Brain Sciences,
Journal Year:
2024,
Volume and Issue:
14(12), P. 1213 - 1213
Published: Nov. 29, 2024
Tinnitus
is
correlated
with
anomalies
of
neural
plasticity
and
has
been
found
to
be
affected
by
inflammatory
status.
The
current
theories
on
tinnitus,
although
still
somewhat
incomplete,
are
based
maladaptive
mechanisms.
Astrocytes
play
a
major
role
in
both
responses
inflammation
regulation;
moreover,
they
have
recently
discovered
encode
“context”
for
neuronal
circuits,
which
similar
the
“expectation”
Bayesian
brain
models.
Therefore,
this
narrative
review
explores
possible
likely
roles
astrocytes
mechanisms
leading
acute
chronic
tinnitus.
Brain Sciences,
Journal Year:
2024,
Volume and Issue:
14(3), P. 284 - 284
Published: March 15, 2024
Diabetes
is
a
chronic
metabolic
condition
associated
with
high
levels
of
blood
glucose
which
leads
to
serious
damage
the
heart,
kidney,
eyes,
and
nerves.
Elevated
brain
function
cognitive
abilities.
They
also
lead
various
neurological
neuropsychiatric
disorders,
including
neurodegeneration
decline.
High
neuronal
can
cause
drastic
due
neurotoxicity.
Astrocytes,
type
glial
cell,
play
vital
role
in
maintaining
through
neuron–astrocyte
coupling.
Hyperglycemia
progressive
decline
networks
impairment,
contributing
dysfunction
fostering
neurodegenerative
environment.
In
this
review,
we
summarize
connections,
functions,
impairments
cells
diabetic
brain.
We
effects
hyperglycemia
on
functions
International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(20), P. 15430 - 15430
Published: Oct. 21, 2023
In
the
last
two
decades,
there
has
been
increasing
evidence
supporting
non-neuronal
cells
as
active
contributors
to
neurodegenerative
disorders.
Among
glial
cells,
astrocytes
play
a
pivotal
role
in
driving
amyotrophic
lateral
sclerosis
(ALS)
progression,
leading
scientific
community
focus
on
"astrocytic
signature"
ALS.
Here,
we
summarized
main
pathological
mechanisms
characterizing
astrocyte
contribution
MN
damage
and
ALS
such
neuroinflammation,
mitochondrial
dysfunction,
oxidative
stress,
energy
metabolism
impairment,
miRNAs
extracellular
vesicles
contribution,
autophagy
protein
misfolding,
altered
neurotrophic
factor
release.
Since
glutamate
excitotoxicity
is
one
of
most
relevant
features,
focused
specific
this
aspect,
highlighting
known
or
potential
molecular
by
which
participate
level
and,
conversely,
undergo
toxic
effect
excessive
glutamate.
scenario,
can
behave
"producers"
"targets"
high
levels,
going
through
changes
that
affect
themselves
turn,
neuronal
surrounding
thus
actively
impacting
course.
Moreover,
review
aims
point
out
knowledge
gaps
deserve
further
investigation.
Cells,
Journal Year:
2024,
Volume and Issue:
13(7), P. 606 - 606
Published: March 30, 2024
In
vitro
and
preclinical
in
vivo
research
the
last
35
years
has
clearly
highlighted
crucial
physiopathological
role
of
glial
cells,
namely
astrocytes/microglia/oligodendrocytes
satellite
cells/Schwann
cells
central
peripheral
nervous
system,
respectively.
Several
possible
pharmacological
targets
to
various
neurodegenerative
disorders
painful
conditions
have
therefore
been
successfully
identified,
including
receptors
enzymes,
mediators
neuroinflammation.
However,
translation
these
promising
data
a
clinical
setting
is
often
hampered
by
both
technical
biological
difficulties,
making
it
necessary
perform
experiments
on
human
models
diseases.
this
review
we
will,
therefore,
summarize
most
relevant
contribution
pathologies
their
modulation
based
obtained
post-mortem
tissues
iPSC-derived
brain
organoids.
The
possibility
an
visualization
glia
reaction
neuroinflammation
patients
will
be
also
discussed.
Extracellular Vesicle,
Journal Year:
2024,
Volume and Issue:
3, P. 100044 - 100044
Published: May 13, 2024
Spinal
cord
injury
(SCI)
is
the
damage
to
spinal
causing
paralysis
below
site
compromised
patient
life
quality.
Exosomes
are
nanosized
vesicles
released
during
physiological
or
pathological
processes.
They
present
a
promising
avenue
for
therapeutic
drug
delivery
due
their
tissue
specificity
and
biocompatibility,
offering
enhanced
efficacy
with
reduced
accumulation-based
toxicity.
