Cells,
Journal Year:
2023,
Volume and Issue:
12(12), P. 1557 - 1557
Published: June 6, 2023
Sulfite
predominantly
accumulates
in
the
brain
of
patients
with
isolated
sulfite
oxidase
(ISOD)
and
molybdenum
cofactor
(MoCD)
deficiencies.
Patients
present
severe
neurological
symptoms
basal
ganglia
alterations,
pathophysiology
which
is
not
fully
established.
Therapies
are
ineffective.
To
elucidate
pathomechanisms
ISOD
MoCD,
we
investigated
effects
intrastriatal
administration
on
myelin
structure,
neuroinflammation,
oxidative
stress
rat
striatum.
decreased
FluoromyelinTM
basic
protein
staining,
suggesting
abnormalities.
also
increased
staining
NG2,
a
marker
oligodendrocyte
progenitor
cells.
In
line
this,
reduced
viability
MO3.13
cells,
express
oligodendroglial
markers.
Furthermore,
altered
expression
interleukin-1β
(IL-1β),
interleukin-6
(IL-6),
interleukin-10
(IL-10),
cyclooxygenase-2
(COX-2),
inducible
nitric
oxide
synthase
(iNOS)
heme
oxygenase-1
(HO-1),
indicating
neuroinflammation
redox
homeostasis
disturbances.
Iba1
another
was
by
sulfite.
These
data
suggest
that
changes
induced
contribute
to
MoCD.
Notably,
post-treatment
bezafibrate
(BEZ),
pan-PPAR
agonist,
mitigated
alterations
markers
IL-1β,
IL-6,
iNOS
HO-1
cell
decrease
further
prevented.
Moreover,
pre-treatment
BEZ
attenuated
some
effects.
findings
show
modulation
PPAR
as
potential
opportunity
for
therapeutic
intervention
these
disorders.
International Journal of Molecular Sciences,
Journal Year:
2022,
Volume and Issue:
23(23), P. 15272 - 15272
Published: Dec. 3, 2022
Huntington’s
disease
(HD)
is
an
autosomal
dominant
neurodegenerative
that
occurs
worldwide.
Despite
some
progress
in
understanding
the
onset
of
HD,
drugs
block
or
delay
symptoms
are
still
not
available.
In
recent
years,
many
treatments
have
been
proposed;
among
them,
nuclear
transcriptional
factor-2
(Nrf2)
enhancer
compounds
proposed
as
potential
therapeutic
agents
to
treat
HD.
Nrf2
triggers
endogenous
antioxidant
pathway
activated
different
disorders.
Probably,
stimulation
during
either
early
phase
before
HD
symptoms’
onset,
could
slow
prevent
striatum
degeneration.
this
review,
we
present
scientific
literature
supporting
role
and
prophylactic
compound.
AbstractBackgroud
Alzheimer's
disease
(AD)
is
a
chronic,
progressive,
and
destructive
neurodegenerative
disorder
that
severely
affects
human
memory,
intelligence,
behavioral
abilities.
Jiao
Tai
Wan
(JTW)
classic
formula
composed
of
two
traditional
Chinese
medicines,
coptis
chinensis
(CC)
cinnamon
(CIN),
the
ratio
CC
CIN
10:1.
JTW
has
effects
promoting
cognitive
function,
improving
learning
memory
function.
But
specific
mechanism
not
been
systematically
studied.
Method:
We
conducted
Morris
water
maze
Y-maze
tests,
polymerase
chain
reaction
(PCR),
assay
kit
ELISA,
nissl's
staining,
western
blotting
to
verified
improvement
function
on
APP/PS1
mice.
Result:
Through
experiments,
can
improved
spatial
exploration
abilities
Nissl’s
staining
PCR
detection
BDNF,
NGF,
SYP
showed
lesions
in
By
detecting
activities
A
β
1-40,
1-42,
α
-
secretase,
γ
as
well
cholinergic
labeling
enzymes
Ach,
AchE,
ChAT
cerebral
amyloidosis
nervous
system
model
The
inflammatory
factors
oxidative
stress
indicators
revealed
inhibited
activity
stress.
