Annual Review of Cell and Developmental Biology,
Год журнала:
2023,
Номер
39(1), С. 409 - 434
Опубликована: Июль 5, 2023
The
life
of
eukaryotic
cells
requires
the
transport
lipids
between
membranes,
which
are
separated
by
aqueous
environment
cytosol.
Vesicle-mediated
traffic
along
secretory
and
endocytic
pathways
lipid
transfer
proteins
(LTPs)
cooperate
in
this
transport.
Until
recently,
known
LTPs
were
shown
to
carry
one
or
a
few
at
time
thought
mediate
shuttle-like
mechanisms.
Over
last
years,
new
family
has
been
discovered
that
is
defined
repeating
β-groove
(RBG)
rod-like
structure
with
hydrophobic
channel
running
their
entire
length.
This
localization
these
membrane
contact
sites
suggest
bridge-like
mechanism
Mutations
some
result
neurodegenerative
developmental
disorders.
Here
we
review
properties
well-established
putative
physiological
roles
proteins,
highlight
many
questions
remain
open
about
functions.
Neuronal
circuit
assembly
requires
the
fine
balance
between
synapse
formation
and
elimination.
Microglia,
through
elimination
of
supernumerary
synapses,
have
an
established
role
in
this
process.
While
microglial
receptor
TREM2
soluble
complement
proteins
C1q
C3
are
recognized
as
key
players,
neuronal
molecular
components
that
specify
synapses
to
be
eliminated
still
undefined.
Here,
we
show
exposed
phosphatidylserine
(PS)
represents
a
"eat-me"
signal
involved
microglial-mediated
pruning.
In
hippocampal
neuron
microglia
co-cultures,
can
partially
prevented
by
blocking
accessibility
PS
using
Annexin
V
or
loss
TREM2.
vivo,
exposure
at
both
retinogeniculate
engulfment
PS-labeled
material
occurs
during
developmental
periods
Mice
deficient
C1q,
which
fail
properly
refine
connections,
elevated
presynaptic
reduced
microglia.
These
data
provide
mechanistic
insight
into
pruning
identify
novel
developmentally
regulated
is
common
among
developing
brain
structures.
Science,
Год журнала:
2020,
Номер
370(6512), С. 66 - 69
Опубликована: Окт. 2, 2020
Dementia
is
a
rapidly
rising
global
health
crisis
that
silently
disables
families
and
ends
lives
livelihoods
around
the
world.
To
date,
however,
no
early
biomarkers
or
effective
therapies
exist.
It
now
clear
brain
microglia
are
more
than
mere
bystanders
amyloid
phagocytes;
they
can
act
as
governors
of
neuronal
function
homeostasis
in
adult
brain.
Here,
we
highlight
fundamental
role
tissue-resident
macrophages
health.
Then,
suggest
how
chronic
impairment
microglia-neuron
cross-talk
may
secure
permanence
failure
synaptic
Alzheimer's
Parkinson's
diseases.
Understanding
to
assess
modulate
interactions
critical
for
will
be
key
developing
dementia.
Neural Regeneration Research,
Год журнала:
2021,
Номер
17(4), С. 705 - 705
Опубликована: Авг. 29, 2021
Microglia
are
the
resident
macrophages
of
central
nervous
system.
possess
varied
morphologies
and
functions.
Under
normal
physiological
conditions,
microglia
mainly
exist
in
a
resting
state
constantly
monitor
their
microenvironment
survey
neuronal
synaptic
activity.
Through
C1q,
C3
CR3
"Eat
Me"
CD47
SIRPα
"Don't
Eat
complement
pathways,
as
well
other
pathways
such
CX3CR1
signaling,
regulate
pruning,
process
crucial
for
promotion
synapse
formation
regulation
activity
plasticity.
By
mediating
play
an
important
role
experience-dependent
plasticity
barrel
cortex
visual
after
whisker
removal
or
monocular
deprivation,
also
learning
memory,
including
modulation
memory
strength,
forgetfulness,
quality.
As
response
to
brain
injury,
infection
neuroinflammation,
become
activated
increase
number.
Activated
change
amoeboid
shape,
migrate
sites
inflammation
secrete
proteins
cytokines,
chemokines
reactive
oxygen
species.
These
molecules
released
by
can
lead
deficits
associated
with
aging,
Alzheimer's
disease,
traumatic
HIV-associated
neurocognitive
disorder,
neurological
mental
disorders
autism,
depression
post-traumatic
stress
disorder.
With
focus
on
recently
published
literature,
here
we
reviewed
studies
investigating
how
modulate
disease-related
deficits.
summarizing
function
these
processes,
aim
provide
overview
discuss
possibility
manipulation
therapeutic
ameliorate
cognitive
disorders.
Brain
organoids
have
been
used
to
recapitulate
the
processes
of
brain
development
and
related
diseases.
However,
lack
vasculatures,
which
regulate
neurogenesis
disorders,
limits
utility
organoids.
In
this
study,
we
induced
vessel
organoids,
respectively,
then
fused
two
types
together
obtain
vascularized
The
were
engrafted
with
robust
vascular
network-like
structures
exhibited
increased
number
neural
progenitors,
in
line
possibility
that
vessels
development.
Fusion
also
contained
functional
blood–brain
barrier-like
structures,
as
well
microglial
cells,
a
specific
population
immune
cells
brain.
incorporated
microglia
responded
actively
stimuli
showed
ability
engulfing
synapses.
Thus,
fusion
established
study
allow
modeling
interactions
between
neuronal
non-neuronal
components
vitro,
particularly
vasculature
niche.