In
SCI,
exosomes
target
inflammation,
apoptosis,
microglial
polarization,
autophagy,
contributing
interventions.
This
article
comprehensively
explores
pathophysiology
of
diverse
exosome
synthesis
processes,
limitations
challenges
overcome,
potential
from
various
cellular
sources
in
SCI
treatment.
Journal of Neurochemistry,
Journal Year:
2025,
Volume and Issue:
169(2)
Published: Feb. 1, 2025
Oxidative
stress-mediated
astrocytic
damage
contributes
to
nerve
injury
and
the
development
of
depression,
especially
under
stress
conditions.
Peroxisomes
pexophagy
are
essential
for
balancing
oxidative
protein
degradation
products.
Our
previous
findings
suggest
that
peroxisome
proliferators-activated
receptor
β/δ
(PPARβ/δ)
activation
significantly
alleviates
depressive
behaviors
by
preventing
injury.
However,
underlying
mechanisms
remain
unclear.
In
present
study,
we
established
treating
astrocytes
with
corticosterone.
Subsequently,
PPARβ/δ
agonists
antagonists
were
applied
determine
effects
on
peroxisomes
in
astrocytes.
The
agonist
(GW0742)
improved
cell
viability
decreased
intracellular
reactive
oxygen
species
(ROS)
production
induced
corticosterone,
while
pretreatment
PPARβ/δ,
antagonist
GSK3787
reversed
GW0742.
Moreover,
activating
promoted
peroxisomal
biogenesis
factor
5
(PEX5)-mediated
enhancing
phosphorylation
ataxia-telangiectasia
mutated
(ATM)
kinase.
Conversely,
blocking
partially
abolished
Further
investigations
demonstrated
not
only
transcription
ubiquitin
ligase
E3
component
n-recognin
(UBR5)
but
also
enhanced
interaction
between
UBR5,
contributing
ATM
interactor
(ATMIN)
degradation,
increased
phosphorylated
kinase
levels.
Therefore,
this
study
revealed
improves
corticosterone-induced
pexophagy.
directly
interacts
UBR5
facilitate
ATMIN
promotes
phosphorylation,
thereby
maintaining
balance
These
is
a
potential
target
promoting
upon
stress.
Frontiers in Cellular Neuroscience,
Journal Year:
2025,
Volume and Issue:
19
Published: April 23, 2025
Major
depressive
disorder
(MDD)
is
one
of
the
most
common
mental
health
conditions,
characterized
by
pervasive
and
persistent
low
mood,
self-esteem,
a
loss
interest
or
pleasure
in
activities
that
are
typically
enjoyable.
Despite
decades
research
into
etiology
pathophysiological
mechanisms
depression,
therapeutic
outcomes
for
many
individuals
remain
less
than
expected.
A
promising
new
area
focuses
on
stress-induced
neuroinflammatory
processes,
such
as
excessive
activation
crosstalk
microglia
astrocytes
central
nervous
system
under
stress,
well
elevated
levels
pro-inflammatory
cytokines,
which
closely
linked
to
onset
progression
depression.
This
review
summarizes
through
neuroinflammation
induces
promotes
development
also
highlights
effective
roles
small
molecules
with
anti-inflammatory
activity
treatment
MDD.
Understanding
specific
further
impacts
using
technologies
single-cell
RNA
sequencing
elucidate
subtypes
interactions
great
importance
developing
more
strategies
Physiology,
Journal Year:
2024,
Volume and Issue:
39(4), P. 208 - 217
Published: March 26, 2024
Astrocytes
are
no
longer
considered
as
passive
support
cells.
In
the
hypothalamus,
these
glial
cells
actively
participate
in
control
of
appetite,
energy
expenditure,
and
processes
leading
to
obesity
its
secondary
complications.
Here
we
briefly
review
studies
supporting
this
conclusion
advances
made
understanding
underlying
mechanisms.
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(11), P. 5711 - 5711
Published: May 24, 2024
Toll-like
receptors
(TLRs)
are
among
the
main
components
of
innate
immune
system.
They
can
detect
conserved
structures
in
microorganisms
and
molecules
associated
with
stress
cellular
damage.
TLRs
expressed
resident
cells
both
neurons
glial
nervous
Increasing
evidence
is
emerging
on
participation
not
only
response
but
also
processes
system,
such
as
neurogenesis
cognition.
Below,
we
present
a
review
literature
that
evaluates
expression
role
neurodevelopment,
behavior,
cognition,
infection,
neuroinflammation,
neurodegeneration.
