Neural Plasticity,
Journal Year:
2020,
Volume and Issue:
2020, P. 1 - 13
Published: Jan. 27, 2020
With
the
rise
in
aging
global
population,
stroke
comorbidities
have
become
a
serious
health
threat
and
tremendous
economic
burden
on
human
society.
Current
therapeutic
strategies
mainly
focus
protecting
neurons
from
cytotoxic
damage
at
acute
phase
upon
onset,
which
not
only
is
difficult
way
to
ameliorate
symptoms
but
also
presents
challenge
for
patients
receive
effective
treatment
time.
The
brain-derived
neurotrophic
factor
(BDNF)
most
abundant
neurotrophin
adult
brain,
possesses
remarkable
capability
repair
brain
damage.
Recent
promising
preclinical
outcomes
made
BDNF
popular
late-stage
target
development
of
novel
treatments.
In
this
review,
we
aim
summarize
latest
progress
understanding
cellular/molecular
mechanisms
underlying
pathogenesis,
current
difficulties
drug
development,
mechanism
action
poststroke
neurorehabilitation
neuroplasticity,
recent
updates
methods.
Journal of Neuroinflammation,
Journal Year:
2020,
Volume and Issue:
17(1)
Published: Jan. 13, 2020
Patients
with
interstitial
cystitis/bladder
pain
syndrome
(IC/BPS)
often
grieve
over
a
low
quality
of
life
brought
about
by
chronic
pain.
In
our
previous
studies,
we
determined
that
neuroinflammation
the
spinal
dorsal
horn
(SDH)
was
associated
mechanisms
cystitis.
Moreover,
it
has
been
shown
brain-derived
neurotrophic
factor
(BDNF)
participates
in
regulation
and
pathological
through
BDNF-TrkB
signaling;
however,
whether
plays
role
cyclophosphamide
(CYP)-induced
cystitis
remains
unclear.
This
study
aimed
to
confirm
signaling
modulates
mechanical
allodynia
CYP-induced
determine
how
occurs.Systemic
intraperitoneal
injection
CYP
performed
establish
rat
model.
modulated
TrkB
receptor
antagonist,
ANA-12,
or
intrathecal
exogenous
BDNF.
Mechanical
suprapubic
region
assessed
using
von
Frey
filaments
test.
The
expression
BDNF,
TrkB,
p-TrkB,
Iba1,
GFAP,
p-p38,
p-JNK,
IL-1β,
TNF-α
L6-S1
SDH
measured
Western
blotting
immunofluorescence
analysis.BDNF-TrkB
upregulated
significantly
after
injected.
Similarly,
expressions
were
all
upregulated.
Treatment
ANA-12
could
attenuate
allodynia,
restrain
activation
astrocytes
microglia
alleviate
neuroinflammation.
Besides,
BDNF
further
decreased
withdrawal
threshold,
promoted
microglia,
increased
release
IL-1β
model.In
model,
aggravating
leading
BDNF-TrkB-p38/JNK
signaling.
Life,
Journal Year:
2021,
Volume and Issue:
11(2), P. 173 - 173
Published: Feb. 23, 2021
Sarcopenia
is
a
geriatric
syndrome
characterized
by
the
progressive
degeneration
of
muscle
mass
and
function,
it
associated
with
severe
complications,
which
are
falls,
functional
decline,
frailty,
mortality.
cognitive
impairment,
defined
as
decline
in
one
or
more
domains
language,
memory,
reasoning,
social
cognition,
planning,
making
decisions,
solving
problems.
Although
exact
mechanism
relating
to
sarcopenia
function
has
not
yet
been
defined,
several
studies
have
shown
that
skeletal
produces
secrete
molecules,
called
myokines,
regulate
brain
functions,
including
mood,
learning,
locomotor
activity,
neuronal
injury
protection,
showing
existence
muscle-brain
cross-talk.
Moreover,
conducted
on
physical
exercise
supported
cross-talk,
how
changing
myokines'
circulating
levels,
exerts
beneficial
effects
brain.
The
review
mainly
focuses
describing
role
myokines
their
involvement
impairment
sarcopenia.