Molecular Neurobiology,
Год журнала:
2022,
Номер
60(3), С. 1369 - 1390
Опубликована: Ноя. 29, 2022
Abstract
Sepsis
is
a
leading
cause
of
intensive
care
unit
admission
and
death
worldwide.
Most
surviving
patients
show
acute
or
chronic
mental
disorders,
which
are
known
as
sepsis-associated
encephalopathy
(SAE).
Although
accumulating
studies
in
the
past
two
decades
focused
on
pathogenesis
SAE,
systematic
review
retrospective
exclusively
focuses
inflammatory
mechanisms
SAE
has
been
lacking
yet.
This
summarizes
recent
advance
field
neuroinflammation
sheds
light
activation
microglia
SAE.
Activation
predominates
neuroinflammation.
As
gene
expression
profile
changes,
heterogeneous
characterizations
throughout
all
stages
Here,
we
summarize
systemic
inflammation
following
sepsis
also
relationship
microglial
diversity
Moreover,
collection
neuroinflammation-related
dysfunction
reviewed
to
illustrate
possible
for
In
addition,
promising
pharmacological
non-pharmacological
therapeutic
strategies,
especially
those
target
microglia,
concluded
final
part
this
review.
Collectively,
clarification
vital
between
SAE-related
disorders
would
significantly
improve
our
understanding
pathophysiological
therefore
provide
potential
targets
therapies
aimed
at
inhibiting
Journal of Neuroinflammation,
Год журнала:
2022,
Номер
19(1)
Опубликована: Июнь 6, 2022
Abstract
Major
depressive
disorder
is
a
highly
debilitating
psychiatric
involving
the
dysfunction
of
different
cell
types
in
brain.
Microglia
are
predominant
resident
immune
cells
brain
and
exhibit
critical
role
depression.
Recent
studies
have
suggested
that
depression
can
be
regarded
as
microglial
disease.
regulate
inflammation,
synaptic
plasticity,
formation
neural
networks,
all
which
affect
In
this
review,
we
highlighted
microglia
pathology
First,
described
activation
animal
models
clinically
depressed
patients.
Second,
emphasized
possible
mechanisms
by
recognize
depression-associated
stress
conditions.
Third,
how
antidepressants
(clinical
medicines
natural
products)
activation.
Thus,
review
aimed
to
objectively
analyze
focus
on
potential
antidepressants.
These
data
regulation
actions
might
novel
therapeutic
strategy
counteract
adverse
effects
devastating
mental
disorders.
Advanced Materials,
Год журнала:
2022,
Номер
34(27)
Опубликована: Апрель 28, 2022
Microglial
polarization
is
one
of
the
most
promising
therapeutic
strategies
for
multiple
central
nervous
system
(CNS)
disorders.
However,
safe,
effective,
and
controllable
microglial
regulation
still
faces
formidable
challenges.
Although
some
anti-inflammatory
factors
promote
microglia
polarization,
their
short
half-life,
high
cost,
unpredictable
in
vivo
behavior,
complex
delivery
operations,
hamper
clinical
application.
Here,
inspired
by
natural
microhemorrhage
cleaning
mechanism,
an
MG1
peptide
RVG29
engineered
nanoerythrocyte
(NEMR)
that
can
reprogram
are
developed
from
classical
M1
toward
alternative
M2
inducing
heme
oxygenase-1
(HO-1),
stimulating
Notch1/Hes1/Stat3
signaling,
further
inhibiting
NF-κB
p65
translocation.
Moreover,
carbon
monoxide
(CO)
bilirubin
produced
endogenous
metabolism
reinforces
effect.
In
middle
cerebral
artery
occlusion
experimental
autoimmune
encephalomyelitis
models,
a
satisfactory
prognosis
achieved,
with
precise
inflammatory
lesion
sites,
increased
expression
factors,
reduced
blood-brain
barrier
permeability,
as
well
promotion
neurogenesis
functional
recovery.
Furthermore,
NEMR
be
integrated
agents,
which
facilitates
drug
to
enhance
effects.
Hence,
nanoerythrocytes,
feasible,
efficient,
practical
tool,
provides
new
strategy
rebalancing
immune
environment
CNS
International Journal of Molecular Sciences,
Год журнала:
2022,
Номер
23(19), С. 11076 - 11076
Опубликована: Сен. 21, 2022
Depression
and
anxiety
disorders
are
the
two
most
prevalent
psychiatric
diseases
that
affect
hundreds
of
millions
individuals
worldwide.
