Frontiers in Cellular Neuroscience,
Journal Year:
2019,
Volume and Issue:
13
Published: Feb. 25, 2019
Synapse
loss
is
an
early
feature
shared
by
many
neurodegenerative
diseases,
and
it
represents
the
major
correlate
of
cognitive
impairment.
Recent
studies
reveal
that
microglia
astrocytes
play
a
role
in
synapse
elimination,
contributing
to
network
dysfunction
associated
with
neurodegeneration.
Excitatory
inhibitory
activity
can
be
affected
glia-mediated
loss,
resulting
imbalanced
synaptic
transmission
subsequent
dysfunction.
Here
we
review
recent
literature
on
contribution
glia
excitatory/inhibitory
imbalance,
context
most
common
disorders.
A
better
understanding
mechanisms
underlying
pathological
will
instrumental
design
targeted
therapeutic
interventions,
taking
account
emerging
roles
remodeling.
Cell Reports Medicine,
Journal Year:
2023,
Volume and Issue:
4(9), P. 101175 - 101175
Published: Aug. 30, 2023
Synapse
loss
correlates
with
cognitive
decline
in
Alzheimer's
disease
(AD).
Data
from
mouse
models
suggests
microglia
are
important
for
synapse
degeneration,
but
direct
human
evidence
any
glial
involvement
removal
AD
remains
to
be
established.
Here
we
observe
astrocytes
and
brains
contain
greater
amounts
of
synaptic
protein
compared
non-disease
controls,
that
proximity
amyloid-β
plaques
the
APOE4
risk
gene
exacerbate
this
effect.
In
culture,
primary
phagocytose
patient-derived
synapses
more
than
controls.
Inhibiting
interactions
MFG-E8
rescues
elevated
engulfment
by
without
affecting
control
uptake.
Thus,
promotes
increased
ingestion
cells
at
least
part
via
an
opsonophagocytic
mechanism
potential
targeted
therapeutic
manipulation.
Frontiers in Molecular Neuroscience,
Journal Year:
2023,
Volume and Issue:
16
Published: June 8, 2023
Astrocytes
are
an
abundantly
distributed
population
of
glial
cells
in
the
central
nervous
system
(CNS)
that
perform
myriad
functions
normal
and
injured/diseased
brain.
exhibit
heterogeneous
phenotypes
response
to
various
insults,
a
process
known
as
astrocyte
reactivity.
The
accuracy
precision
brain
signaling
primarily
based
on
interactions
involving
neurons,
astrocytes,
oligodendrocytes,
microglia,
pericytes,
dendritic
within
CNS.
have
emerged
critical
entity
because
their
unique
role
recycling
neurotransmitters,
actively
modulating
ionic
environment,
regulating
cholesterol
sphingolipid
metabolism,
influencing
cellular
crosstalk
diverse
neural
injury
conditions
neurodegenerative
disorders.
However,
little
is
about
how
synapse
formation,
axon
specification,
neuroplasticity,
homeostasis,
network
activity
following
dynamic
surveillance,
CNS
structure
neurological
diseases.
Interestingly,
tripartite
hypothesis
came
light
fill
some
knowledge
gaps
constitute
interaction
subpopulation
synapses.
This
review
highlights
astrocytes'
health
neurological/neurodegenerative
diseases
arising
from
omnidirectional
between
astrocytes
neurons
at
synapse.
also
recapitulates
disruption
with
focus
perturbations
homeostatic
astrocytic
function
key
driver
modulate
molecular
physiological
processes
toward
Proceedings of the National Academy of Sciences,
Journal Year:
2024,
Volume and Issue:
121(22)
Published: May 23, 2024
The
prion-like
spread
of
protein
aggregates
is
a
leading
hypothesis
for
the
propagation
neurofibrillary
lesions
in
brain,
including
tau
inclusions
associated
with
Alzheimer’s
disease.
mechanisms
cellular
uptake
seeds
and
subsequent
nucleated
polymerization
cytosolic
are
major
questions
field,
potential
coupling
between
entry
nucleation
has
been
little
explored.
We
found
that
primary
astrocytes
neurons,
endocytosis
leads
to
their
accumulation
lysosomes.
This
turn
lysosomal
swelling,
deacidification,
recruitment
ESCRT
proteins,
but
not
Galectin-3,
membrane.
These
observations
consistent
nanoscale
damage
Live
cell
imaging
STORM
superresolution
microscopy
further
show
occurs
primarily
at
lysosome
membrane
under
these
conditions.
data
suggest
escape
from
lysosomes
via
rather
than
wholesale
rupture
commences
as
soon
fibril
ends
emerge
International Journal of Molecular Sciences,
Journal Year:
2018,
Volume and Issue:
19(9), P. 2834 - 2834
Published: Sept. 19, 2018
When
a
main
artery
of
the
brain
occludes,
cellular
response
involving
multiple
cell
types
follows.
Cells
directly
affected
by
lack
glucose
and
oxygen
in
neuronal
core
die
necrosis.
In
periphery
surrounding
ischemic
(the
so-called
penumbra)
neurons,
astrocytes,
microglia,
oligodendrocytes,
pericytes,
endothelial
cells
react
to
detrimental
factors
such
as
excitotoxicity,
oxidative
stress,
inflammation
different
ways.
The
fate
neurons
this
area
is
multifactorial,
communication
between
all
players
important
for
survival.
This
review
focuses
on
latest
research
relating
synaptic
loss
release
apoptotic
bodies
other
extracellular
vesicles
stroke.
We
also
point
out
possible
treatment
options
related
increasing
survival
regeneration
penumbra.
Frontiers in Cellular Neuroscience,
Journal Year:
2019,
Volume and Issue:
13
Published: Feb. 25, 2019
Synapse
loss
is
an
early
feature
shared
by
many
neurodegenerative
diseases,
and
it
represents
the
major
correlate
of
cognitive
impairment.
Recent
studies
reveal
that
microglia
astrocytes
play
a
role
in
synapse
elimination,
contributing
to
network
dysfunction
associated
with
neurodegeneration.
Excitatory
inhibitory
activity
can
be
affected
glia-mediated
loss,
resulting
imbalanced
synaptic
transmission
subsequent
dysfunction.
Here
we
review
recent
literature
on
contribution
glia
excitatory/inhibitory
imbalance,
context
most
common
disorders.
A
better
understanding
mechanisms
underlying
pathological
will
instrumental
design
targeted
therapeutic
interventions,
taking
account
emerging
roles
remodeling.
