Annals of Neurology,
Journal Year:
2021,
Volume and Issue:
89(5), P. 895 - 910
Published: March 16, 2021
Blood
tests
to
monitor
disease
activity,
attack
severity,
or
treatment
impact
in
neuromyelitis
optica
spectrum
disorder
(NMOSD)
have
not
been
developed.
This
study
investigated
the
relationship
between
serum
glial
fibrillary
acidic
protein
(sGFAP)
concentration
and
NMOSD
activity
assessed
of
inebilizumab
treatment.N-MOmentum
was
a
prospective,
multicenter,
double-blind,
placebo-controlled,
randomized
clinical
trial
adults
with
NMOSD.
sGFAP
levels
were
measured
by
single-molecule
arrays
(SIMOA)
1,260
serial
attack-related
samples
from
215
N-MOmentum
participants
(92%
aquaporin
4-immunoglobulin
G-seropositive)
control
(from
healthy
donors
patients
relapsing-remitting
multiple
sclerosis).At
baseline,
62
(29%)
exhibited
high
concentrations
(≥170
pg/ml;
≥2
standard
deviations
above
donor
mean
concentration)
more
likely
experience
an
adjudicated
than
lower
baseline
(hazard
ratio
[95%
confidence
interval],
3.09
[1.6-6.1],
p
=
0.001).
Median
(interquartile
range
[IQR])
increased
within
1
week
(baseline:
168.4,
IQR
128.9-449.7
attack:
2,160.1,
302.7-9,455.0
pg/ml,
0.0015)
correlated
severity
(median
fold
change
[FC],
minor
attacks:
1.06,
0.9-7.4;
major
34.32,
8.7-107.5,
0.023).
increase
occurred
primarily
placebo-treated
(FC:
20.2,
4.4-98.3,
0.001)
observed
inebilizumab-treated
1.1,
0.8-24.6,
>
0.05).
Five
(28%)
elevated
reported
neurological
symptoms
leading
nonadjudicated
assessments.Serum
GFAP
may
serve
as
biomarker
risk,
effects.
ANN
NEUROL
2021;89:895-910.
Signal Transduction and Targeted Therapy,
Journal Year:
2019,
Volume and Issue:
4(1)
Published: Aug. 23, 2019
Abstract
Alzheimer’s
disease
(AD)
is
a
neurodegenerative
characterized
by
progressive
memory
loss
along
with
neuropsychiatric
symptoms
and
decline
in
activities
of
daily
life.
Its
main
pathological
features
are
cerebral
atrophy,
amyloid
plaques,
neurofibrillary
tangles
the
brains
patients.
There
various
descriptive
hypotheses
regarding
causes
AD,
including
cholinergic
hypothesis,
tau
propagation
mitochondrial
cascade
calcium
homeostasis
neurovascular
inflammatory
metal
ion
lymphatic
system
hypothesis.
However,
ultimate
etiology
AD
remains
obscure.
In
this
review,
we
discuss
related
clinical
trials.
Wealthy
puzzles
lessons
have
made
it
possible
to
develop
explanatory
theories
identify
potential
strategies
for
therapeutic
interventions
AD.
The
combination
hypometabolism
autophagy
deficiency
likely
be
causative
factor
We
further
propose
that
fluoxetine,
selective
serotonin
reuptake
inhibitor,
has
treat
Signal Transduction and Targeted Therapy,
Journal Year:
2023,
Volume and Issue:
8(1)
Published: July 12, 2023
Abstract
Studies
in
neurodegenerative
diseases,
including
Alzheimer’s
disease,
Parkinson’s
disease
and
Amyotrophic
lateral
sclerosis,
Huntington’s
so
on,
have
suggested
that
inflammation
is
not
only
a
result
of
neurodegeneration
but
also
crucial
player
this
process.
Protein
aggregates
which
are
very
common
pathological
phenomenon
can
induce
neuroinflammation
further
aggravates
protein
aggregation
neurodegeneration.
Actually,
even
happens
earlier
than
aggregation.
Neuroinflammation
induced
by
genetic
variations
CNS
cells
or
peripheral
immune
may
deposition
some
susceptible
population.
Numerous
signaling
pathways
range
been
to
be
involved
the
pathogenesis
neurodegeneration,
although
they
still
far
from
being
completely
understood.
Due
limited
success
traditional
treatment
methods,
blocking
enhancing
inflammatory
considered
promising
strategies
for
therapy
many
them
got
exciting
results
animal
models
clinical
trials.
Some
them,
few,
approved
FDA
usage.
Here
we
comprehensively
review
factors
affecting
major
pathogenicity
sclerosis.
We
summarize
current
strategies,
both
clinic,
diseases.
Nature Communications,
Journal Year:
2020,
Volume and Issue:
11(1)
Published: Sept. 2, 2020
The
glymphatic
system
is
a
network
of
perivascular
spaces
that
promotes
movement
cerebrospinal
fluid
(CSF)
into
the
brain
and
clearance
metabolic
waste.
This
transport
supported
by
water
channel
aquaporin-4
(AQP4)
localized
to
vascular
endfeet
astrocytes.
more
effective
during
sleep,
but
whether
sleep
timing
function
remains
unknown.
We
here
show
influx
exhibit
endogenous,
circadian
rhythms
peaking
mid-rest
phase
mice.
Drainage
CSF
from
cisterna
magna
lymph
nodes
exhibits
daily
variation
opposite
influx,
suggesting
distribution
throughout
animal
depends
on
time-of-day.
polarization
AQP4
highest
rest
loss
eliminates
day-night
difference
in
both
drainage
nodes.
conclude
under
control
supports
this
rhythm.
Physiological Reviews,
Journal Year:
2021,
Volume and Issue:
102(2), P. 1025 - 1151
Published: May 5, 2021
The
brain
harbors
a
unique
ability
to,
figuratively
speaking,
shift
its
gears.
During
wakefulness,
the
is
geared
fully
toward
processing
information
and
behaving,
while
homeostatic
functions
predominate
during
sleep.
blood-brain
barrier
establishes
stable
environment
that
optimal
for
neuronal
function,
yet
imposes
physiological
problem;
transcapillary
filtration
forms
extracellular
fluid
in
other
organs
reduced
to
minimum
brain.
Consequently,
depends
on
special
[the
cerebrospinal
(CSF)]
flushed
into
along
perivascular
spaces
created
by
astrocytic
vascular
endfeet.
We
describe
this
pathway,
coined
term
glymphatic
system,
based
dependency
endfeet
their
adluminal
expression
of
aquaporin-4
water
channels
facing
CSF-filled
spaces.
Glymphatic
clearance
potentially
harmful
metabolic
or
protein
waste
products,
such
as
amyloid-β,
primarily
active
sleep,
when
drivers,
cardiac
cycle,
respiration,
slow
vasomotion,
together
efficiently
propel
CSF
inflow
periarterial
brain's
space
contains
an
abundance
proteoglycans
hyaluronan,
which
provide
low-resistance
hydraulic
conduit
rapidly
can
expand
shrink
sleep-wake
cycle.
system
brain,
meets
requisites
maintain
homeostasis
similar
peripheral
organs,
considering
blood-brain-barrier
paths
formation
egress
CSF.