Understanding
etiology
related
mechanisms
is
great
importance
might
yield
new
therapeutic
strategies
to
treat
these
effectively.
During
past
decades,
a
growing
number
studies
have
pointed
out
stress-induced
inflammatory
response
in
amygdala,
kernel
region
for
processing
emotional
stimuli,
as
potentially
critical
contributor
pathophysiology
depression
disorders.
In
this
review,
we
first
summarized
recent
progress
from
both
animal
human
toward
understanding
causal
link
between
inflammation
disorders,
with
particular
emphasis
on
findings
showing
effect
functional
changes
neurons
at
levels
ranging
molecular
signaling,
cellular
function,
synaptic
plasticity,
neural
circuit
behavior,
well
their
contributions
pathology
inflammation-related
Finally,
concluded
by
discussing
some
difficulties
surrounding
current
research
propose
issues
worth
future
study
field.
Cells,
Год журнала:
2024,
Номер
13(5), С. 423 - 423
Опубликована: Фев. 28, 2024
The
involvement
of
central
and
peripheral
inflammation
in
the
pathogenesis
prognosis
major
depressive
disorder
(MDD)
has
been
demonstrated.
increase
pro-inflammatory
cytokines
(interleukin
(IL)-1β,
IL-6,
IL-18,
TNF-α)
individuals
with
depression
may
elicit
neuroinflammatory
processes
inflammation,
mechanisms
that,
turn,
can
contribute
to
gut
microbiota
dysbiosis.
Together,
neuroinflammation
dysbiosis
induce
alterations
tryptophan
metabolism,
culminating
decreased
serotonin
synthesis,
impairments
neuroplasticity-related
mechanisms,
glutamate-mediated
excitotoxicity.
This
review
aims
highlight
inflammatory
(neuroinflammation,
dysbiosis)
involved
pathophysiology
MDD
explore
novel
anti-inflammatory
therapeutic
approaches
for
this
psychiatric
disturbance.
Several
lines
evidence
have
indicated
that
addition
antidepressants,
physical
exercise,
probiotics,
nutraceuticals
(agmatine,
ascorbic
acid,
vitamin
D)
possess
effects
their
antidepressant
properties.
Further
studies
are
necessary
benefits
these
alternative
therapies
MDD.
Abstract
Background
Adolescent
depression
is
becoming
one
of
the
major
public
health
concerns,
because
its
increased
prevalence
and
risk
significant
functional
impairment
suicidality.
Clinical
commonly
emerges
in
adolescence;
therefore,
prevention
intervention
at
this
stage
crucial.
Recent
evidence
supports
importance
gut
microbiota
(GM)
modulation
multiple
functions
associated
with
through
gut-brain
axis
(GBA).
However,
underlying
mechanisms
remain
poorly
understood.
Therefore,
current
study,
we
aimed
to
screen
out
from
healthy
depressive
adolescents,
delineate
association
targeted
adolescent
depression,
address
salutary
effects
on
anti-depressive
behaviors
mice
involving
metabolism
tryptophan
(Trp)-derived
neurotransmitters
along
GBA.
Results
Here,
found
volunteers,
first
diagnosis
patients
sertraline
interveners
after
displayed
difference,
relative
abundance
Faecalibacterium
,
Roseburia
Collinsella
Blautia
Phascolarctobacterium
Lachnospiraceae-unclassified
decreased
patients,
while
restored
treatment.
Of
note,
exhibited
a
high
efficiency
predicting
depression.
Intriguingly,
transplantation
fecal
volunteers
chronic
restraint
stress
(CRS)-induced
depressed
significantly
ameliorated
mouse
behaviors,
which
exerted
critical
roles,
since
effective
colonization
colon
resulted
remarkably
5-HT
level
reciprocally
kynurenine
(Kyn)
toxic
metabolites
quinolinic
acid
(Quin)
3-hydroxykynurenine
(3-HK)
levels
both
brain
colon.
The
specific
roles
were
further
validated
by
target
bacteria
model,
intestinalis
(
Ri
.)
was
gavaged
importantly,
it
dramatically
CRS-induced
via
promoting
hydroxylase-2
(TPH2)
or
-1
(TPH1)
expression.
