Neuropathology and Applied Neurobiology,
Год журнала:
2017,
Номер
44(1), С. 91 - 111
Опубликована: Окт. 4, 2017
Accumulating
evidence
indicates
an
important
pathophysiological
role
of
brain
inflammation
in
epilepsy.
In
this
review,
we
will
provide
update
specific
inflammatory
pathways
that
have
been
proposed
to
be
crucial
the
underlying
molecular
mechanisms
epilepsy,
including
interleukin-1
receptor/toll-like
receptor
signalling,
cyclooxygenase-2,
tumour
necrosis
factor-alpha,
complement
signalling
and
chemokines.
Furthermore,
by
drawing
on
from
preclinical
clinical
studies
discuss
potential
these
targets
for
novel
therapeutic
interventions
control
drug-resistant
seizures
or
disease-modifying
effects.
Finally,
assess
use
as
biomarkers
development
epilepsy
measure
effectiveness
interventions.
Science,
Год журнала:
2016,
Номер
354(6312), С. 572 - 577
Опубликована: Ноя. 3, 2016
Acute
pain
is
protective
and
a
cardinal
feature
of
inflammation.
Chronic
after
arthritis,
nerve
injury,
cancer,
chemotherapy
associated
with
chronic
neuroinflammation,
local
inflammation
in
the
peripheral
or
central
nervous
system.
Accumulating
evidence
suggests
that
non-neuronal
cells
such
as
immune
cells,
glial
keratinocytes,
cancer
stem
play
active
roles
pathogenesis
resolution
pain.
We
review
how
interact
nociceptive
neurons
by
secreting
neuroactive
signaling
molecules
modulate
Recent
studies
also
suggest
bacterial
infections
regulate
through
direct
actions
on
sensory
neurons,
specific
receptors
are
present
nociceptors
to
detect
danger
signals
from
infections.
discuss
new
therapeutic
strategies
control
neuroinflammation
for
prevention
treatment
Physiological Reviews,
Год журнала:
2019,
Номер
99(3), С. 1325 - 1380
Опубликована: Март 28, 2019
Sleep
and
immunity
are
bidirectionally
linked.
Immune
system
activation
alters
sleep,
sleep
in
turn
affects
the
innate
adaptive
arm
of
our
body’s
defense
system.
Stimulation
immune
by
microbial
challenges
triggers
an
inflammatory
response,
which,
depending
on
its
magnitude
time
course,
can
induce
increase
duration
intensity,
but
also
a
disruption
sleep.
Enhancement
during
infection
is
assumed
to
feedback
promote
host
defense.
Indeed,
various
parameters,
associated
with
reduced
risk,
improve
outcome
vaccination
responses.
The
induction
hormonal
constellation
that
supports
functions
one
likely
mechanism
underlying
immune-supporting
effects
In
absence
infectious
challenge,
appears
homeostasis
through
several
mediators,
such
as
cytokines.
This
notion
supported
findings
prolonged
deficiency
(e.g.,
short
duration,
disturbance)
lead
chronic,
systemic
low-grade
inflammation
diseases
have
component,
like
diabetes,
atherosclerosis,
neurodegeneration.
Here,
we
review
available
data
this
regulatory
sleep-immune
crosstalk,
point
out
methodological
challenges,
suggest
questions
open
for
future
research.
Anesthesiology,
Год журнала:
2018,
Номер
129(2), С. 343 - 366
Опубликована: Фев. 16, 2018
Abstract
Chronic
pain
is
maintained
in
part
by
central
sensitization,
a
phenomenon
of
synaptic
plasticity,
and
increased
neuronal
responsiveness
pathways
after
painful
insults.
Accumulating
evidence
suggests
that
sensitization
also
driven
neuroinflammation
the
peripheral
nervous
system.
A
characteristic
feature
activation
glial
cells,
such
as
microglia
astrocytes,
spinal
cord
brain,
leading
to
release
proinflammatory
cytokines
chemokines.
Recent
studies
suggest
chemokines
are
powerful
neuromodulators
play
sufficient
role
inducing
hyperalgesia
allodynia
system
administration.
Sustained
increase
promotes
chronic
widespread
affects
multiple
body
sites.
Thus,
drives
via
sensitization.
We
discuss
sex-dependent
glial/immune
signaling
new
therapeutic
approaches
control
for
resolution
pain.
Frontiers in Cellular Neuroscience,
Год журнала:
2015,
Номер
9
Опубликована: Дек. 17, 2015
Patients
with
chronic
inflammation
are
often
associated
the
emergence
of
depression
symptoms,
while
diagnosed
depressed
patients
show
increased
levels
circulating
cytokines.
Further
studies
revealed
activation
brain
immune
cell
microglia
in
a
greater
magnitude
individuals
that
committed
suicide,
indicating
crucial
role
for
neuroinflammation
pathogenesis.
Rapid
advances
understanding
microglial
and
astrocytic
neurobiology
were
obtained
past
fifteen
to
twenty
years.
Indeed,
recent
data
reveal
play
an
important
managing
neuronal
death,
neurogenesis,
synaptic
interactions,
besides
their
involvement
immune-response
generating
The
communication
between
neurons
is
essential
synchronize
these
diverse
functions
activity.
Evidence
accumulating
secreted
extracellular
vesicles
(EVs),
comprising
ectosomes
exosomes
size
ranging
from
0.1
1
μm,
key
players
intercellular
signaling.
These
EVs
may
carry
specific
proteins,
mRNAs
microRNAs
(miRNAs).
Transfer
was
shown
be
mediated
by
oligodendrocytes,
astrocytes
either
supportive
neurons,
or
instead
disseminate
disease.
Interestingly,
several
reports
have
identified
changes
miRNAs
patients,
which
target
not
only
pathways
plasticity,
learning
memory
but
also
production
neurotrophic
factors
modulation.
In
this
article,
we
discuss
depression,
namely
dynamic
alterations
status
response
stimulation,
how
phenotypes
etiological
neurodegeneneration,
particular
depressive-like
behavior.
We
will
overview
miRNAs,
exosomes,
regulating
critical
they
contribute
other
disorders
including
amyotrophic
lateral
sclerosis,
Alzheimer's
disease
Parkinson
disease,
share
neuroinflammatory-associated
processes.
Specific
reference
made
as
potential
biomarkers
monitoring
approaches,
focusing
on
potentialities
drug
delivery
vehicles
putative
therapeutic
strategies
using
autologous
exosome-based
systems
treat
neurodegenerative
psychiatric
disorders.
