usually
depression.
Journal of Child Psychology and Psychiatry,
Год журнала:
2024,
Номер
65(4), С. 538 - 567
Опубликована: Март 1, 2024
Depression
is
a
serious
public
health
problem,
and
adolescence
an
‘age
of
risk’
for
the
onset
Major
Depressive
Disorder.
Recently,
we
others
have
proposed
neuroimmune
network
models
that
highlight
bidirectional
communication
between
brain
immune
system
in
both
mental
physical
health,
including
depression.
These
draw
on
research
indicating
cellular
actors
(particularly
monocytes)
signaling
molecules
cytokines)
orchestrate
inflammation
periphery
can
directly
modulate
structure
function
brain.
In
brain,
inflammatory
activity
heightens
sensitivity
to
threats
cortico‐amygdala
circuit,
lowers
rewards
cortico‐striatal
alters
executive
control
emotion
regulation
prefrontal
cortex.
When
dysregulated,
particularly
under
conditions
chronic
stress,
generate
feelings
dysphoria,
distress,
anhedonia.
This
initiate
unhealthy,
self‐medicating
behaviors
(e.g.
substance
use,
poor
diet)
manage
which
further
heighten
inflammation.
Over
time,
dysregulation
these
circuits
response
may
compound
each
other
form
positive
feedback
loop,
whereby
one
organ
exacerbates
other.
We
suggest
this
dynamic
joint
vulnerability
depression,
during
adolescence.
three
goals
present
paper.
First,
extend
developmental
framework
risk
depression
Second,
examine
how
perspective
help
explain
high
rates
comorbidity
psychiatric
disorders
across
development,
multimorbidity
stress‐related
medical
illnesses.
Finally,
consider
identifying
pathways
facilitate
‘next
generation’
behavioral
biological
interventions
target
treat,
ideally
prevent,
youth
adolescents.