International Journal of Molecular Sciences,
Journal Year:
2021,
Volume and Issue:
22(4), P. 1636 - 1636
Published: Feb. 6, 2021
Microglia
are
immune
brain
cells
involved
in
neuroinflammation.
They
express
a
lot
of
proteins
on
their
surface
such
as
receptors
that
can
be
activated
by
mediators
released
the
microglial
environment.
Among
these
receptors,
purinergic
receptor
expression
could
modified
depending
activation
status
microglia.
In
this
review,
we
focus
P2Y
and
more
specifically
P2RY12
is
motility
migration,
first
step
neuroinflammation
process.
We
describe
families,
structure,
physiological
functions.
The
pharmacological
genetic
tools
for
studying
detailed
thereafter.
Last
but
not
least,
report
contribution
to
acute
chronic
pathologies
order
better
understand
role.
Glia,
Journal Year:
2020,
Volume and Issue:
69(7), P. 1637 - 1653
Published: Dec. 28, 2020
Microglia
are
innate
immune
cells
of
the
central
nervous
system
that
sense
extracellular
cues.
Brain
injuries,
inflammation,
and
pathology
evoke
dynamic
structural
responses
in
microglia,
altering
their
morphology
motility.
The
motility
microglia
is
hypothesized
to
be
a
critical
first
step
sensing
local
alterations
engaging
pattern-specific
responses.
Alongside
pathological
responses,
also
regulate
neuronal
activity.
In
this
review,
we
consider
molecules,
receptors,
mechanisms
allow
activity
changes
under
both
hypoactivity
hyperactivity.
We
highlight
emerging
vivo
evidence
activity,
ranging
from
physiological
pathophysiological
conditions.
addition,
discuss
role
calcium
signaling
microglial
environment.
function
monitoring
influencing
may
for
brain
homeostasis
circuit
modification
health
disease.
Nature Neuroscience,
Journal Year:
2023,
Volume and Issue:
26(3), P. 406 - 415
Published: Feb. 6, 2023
Alzheimer's
disease
(AD)
is
characterized
by
synaptic
loss,
which
can
result
from
dysfunctional
microglial
phagocytosis
and
complement
activation.
However,
what
signals
drive
aberrant
microglia-mediated
engulfment
of
synapses
in
AD
unclear.
Here
we
report
that
secreted
phosphoprotein
1
(SPP1/osteopontin)
upregulated
predominantly
perivascular
macrophages
and,
to
a
lesser
extent,
fibroblasts.
Perivascular
SPP1
required
for
microglia
engulf
upregulate
phagocytic
markers
including
C1qa,
Grn
Ctsb
presence
amyloid-β
oligomers.
Absence
Spp1
expression
mouse
models
results
prevention
loss.
Furthermore,
single-cell
RNA
sequencing
putative
cell-cell
interaction
analyses
reveal
induces
states
the
hippocampus
model
AD.
Altogether,
suggest
functional
role
cells-to-microglia
crosstalk,
whereby
modulates
Frontiers in Aging Neuroscience,
Journal Year:
2022,
Volume and Issue:
14
Published: March 25, 2022
Traumatic
brain
injury
(TBI)
is
one
of
the
most
common
diseases
in
central
nervous
system
(CNS)
with
high
mortality
and
morbidity.
Patients
TBI
usually
suffer
many
sequelae
life
time
post
injury,
including
neurodegenerative
disorders
such
as
Alzheimer’s
disease
(AD)
Parkinson’s
(PD).
However,
pathological
mechanisms
connecting
these
two
processes
have
not
yet
been
fully
elucidated.
It
important
to
further
investigate
pathophysiological
underlying
TBI-induced
neurodegeneration,
which
will
promote
development
precise
treatment
target
for
notorious
consequences
after
TBI.
A
growing
body
evidence
shows
that
neuroinflammation
a
pivotal
process
chronic
neurodegeneration
following
Microglia,
immune
cells
CNS,
play
crucial
roles
other
CNS
diseases.
Of
interest,
microglial
activation
functional
alteration
has
proposed
key
mediators
evolution
pathology
Here,
we
review
updated
studies
involving
phenotypical
alterations
microglia
survey
molecules
regulating
activities
responses
pathology,
explore
their
potential
implications
injury.
The
work
give
us
comprehensive
understanding
driving
TBI-related
offer
novel
ideas
developing
corresponding
prevention
strategies
this
disease.
International Journal of Molecular Sciences,
Journal Year:
2021,
Volume and Issue:
22(4), P. 1636 - 1636
Published: Feb. 6, 2021
Microglia
are
immune
brain
cells
involved
in
neuroinflammation.
They
express
a
lot
of
proteins
on
their
surface
such
as
receptors
that
can
be
activated
by
mediators
released
the
microglial
environment.
Among
these
receptors,
purinergic
receptor
expression
could
modified
depending
activation
status
microglia.
In
this
review,
we
focus
P2Y
and
more
specifically
P2RY12
is
motility
migration,
first
step
neuroinflammation
process.
We
describe
families,
structure,
physiological
functions.
The
pharmacological
genetic
tools
for
studying
detailed
thereafter.
Last
but
not
least,
report
contribution
to
acute
chronic
pathologies
order
better
understand
role.