bioRxiv (Cold Spring Harbor Laboratory),
Год журнала:
2024,
Номер
unknown
Опубликована: Дек. 21, 2024
Abstract
Oligodendrocytes
are
the
myelinating
cells
of
central
nervous
system.
Regulation
early
stages
oligodendrocyte
development
is
critical
to
function
cell.
Specifically,
myelin
sheath
formation
an
energetically
demanding
event
that
requires
precision,
as
alterations
may
lead
dysmyelination.
Recent
work
has
established
fatty
acid
β-oxidation
required
for
oligodendrocytes.
We
have
shown
MCL-1,
a
well-characterized
anti-apoptotic
protein,
oligodendrocytes
in
vivo
.
Further,
it
was
recently
uncovered
MCL-1
regulates
long-
chain
through
its
interaction
with
acyl-CoA
synthetase
long-chain
family
member
1
(ACSL1),
enzyme
responsible
conversion
acids
into
acyl-CoA.
Here,
we
introduce
vitro
system
isolate
human
stem
cell-
derived
progenitor
and
investigate
involvement
during
development.
Using
this
system,
pharmacologically
inhibited
(OPCs)
elucidate
non-apoptotic
protein
at
developmental
stage.
Additionally,
used
motor
neuron
co-culture
downstream
effects
inhibition
later
when
begin
contact
axons
generate
basic
protein.
demonstrate
mitochondrial
network
changes
resemble
those
reported
Our
findings
point
factor
essential
OPC
stage
proper
morphogenesis.
Cell Communication and Signaling,
Год журнала:
2024,
Номер
22(1)
Опубликована: Июнь 7, 2024
Alzheimer's
disease
is
the
most
common
cause
of
dementia
and
characterized
by
amyloid-β
plaques,
tau
neurofibrillary
tangles,
neuronal
loss.
Although
loss
a
primary
hallmark
disease,
it
known
that
non-neuronal
cell
populations
are
ultimately
responsible
for
maintaining
brain
homeostasis
health
through
neuron-glia
glial
crosstalk.
Many
signaling
pathways
have
been
proposed
to
be
dysregulated
in
including
WNT,
TGFβ,
p53,
mTOR,
NFkB,
Pi3k/Akt
signaling.
Here,
we
predict
altered
cell-cell
communication
between
glia
neurons.
Molecular Psychiatry,
Год журнала:
2024,
Номер
unknown
Опубликована: Дек. 5, 2024
Abstract
Dysfunctional
glial
cells
play
a
pre-eminent
role
in
schizophrenia
pathophysiology.
Post-mortem
studies
have
provided
evidence
for
significantly
decreased
cell
numbers
different
brain
regions
of
individuals
with
schizophrenia.
Reduced
are
most
pronounced
oligodendroglia,
but
reduced
astrocyte
densities
also
been
reported.
This
review
highlights
that
oligo-
and
astroglial
deficits
key
histopathological
feature
schizophrenia,
distinct
from
typical
changes
seen
neurodegenerative
disorders.
Significant
oligodendrocytes
may
arise
two
ways:
(i)
demise
mature
functionally
compromised
oligodendrocytes;
(ii)
lack
due
to
failed
maturation
progenitor
cells.
We
analyse
detail
the
controversy
regarding
astrocytes.
Regardless
their
origin,
several
pathophysiological
consequences.
Among
these,
myelination
number
be
important
factor,
resulting
disconnectivity
between
neurons
observed
When
die,
it
appears
through
degeneration,
process
which
is
basically
reversible.
Thus,
therapeutic
interventions
help
rescue
or
improve
might
viable
option.
Since
antipsychotic
treatment
alone
does
not
seem
prevent
loss
deficits,
there
intense
search
new
options.
Current
proposals
range
application
antidepressants
other
chemical
agents
as
well
physical
exercise
engrafting
healthy
into
brains
patients.
Nature Communications,
Год журнала:
2025,
Номер
16(1)
Опубликована: Янв. 30, 2025
Abstract
Oligodendrocyte
precursor
cells
(OPCs)
shape
brain
function
through
many
non-canonical
regulatory
mechanisms
beyond
myelination.
Here
we
show
that
OPCs
form
contacts
with
their
processes
on
neuronal
somata
in
a
activity-dependent
manner.
These
facilitate
exocytosis
of
lysosomes.
A
reduction
the
number
or
branching
reduces
these
contacts,
which
is
associated
lysosome
accumulation
and
altered
metabolism
neurons
more
senescent
age.
similar
OPC
seen
an
early-stage
mouse
model
Alzheimer’s
disease.
Our
findings
have
implications
for
prevention
age-related
pathologies
treatment
neurodegenerative
diseases.
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(8), С. 4452 - 4452
Опубликована: Апрель 18, 2024
Schizophrenia
is
a
significant
worldwide
health
concern,
affecting
over
20
million
individuals
and
contributing
to
potential
reduction
in
life
expectancy
by
up
14.5
years.
