Cell Reports,
Journal Year:
2016,
Volume and Issue:
15(2), P. 238 - 246
Published: April 1, 2016
How
aging
impacts
axon
regeneration
after
CNS
injury
is
not
known.
We
assessed
the
impact
of
age
on
induced
by
Pten
deletion
in
corticospinal
and
rubrospinal
neurons,
two
neuronal
populations
with
distinct
innate
regenerative
abilities.
As
young
mice,
older
mice
remains
effective
preventing
axotomy-induced
decline
neuron-intrinsic
growth
state,
as
mTOR
activity,
soma
size,
axonal
proximal
to
a
spinal
cord
injury.
However,
distal
greatly
diminished,
accompanied
increased
expression
astroglial
inflammatory
markers
at
site.
Thus,
mammalian
undergoes
an
age-dependent
regeneration,
revealed
when
state
elevated.
These
results
have
important
implications
for
developing
strategies
promote
repair
injuries
or
diseases,
which
increasingly
affect
middle-aged
populations.
Frontiers in Cellular Neuroscience,
Journal Year:
2017,
Volume and Issue:
11
Published: Feb. 13, 2017
Glial
cells,
consisting
of
microglia,
astrocytes
and
oligodendrocyte
lineage
cells
as
their
major
components,
constitute
a
large
fraction
the
mammalian
brain.
Originally
considered
purely
non-functional
glue
for
neurons,
decades
research
have
highlighted
importance
well
further
functions
glial
cells.
Although
many
aspects
these
are
characterized
nowadays,
different
populations
in
brain
under
both
physiological
pathological
conditions
remain,
at
least
to
certain
extent,
unresolved.
To
tackle
important
questions,
broad
range
depletion
approaches
been
developed
which
or
(i.e.
NG2-glia
oligodendrocytes)
specifically
ablated
from
adult
network
with
subsequent
analysis
consequences.
As
very
heterogeneous,
it
is
imperative
ablate
single
cell
instead
inducing
death
all
general.
Thanks
modern
genetic
manipulation
methods,
can
now
directly
be
targeted
type
interest
making
ablation
more
specific
compared
general
that
used
earlier
on.
In
this
review
we
will
give
detailed
summary
on
studies,
focusing
mouse
central
nervous
system
(CNS)
functional
readouts.
We
also
provide
an
outlook
how
could
exploited
future.
Glia,
Journal Year:
2018,
Volume and Issue:
67(6), P. 1017 - 1035
Published: Dec. 11, 2018
Abstract
Neuroinflammation
in
the
central
nervous
system
(CNS)
is
an
important
subject
of
neuroimmunological
research.
Emerging
evidence
suggests
that
neuroinflammation
a
key
player
various
neurological
disorders,
including
neurodegenerative
diseases
and
CNS
injury.
complex
well‐orchestrated
process
by
groups
glial
cells
peripheral
immune
cells.
The
cross‐talks
between
extremely
dynamic
which
resembles
symphony.
However,
understanding
how
interact
with
each
other
to
shape
distinctive
responses
remains
limited.
In
this
review,
we
will
discuss
joint
actions
three
phases
neuroinflammation,
initiation,
progression,
prognosis,
movements
symphony,
as
role
type
depends
on
nature
inflammatory
cues
specific
course
diseases.
This
perspective
might
provide
helpful
clues
development
early
diagnosis
therapeutic
intervention
Nature Communications,
Journal Year:
2017,
Volume and Issue:
8(1)
Published: March 20, 2017
Abstract
Injury
to
the
central
nervous
system
(CNS)
alters
molecular
and
cellular
composition
of
neural
tissue
leads
glial
scarring,
which
inhibits
regrowth
damaged
axons.
Mammalian
scars
supposedly
form
a
chemical
mechanical
barrier
neuronal
regeneration.
While
tremendous
effort
has
been
devoted
identifying
characteristics
scar,
very
little
is
known
about
its
properties.
Here
we
characterize
spatiotemporal
changes
elastic
stiffness
injured
rat
neocortex
spinal
cord
at
1.5
three
weeks
post-injury
using
atomic
force
microscopy.
In
contrast
in
other
mammalian
tissues,
CNS
significantly
softens
after
injury.
Expression
levels
intermediate
filaments
(GFAP,
vimentin)
extracellular
matrix
components
(laminin,
collagen
IV)
correlate
with
softening.
As
regulator
growth,
our
results
may
help
understand
why
neurons
do
not
regenerate
Disease Models & Mechanisms,
Journal Year:
2016,
Volume and Issue:
9(10), P. 1125 - 1137
Published: Oct. 1, 2016
ABSTRACT
A
long-standing
goal
of
spinal
cord
injury
research
is
to
develop
effective
repair
strategies
for
the
clinic.
Rat
models
provide
an
important
mammalian
model
in
which
evaluate
treatment
and
understand
pathological
basis
injuries.
These
have
facilitated
development
robust
tests
assessing
recovery
locomotor
sensory
functions.
also
allowed
us
how
neuronal
circuitry
changes
following
could
be
promoted
by
enhancing
spontaneous
regenerative
mechanisms
counteracting
intrinsic
inhibitory
factors.
studies
revealed
possible
routes
rescuing
cells
acute
stage
injury.
Spatiotemporal
functional
these
highlight
therapeutic
potential
manipulating
inflammation,
scarring
myelination.
In
addition,
replacement
therapies
injury,
including
grafts
bridges,
stem
primarily
from
rat
studies.
Here,
we
discuss
advantages
disadvantages
experimental
summarize
knowledge
gained
models.
We
emerging
understanding
different
forms
their
pathology
degree
has
inspired
numerous
strategies,
some
led
clinical
trials.
Cell,
Journal Year:
2018,
Volume and Issue:
173(1), P. 153 - 165.e22
Published: March 1, 2018
CNS
injury
often
severs
axons.
Scar
tissue
that
forms
locally
at
the
lesion
site
is
thought
to
block
axonal
regeneration,
resulting
in
permanent
functional
deficits.
We
report
inhibiting
generation
of
progeny
by
a
subclass
pericytes
led
decreased
fibrosis
and
extracellular
matrix
deposition
after
spinal
cord
mice.
Regeneration
raphespinal
corticospinal
tract
axons
was
enhanced
sensorimotor
function
recovery
improved
following
animals
with
attenuated
pericyte-derived
scarring.
Using
optogenetic
stimulation,
we
demonstrate
regenerated
integrated
into
local
circuitry
below
site.
The
number
correlated
recovery.
In
conclusion,
attenuation
represents
promising
therapeutic
approach
facilitate
injury.
Cold Spring Harbor Perspectives in Biology,
Journal Year:
2014,
Volume and Issue:
7(3), P. a020602 - a020602
Published: Dec. 4, 2014
Jerry
Silver1,
Martin
E.
Schwab2
and
Phillip
G.
Popovich3
1Department
of
Neurosciences,
Case
Western
Reserve
University,
Cleveland,
Ohio
44140
2Brain
Research
Institute,
University
Zurich
Department
Health
Sciences
Technology,
ETH
Zurich,
8057
Switzerland
3Center
for
Brain
Spinal
Cord
Repair,
State
Columbus,
43210
Correspondence:
phillip.popovich{at}osumc.edu
