Psychiatry and Clinical Neurosciences,
Journal Year:
2019,
Volume and Issue:
73(5), P. 204 - 215
Published: Jan. 22, 2019
Schizophrenia
is
a
chronic
and
severe
psychiatric
disorder
that
has
profound
impact
on
an
individual's
life
society.
Thus,
developing
more
effective
therapeutic
interventions
essential.
Over
the
past
quarter-century,
abundance
of
evidence
from
pharmacologic
challenges,
post-mortem
studies,
brain
imaging,
genetic
studies
supports
role
glutamatergic
dysregulation
in
pathophysiology
schizophrenia,
results
recent
randomized
clinical
trials
based
this
have
yielded
promising
results.
In
article,
we
review
alterations
neurotransmission,
especially
focusing
N-methyl-d-aspartate
receptor
(NMDAR)
function,
may
be
critical
causative
feature
how
contributes
to
pathologic
circuit
function
brain,
these
insights
are
revealing
whole
new
avenues
for
treatment
development
could
reduce
treatment-resistant
symptoms,
which
account
persistent
disability.
Frontiers in Immunology,
Journal Year:
2020,
Volume and Issue:
11
Published: Feb. 26, 2020
Ischemic
stroke,
which
accounts
for
75-80%
of
strokes,
is
a
predominant
cause
morbidity
and
mortality
worldwide.
Recently,
post-stroke
immune
response
becomes
new
breakthrough
the
treatment
strategy
ischemic
stroke.
Glial
cells,
including
microglia,
astrocytes,
oligodendrocytes,
are
major
components
peri-infarction
environment
in
central
nervous
system
have
been
elucidated
to
play
critical
roles
regulation.
However,
increasing
evidences
suggest
that
glial
cells
exert
different,
even
contrary
effect
Microglia,
survey
CNS
homostasis
regulate
innate
response,
rapidly
activated
following
The
microglia
would
release
inflammatory
cytokines
induce
neuronal
tissue
injuries.
On
contrary,
anti-inflammatory
neurotrophic
factors
secreted
by
alternatively
considered
be
benefit
recovery
Astrocytes
activation
reactive
gliosis
stroke
contribute
limitaion
brain
injury
stabalize
homeostasis.
scar
developed
astrocytes
also
hinder
reconnectivity
extension.
Oligodendrocytes
shown
extensively
involved
demyelination
remyelination
after
Oligodendrocyte
precursor
able
differentiate
into
reactived
supposed
lead
functional
recovery.
Here
we
discuss
mechanisms
regulation
mediated
interaction
between
neurons.
present
review,
from
perspective
various
describes
their
possible
at
different
stages
future
intervention
targets.
Journal of Neuroinflammation,
Journal Year:
2018,
Volume and Issue:
15(1)
Published: Sept. 24, 2018
Alzheimer’s
disease
(AD)
is
a
neurodegenerative
disorder,
most
cases
of
which
lack
clear
causative
event.
This
has
made
the
difficult
to
characterize
and,
thus,
diagnose.
Although
some
are
genetically
linked,
there
many
diseases
and
lifestyle
factors
that
can
lead
an
increased
risk
developing
AD,
including
traumatic
brain
injury,
diabetes,
hypertension,
obesity,
other
metabolic
syndromes,
in
addition
aging.
Identifying
common
trends
between
these
conditions
could
enhance
our
understanding
AD
development
more
effective
treatments.
immune
system
one
body’s
key
defense
mechanisms,
chronic
inflammation
been
increasingly
linked
with
several
age-related
diseases.
Moreover,
it
now
well
accepted
important
role
onset
progression
AD.
In
this
review,
different
inflammatory
signals
associated
its
will
be
outlined
demonstrate
how
may
influencing
individual
susceptibility
Our
goal
bring
attention
potential
shared
presented
by
during
successful
Frontiers in Immunology,
Journal Year:
2020,
Volume and Issue:
11
Published: July 8, 2020
The
interaction
between
microglia
and
astrocytes
significantly
influences
neuroinflammation.
Microglia/astrocytes,
part
of
the
neurovascular
unit
(NVU),
are
activated
by
various
brain
insults.
local
extracellular
intracellular
signals
determine
their
characteristics
switch
phenotypes.
Microglia
into
two
polarization
states:
pro-inflammatory
phenotype
(M1
A1)
anti-inflammatory
(M2
A2).
During
neuroinflammation,
induced
stroke
or
lipopolysaccharides,
more
sensitive
to
pathogens
damage,
thus
initially
M1
phenotype,
produce
common
inflammatory
such
as
IL-
1
TNF-α
trigger
reactive
A1
phenotype.
These
can
be
amplified
not
only
self-feedback
loop
microglial
activation,
but
also
unique
anatomy
structure
astrocytes.
As
pathology
further
progresses,
resulting
in
environmental
changes,
M1-like
M2
crosstalk
with
A2.
While
communicate
simultaneously
neurons
blood
vessels
maintain
function
blood-brain
barrier
(BBB),
subtle
changes
may
identified
responded
astrocytes,
possibly
transferred
microglia.
Although
both
have
different
functional
characteristics,
they
achieve
immune
"optimization"
through
mutual
communication
cooperation
NVU
build
a
cascaded
network
amplification.
