Frontiers in Cell and Developmental Biology,
Год журнала:
2021,
Номер
9
Опубликована: Март 8, 2021
The
myelination
of
axons
by
oligodendrocytes
is
a
highly
complex
cell-to-cell
interaction.
Oligodendrocytes
and
have
reciprocal
signaling
relationship
in
which
receive
cues
from
that
direct
their
myelination,
subsequently
shape
axonal
structure
conduction.
are
necessary
for
the
maturation
excitatory
domains
on
axon
including
nodes
Ranvier,
help
buffer
potassium,
support
neuronal
energy
metabolism.
Disruption
oligodendrocyte-axon
unit
traumatic
injuries,
Alzheimer’s
disease
demyelinating
diseases
such
as
multiple
sclerosis
results
dysfunction
can
culminate
neurodegeneration.
In
this
review,
we
discuss
mechanisms
demyelination
loss
compromise
axons.
We
highlight
intra-axonal
cascades
initiated
result
irreversible
damage.
Both
restoration
oligodendrocyte
or
neuroprotective
therapies
targeting
these
likely
to
therapeutic
potential
disorders
disrupted.
Cell Reports,
Год журнала:
2020,
Номер
32(11), С. 108132 - 108132
Опубликована: Сен. 1, 2020
Gene
and
protein
expression
data
provide
useful
resources
for
understanding
brain
function,
but
little
is
known
about
the
lipid
composition
of
brain.
Here,
we
perform
quantitative
shotgun
lipidomics,
which
enables
a
cell-type-resolved
assessment
mouse
composition.
We
quantify
around
700
species
evaluate
features
including
fatty
acyl
chain
length,
hydroxylation,
number
double
bonds,
thereby
identifying
cell-type-
brain-region-specific
profiles
in
adult
mice,
as
well
aged
apolipoprotein-E-deficient
model
Alzheimer's
disease,
mice
fed
different
diets.
also
integrate
with
to
predict
pathways
enriched
specific
cell
types,
such
acid
β-oxidation
astrocytes
sphingolipid
metabolism
microglia.
This
resource
complements
existing
atlases
gene
may
be
role
lipids
function.
Nature Neuroscience,
Год журнала:
2022,
Номер
25(11), С. 1446 - 1457
Опубликована: Окт. 24, 2022
Abstract
A
hallmark
of
nervous
system
aging
is
a
decline
white
matter
volume
and
function,
but
the
underlying
mechanisms
leading
to
pathology
are
unknown.
In
present
study,
we
found
age-related
alterations
oligodendrocyte
cell
state
with
reduction
in
total
density
murine
matter.
Using
single-cell
RNA-sequencing,
identified
interferon
(IFN)-responsive
oligodendrocytes,
which
localize
proximity
CD8
+
T
cells
Absence
functional
lymphocytes
decreased
number
IFN-responsive
oligodendrocytes
rescued
loss,
whereas
T-cell
checkpoint
inhibition
worsened
response.
addition,
subpopulation
lymphocyte-dependent,
microglia
vicinity
summary,
provide
evidence
that
T-cell-induced,
important
modifiers
aging.
Neural Regeneration Research,
Год журнала:
2021,
Номер
16(9), С. 1702 - 1702
Опубликована: Янв. 1, 2021
Astrocytes
play
multifaceted
and
vital
roles
in
maintaining
neurophysiological
function
of
the
central
nervous
system
by
regulating
homeostasis,
increasing
synaptic
plasticity,
sustaining
neuroprotective
effects.
become
activated
as
a
result
inflammatory
responses
during
progression
pathological
changes
associated
with
neurodegenerative
disorders.
Reactive
astrocytes
(neurotoxic
A1
A2)
are
triggered
disease
pathogenesis
due
to
neuroinflammation
ischemia.
However,
only
limited
body
literature
describes
morphological
functional
diseases.
The
present
review
investigated
detrimental
beneficial
diseases
reported
recent
studies,
these
cells
have
promising
therapeutic
potential
offer
new
approaches
for
treatment
The
brain
is
responsive
to
an
ever-changing
environment,
enabling
the
organism
learn
and
change
behavior
accordingly.
Efforts
understand
underpinnings
of
this
plasticity
have
almost
exclusively
focused
on
functional
underlying
structural
changes
that
neurons
undergo
at
neurochemical
synapses.
What
has
received
comparatively
little
attention
involvement
activity-dependent
myelination
in
such
output
circuits
controlling
behavior.
traditionally
held
view
myelin
as
a
passive
insulator
axons
changing
one
lifelong
myelin,
modulated
by
neuronal
activity
experience.
We
review
nascent
evidence
role
strengthening
circuit
functions
underlie
learning
International Journal of Molecular Sciences,
Год журнала:
2021,
Номер
22(8), С. 4112 - 4112
Опубликована: Апрель 16, 2021
Vincristine-induced
peripheral
neurotoxicity
(VIPN)
is
a
very
common
side
effect
of
vincristine
chemotherapy
among
pediatric
patients
with
cancer.
Neuropathy
may
be
sensory,
motor
and/or
autonomic,
consequent
reduction,
delay
or
discontinuation
vincristine-chemotherapy,
but
also
pain,
disability,
reduced
quality
life
and
an
increase
in
medical
costs.
Vincristine
acts
out
its
antineoplastic
function
by
altering
the
normal
assembly
disassembly
microtubules,
their
mitosis
block
death.
leads
to
VIPN
through
complex
mechanism
damage,
which
occurs
not
only
on
endothelium
mitochondria
nerve
cells.
Furthermore,
both
patient-related
risk
factors
(age,
race,
ethnicity
genetic
polymorphisms)
treatment-related
(dose,
time
infusion
drug–drug
interactions)
are
involved
pathogenesis
VIPN.
There
lack
consensus
about
prophylaxis
treatment
oncologic
patients,
despite
several
molecules
(such
as
gabapentin,
pyridoxine
pyridostigmine,
glutamic
acid
glutamine)
having
been
already
investigated
clinical
trials.
This
review
describes
molecular
mechanisms
analyzes
principal
drugs
adopted
for
Alzheimer s & Dementia,
Год журнала:
2022,
Номер
19(1), С. 9 - 24
Опубликована: Март 2, 2022
Chitinase-3-like
protein
1
(CHI3L1/YKL-40)
has
long
been
known
as
a
biomarker
for
early
detection
of
neuroinflammation
and
disease
diagnosis
Alzheimer's
(AD).
In
the
brain,
CHI3L1
is
primarily
provided
by
astrocytes
heralds
reactive,
neurotoxic
state
triggered
inflammation
other
stress
signals.
However,
how
acts
in
or
it
contributes
to
AD
relevant
neurodegenerative
conditions
remains
unknown.
peripheral
tissues,
our
group
others
have
uncovered
that
master
regulator
wide
range
injury
repair
events,
including
innate
immunity
pathway
resembles
process
governed
microglia
astrocytes.
Based
on
assessment
current
knowledge
regarding
biology,
we
hypothesize
functions
signaling
molecule
mediating
distinct
neuroinflammatory
responses
brain
cells
misfunctions
precipitate
neurodegeneration.
We
also
recommend
future
research
directions
validate
such
assertions
better
understanding
mechanisms.