Despite
its
profound
impact,
the
precise
pathological
mechanisms
underlying
schizophrenia
continue
remain
enigmatic,
with
previous
research
yielding
diverse
occasionally
conflicting
findings.
Nonetheless,
one
consistently
observed
phenomenon
brain
imaging
studies
of
patients
disruption
white
matter,
bundles
myelinated
axons
that
provide
connectivity
rapid
signalling
between
regions.
Myelin
produced
specialised
glial
cells
known
as
oligodendrocytes,
which
have
been
shown
be
disrupted
post-mortem
analyses
patients.
Oligodendrocytes
are
generated
throughout
major
population
oligodendrocyte
progenitor
(OPC),
essential
for
matter
plasticity.
Notably,
decline
specific
subpopulation
OPC
has
identified
principal
factor
loss
aging
brain,
suggesting
this
may
also
schizophrenia.
In
review,
we
analysed
genomic
databases
pinpoint
intersections
identify
shared
cognitive
dysfunction.
Frontiers in Immunology,
Год журнала:
2024,
Номер
15
Опубликована: Июль 9, 2024
Oligodendrocyte
precursor
cells
(OPCs)
have
long
been
regarded
as
progenitors
of
oligodendrocytes,
yet
recent
advances
illuminated
their
multifaceted
nature
including
emerging
immune
functions.
This
review
seeks
to
shed
light
on
the
functions
exhibited
by
OPCs,
spanning
from
phagocytosis
modulation
and
direct
engagement
with
across
various
pathological
scenarios.
Comprehensive
understanding
OPCs
alongside
other
roles
will
pave
way
for
targeted
therapies
in
neurological
disorders.
Journal of Biomedical Science,
Год журнала:
2024,
Номер
31(1)
Опубликована: Сен. 17, 2024
Traumatic
brain
injury
(TBI)
causes
axon
tearing
and
synapse
degradation,
resulting
in
multiple
neurological
dysfunctions
exacerbation
of
early
neurodegeneration;
the
repair
axonal
synaptic
structures
is
critical
for
restoring
neuronal
function.
C-C
Motif
Chemokine
Ligand
5
(CCL5)
shows
many
neuroprotective
activities.
PLoS Biology,
Год журнала:
2025,
Номер
23(1), С. e3002977 - e3002977
Опубликована: Янв. 8, 2025
The
major
pathological
feature
of
Parkinson
‘s
disease
(PD),
the
second
most
common
neurodegenerative
and
movement
disorder,
is
predominant
degeneration
dopaminergic
neurons
in
substantia
nigra,
a
part
midbrain.
Despite
decades
research,
molecular
mechanisms
origin
remain
unknown.
While
was
initially
viewed
as
purely
neuronal
results
from
single-cell
transcriptomics
have
suggested
that
oligodendrocytes
may
play
an
important
role
early
stages
Parkinson’s.
Although
these
findings
are
high
relevance,
particularly
to
search
for
effective
disease-modifying
therapies,
actual
functional
Parkinson’s
remains
highly
speculative
requires
concerted
scientific
effort
be
better
understood.
This
Unsolved
Mystery
discusses
limited
understanding
PD,
highlighting
unresolved
questions
regarding
changes
oligodendroglia,
myelin
nigral
neurons,
impact
toxic
environment,
aggregation
alpha-synuclein
within
oligodendrocytes.
Epilepsy
is
a
chronic
neurological
disorder
marked
by
recurrent
seizures,
significantly
impacting
individuals
worldwide.
Current
treatments
are
often
ineffective
for
third
of
patients
and
can
cause
severe
side
effects,
necessitating
new
therapeutic
approaches.
Glial
cells,
particularly
astrocytes,
microglia,
oligodendrocytes,
emerging
as
crucial
targets
in
epilepsy
management.
Astrocytes
regulate
neuronal
homeostasis,
excitability,
synaptic
plasticity,
playing
key
roles
maintaining
the
blood-brain
barrier
(BBB)
mediating
neuroinflammatory
responses.
Dysregulated
astrocyte
functions,
such
reactive
astrogliosis,
lead
to
abnormal
activity
seizure
generation.
They
release
gliotransmitters,
cytokines,
chemokines
that
may
exacerbate
or
mitigate
seizures.
Microglia,
innate
immune
cells
CNS,
contribute
neuroinflammation,
glutamate
excitotoxicity,
balance
between
excitatory
inhibitory
neurotransmission,
underscoring
their
dual
role
promotion
protection.
Meanwhile,
primarily
involved
myelination,
also
modulate
axonal
excitability
neuron-glia
network
underlying
pathogenesis.
Understanding
dynamic
interactions
glial
with
neurons
provides
promising
avenues
novel
therapies.
Targeting
these
improved
control
better
clinical
outcomes,
offering
hope
refractory
epilepsy.
