Cell Proliferation,
Год журнала:
2022,
Номер
55(10)
Опубликована: Июль 20, 2022
Abstract
Objectives
Cognitive
dysfunction
has
been
identified
as
a
major
symptom
of
series
psychiatric
disorders.
Multidisciplinary
studies
have
shown
that
cognitive
is
monitored
by
two‐way
interaction
between
the
neural
and
immune
systems.
However,
specific
mechanisms
in
response
brain
remain
unclear.
Materials
methods
In
this
review,
we
summarized
relevant
research
to
uncover
our
comprehension
brain–immune
underlying
decline.
Results
The
pathophysiological
brain‐immune
interactions
psychiatric‐based
involve
several
molecules
their
associated
signaling
pathways,
impairments
synaptic
plasticity,
potential
neuro‐immunological
mechanism
stress.
Conclusions
Therefore,
review
may
provide
better
theoretical
basis
for
integrative
therapeutic
considerations
disorders
with
dysfunction.
Cell,
Год журнала:
2022,
Номер
186(1), С. 194 - 208.e18
Опубликована: Дек. 28, 2022
The
diversity
and
complex
organization
of
cells
in
the
brain
have
hindered
systematic
characterization
age-related
changes
its
cellular
molecular
architecture,
limiting
our
ability
to
understand
mechanisms
underlying
functional
decline
during
aging.
Here,
we
generated
a
high-resolution
cell
atlas
aging
within
frontal
cortex
striatum
using
spatially
resolved
single-cell
transcriptomics
quantified
gene
expression
spatial
major
types
these
regions
over
mouse
lifespan.
We
observed
substantially
more
pronounced
state,
expression,
non-neuronal
neurons.
Our
data
revealed
signatures
glial
immune
activation
aging,
particularly
enriched
subcortical
white
matter,
identified
both
similarities
notable
differences
cell-activation
patterns
induced
by
systemic
inflammatory
challenge.
These
results
provide
critical
insights
into
inflammation
brain.
Circulation Research,
Год журнала:
2022,
Номер
130(8), С. 1167 - 1186
Опубликована: Апрель 14, 2022
Inflammation
and
immune
mechanisms
are
crucially
involved
in
the
pathophysiology
of
development,
acute
damage
cascades,
chronic
course
after
ischemic
stroke.
Atherosclerosis
is
an
inflammatory
disease,
and,
addition
to
classical
risk
factors,
maladaptive
lead
increased
Accordingly,
individuals
with
signs
inflammation
or
corresponding
biomarkers
have
Anti-inflammatory
drugs,
such
as
IL
(interleukin)-1β
blockers,
methotrexate,
colchicine,
represent
attractive
treatment
strategies
prevent
vascular
events
Lately,
COVID-19
pandemic
shows
a
clear
association
between
SARS-CoV2
infections
cerebrovascular
events.
Furthermore,
both
innate
adaptive
systems
influence
cerebral
cascades
Neutrophils,
monocytes,
microglia,
well
T
B
lymphocytes
each
play
complex
interdependent
roles
that
synergize
remove
dead
tissue
but
also
can
cause
bystander
injury
intact
brain
cells
generate
inflammation.
Chronic
systemic
comorbid
may
unfavorably
outcome
stroke
recurrence
for
further
In
addition,
triggers
specific
depression,
which
turn
promote
infections.
Recent
research
now
increasingly
addressing
question
extent
long-term
particular,
complications
poststroke
dementia
even
depression.
Abstract
Alzheimer’s
disease
(AD)
is
a
genetically
complex
and
heterogeneous
disorder
with
multifaceted
neuropathological
features,
including
β-amyloid
plaques,
neurofibrillary
tangles,
neuroinflammation.
Over
the
past
decade,
emerging
evidence
has
implicated
both
beneficial
pathological
roles
for
innate
immune
genes
cells,
peripheral
cells
such
as
T
which
can
infiltrate
brain
either
ameliorate
or
exacerbate
AD
neuropathogenesis.
These
findings
support
neuroimmune
axis
of
AD,
in
interplay
adaptive
systems
inside
outside
critically
impacts
etiology
pathogenesis
AD.
In
this
review,
we
discuss
complexities
neuropathology
at
levels
genetics
cellular
physiology,
highlighting
signaling
pathways
associated
risk
interactions
among
brain.
We
emphasize
role
mechanisms
by
monocytes,
influence
neuropathology,
microglial
clearance
amyloid-β
peptide,
key
component
plaque
cores,
pro-inflammatory
cytotoxic
activity
microglia,
astrogliosis,
their
vasculature.
Finally,
review
challenges
outlook
establishing
immune-based
therapies
treating
preventing
Translational Psychiatry,
Год журнала:
2024,
Номер
14(1)
Опубликована: Июнь 8, 2024
Abstract
Major
depressive
disorder
(MDD)
and
bipolar
(BD)
are
highly
disabling
illnesses
defined
by
different
psychopathological,
neuroimaging,
cognitive
profiles.
In
the
last
decades,
immune
dysregulation
has
received
increasing
attention
as
a
central
factor
in
pathophysiology
of
these
disorders.
Several
aspects
dysregulations
have
been
investigated,
including,
low-grade
inflammation
cytokines,
chemokines,
cell
populations,
gene
expression,
markers
both
peripheral
activation.
Understanding
distinct
profiles
characterizing
two
disorders
is
indeed
crucial
importance
for
differential
diagnosis
implementation
personalized
treatment
strategies.
this
paper,
we
reviewed
current
literature
on
response
system
focusing
our
studies
using
inflammatory
to
discriminate
between
MDD
BD.
High
heterogeneity
characterized
available
literature,
reflecting
Common
alterations
include
high
pro-inflammatory
cytokines
such
IL-6
TNF-α.
On
contrary,
greater
involvement
chemokines
associated
with
innate
immunity
reported
BD
together
dynamic
changes
T
cells
differentiation
defects
during
childhood
which
normalize
adulthood,
whereas
classic
mediators
responses
IL-4
IL-10
present
signs
immune-senescence.
Frontiers in Aging Neuroscience,
Год журнала:
2022,
Номер
14
Опубликована: Апрель 25, 2022
For
decades,
it
has
been
widely
believed
that
the
blood–brain
barrier
(BBB)
provides
an
immune
privileged
environment
in
central
nervous
system
(CNS)
by
blocking
peripheral
cells
and
humoral
factors.
This
view
revised
recent
years,
with
increasing
evidence
revealing
plays
a
critical
role
regulating
CNS
homeostasis
disease.
Neurodegenerative
diseases
are
characterized
progressive
dysfunction
loss
of
neurons
CNS.
An
number
studies
have
focused
on
connection
between
neurodegenerative
diseases.
On
one
hand,
peripherally
released
cytokines
can
cross
BBB,
cause
direct
neurotoxicity
contribute
to
activation
microglia
astrocytes.
other
also
infiltrate
brain
participate
progression
neuroinflammatory
high
morbidity
disability
rate,
yet
there
no
effective
therapies
stop
or
reverse
their
progression.
In
neuroinflammation
received
much
attention
as
therapeutic
target
for
many
this
review,
we
highlight
emerging
systems
diseases,
well
interactions.
A
better
understanding
may
improve
strategies