Western
Blotting
was
used
detect
Nrf2/ARE/HO-1
pathway,
result
regulate
pathway
Conclusion:
JTW
enhanced
Nrf2,
regulated
increased
nerve
growth
factors,
system,
stress,
ameliorated
dysfunction
International Journal of Molecular Sciences,
Journal Year:
2022,
Volume and Issue:
23(4), P. 2017 - 2017
Published: Feb. 11, 2022
Normal
embryogenesis
requires
complex
regulation
and
precision,
which
depends
on
multiple
mechanistic
details.
Defective
can
occur
by
various
mechanisms.
Maintaining
redox
homeostasis
is
of
importance
during
embryogenesis.
NADPH,
as
produced
from
the
action
glucose-6-phosphate
dehydrogenase
(G6PD),
has
an
important
role
in
homeostasis,
serving
a
cofactor
for
glutathione
reductase
recycling
oxidized
NADPH
oxidases
nitric
oxide
synthases
generation
reactive
oxygen
(ROS)
nitrogen
species
(RNS).
Oxidative
stress
differentially
influences
cell
fate
While
low
levels
(eustress)
ROS
RNS
promote
growth
differentiation,
supra-physiological
concentrations
lead
to
demise
embryonic
lethality.
G6PD-deficient
cells
organisms
have
been
used
models
determining
signaling
regulating
proliferation,
differentiation
migration.
Embryogenesis
also
modulated
anti-oxidant
enzymes,
transcription
factors,
microRNAs,
factors
pathways,
are
dependent
regulation.
Crosstalk
among
microRNAs
essential
Journal of Alzheimer s Disease,
Journal Year:
2022,
Volume and Issue:
90(2), P. 475 - 493
Published: Sept. 20, 2022
Alzheimer's
disease
(AD)
represents
a
global
health
challenge,
with
an
estimated
55
million
people
suffering
from
the
non-curable
across
world.
While
amyloid-β
plaques
and
tau
neurofibrillary
tangles
in
brain
define
AD
proteinopathy,
it
has
become
evident
that
diverse
coding
non-coding
regions
of
genome
may
significantly
contribute
to
neurodegeneration.
The
diversity
factors
associated
pathogenesis,
coupled
age-associated
damage,
suggests
series
triggering
events
be
required
initiate
AD.
Since
somatic
mutations
accumulate
aging,
aging
is
major
risk
factor
for
AD,
there
great
potential
mutational
drive
disease.
Indeed,
recent
data
Gozes
team/laboratories
as
well
other
leading
laboratories
correlated
accumulation
progression
tauopathy.
In
this
review,
we
lay
current
perspectives
on
principal
genetic
causes,
highlighting
contribution
pathogenesis
late
onset
roles
artificial
intelligence
big
can
play
accelerating
progress
causal
mutation
markers/biomarkers
identification,
drug
discovery/repurposing,
have
been
highlighted
future
neurodegenerations,
aim
bring
hope
vulnerable
population.
Pharmaceuticals,
Journal Year:
2022,
Volume and Issue:
15(9), P. 1054 - 1054
Published: Aug. 26, 2022
Glucoraphanin
(GRA)
is
a
natural
compound
that
has
shown
beneficial
effects
in
chronic
diseases
and
central
nervous
system
disorders.
Moreover,
GRA
displayed
antidepressant
activity
preclinical
models.
We
have
previously
demonstrated
single
intracerebroventricular
administration
of
soluble
amyloid-beta
1-42
(sAβ
1-42)
rat
evokes
depressive-like
phenotype
by
increasing
immobility
frequency
the
forced
swimming
test
(FST).
The
aim
this
work
was
to
investigate
effect
naïve
sAβ-1-42-treated
rats
using
FST.
Behavioural
analyses
were
accompanied
neurochemical
biochemical
measurements
prefrontal
cortex
(PFC),
such
as
serotonin
(5-HT),
noradrenaline
(NA),
kynurenine
(KYN),
tryptophan
(TRP),
reactive
oxygen
species
(ROS)
transcription
nuclear
factor
kappa
B
(NF-kB)
levels.
reported
at
dose
50
mg/kg
reduced
FST
increased
5-HT
NA
levels
PFC
compared
controls.
At
same
dose,
reverted
sAβ
administration,
restored
NF-kB,
KYN
ROS
PFC.
In
conclusion,
rapidly
reverting
behaviour,
together
with
alterations,
might
represent
safe
candidate
for
treatment
depression.