Reciprocally,
Ri.
markedly
restrained
limit-step
enzyme
responsible
for
(indoleamine2,3-dioxygenase
1,
IDO1)
(3-hydroxyanthranilic
3,4-dioxygenase,
3HAO)
generation,
thereby
Kyn
Quin
levels.
Additionally,
.
administration
pivotal
role
protection
synaptic
loss,
microglial
activation,
astrocyte
maintenance.
Conclusions
This
study
beneficial
balancing
Trp-derived
neurotransmitter
improving
synaptogenesis
glial
maintenance,
may
yield
novel
insights
into
microbial
markers
therapeutic
strategies
GBA
Advanced Materials,
Год журнала:
2023,
Номер
35(47)
Опубликована: Май 5, 2023
Abstract
Brain–computer
interface
(BCI)
has
been
the
subject
of
extensive
research
recently.
Governments
and
companies
have
substantially
invested
in
relevant
applications.
The
restoration
communication
motor
function,
treatment
psychological
disorders,
gaming,
other
daily
therapeutic
applications
all
benefit
from
BCI.
electrodes
hold
key
to
essential,
fundamental
BCI
precondition
electrical
brain
activity
detection
delivery.
However,
traditional
rigid
are
limited
due
their
mismatch
Young's
modulus,
potential
damages
human
body,
a
decline
signal
quality
with
time.
These
factors
make
development
flexible
vital
urgent.
Flexible
made
soft
materials
grown
popularity
recent
years
as
an
alternative
conventional
because
they
offer
greater
conformance,
for
higher
signal‐to‐noise
ratio
(SNR)
signals,
wider
range
Therefore,
latest
classifications
future
developmental
directions
fabricating
these
explored
this
paper
further
encourage
speedy
advent
In
summary,
perspectives
outlook
developing
discipline
provided.
Nature Communications,
Год журнала:
2024,
Номер
15(1)
Опубликована: Янв. 10, 2024
Abstract
Anxiety-associated
symptoms
following
acute
stress
usually
become
extinct
gradually
within
a
period
of
time.
However,
the
mechanisms
underlying
how
individuals
cope
with
to
achieve
extinction
anxiety
are
not
clear.
Here
we
show
that
restraint
causes
an
increase
in
activity
GABAergic
neurons
CeA
(GABA
)
male
mice,
resulting
anxiety-like
behaviors
12
hours;
meanwhile,
elevated
GABA
neuronal
CX3CL1
secretion
via
MST4
(mammalian
sterile-20-like
kinase
4)-NF-κB-CX3CL1
signaling
consequently
activates
microglia
CeA.
Activated
turn
inhibit
engulfment
their
dendritic
spines,
ultimately
leading
induced
by
stress.
These
findings
reveal
dynamic
molecular
and
cellular
mechanism
which
drive
negative
feedback
activity,
thus
facilitating
maintenance
brain
homeostasis
response
Molecular Neurodegeneration,
Год журнала:
2024,
Номер
19(1)
Опубликована: Апрель 1, 2024
Abstract
Lipopolysaccharide
(LPS)
constitutes
much
of
the
surface
Gram-negative
bacteria,
and
if
LPS
enters
human
body
or
brain
can
induce
inflammation
act
as
an
endotoxin.
We
outline
hypothesis
here
that
may
contribute
to
pathophysiology
Alzheimer’s
disease
(AD)
via
peripheral
infections
gut
dysfunction
elevating
levels
in
blood
brain,
which
promotes:
amyloid
pathology,
tau
pathology
microglial
activation,
contributing
neurodegeneration
AD.
The
evidence
supporting
this
includes:
i)
are
elevated
AD
patients,
ii)
risk
factors
increase
response,
iii)
induces
Aβ
expression,
aggregation,
neurotoxicity,
iv)
TAU
phosphorylation,
aggregation
spreading,
v)
priming,
activation
vi)
loss
synapses,
neurons
memory
mouse
models,
cognitive
humans.
However,
test
hypothesis,
it
is
necessary
whether
reducing
reduces
progression.
If
endotoxin
correct,
then
treatments
might
include:
infections,
changing
microbiome,
leaky
gut,
decreasing
LPS,
blocking
response.