Antioxidants,
Journal Year:
2023,
Volume and Issue:
12(10), P. 1811 - 1811
Published: Sept. 29, 2023
In
diseases
of
the
central
nervous
system,
such
as
Alzheimer's
disease
(AD),
Parkinson's
(PD),
stroke,
amyotrophic
lateral
sclerosis
(ALS),
Huntington's
(HD),
and
even
epilepsy
migraine,
oxidative
stress
load
commonly
surpasses
endogenous
antioxidative
capacity.
While
processes
have
been
robustly
implicated
in
pathogenesis
these
diseases,
significance
particular
antioxidants,
both
especially
exogenous,
maintaining
redox
homeostasis
requires
further
research.
Among
enzymes
catalase,
superoxide
dismutase,
glutathione
peroxidase
are
to
disabling
free
radicals,
thereby
preventing
damage
cellular
lipids,
proteins,
nucleic
acids.
Whether
supplementation
with
endogenously
occurring
antioxidant
compounds
melatonin
carries
any
benefit,
however,
remains
equivocal.
Similarly,
while
health
benefits
certain
exogenous
including
ascorbic
acid
(vitamin
C),
carotenoids,
polyphenols,
sulforaphanes,
anthocyanins
touted,
their
clinical
efficacy
effectiveness
neurological
contexts
need
be
more
defined.
Here,
we
review
current
literature
on
mechanisms
mitigating
comment
possible
benefit
most
common
antioxidants
AD,
PD,
ALS,
HD,
epilepsy,
migraine.
We
selected
a
basically
neurodegenerative
nature.
Annual Review of Nutrition,
Journal Year:
2022,
Volume and Issue:
42(1), P. 275 - 309
Published: June 2, 2022
Ferroptosis
is
a
type
of
regulated
cell
death
characterized
by
an
excessive
lipid
peroxidation
cellular
membranes
caused
the
disruption
antioxidant
defense
system
and/or
imbalanced
metabolism.
differentiates
from
other
forms
in
that
several
metabolic
pathways
and
nutritional
aspects,
including
endogenous
antioxidants
(such
as
coenzyme
Q10,
vitamin
E,
di/tetrahydrobiopterin),
iron
handling,
energy
sensing,
selenium
utilization,
amino
acids,
fatty
directly
regulate
cells'
sensitivity
to
ferroptosis.
As
hallmarks
ferroptosis
have
been
documented
variety
diseases,
neurodegeneration,
acute
organ
injury,
therapy-resistant
tumors,
modulation
using
pharmacological
tools
or
reprogramming
holds
great
potential
for
treatment
ferroptosis-associated
diseases
cancer
therapy.
Hence,
this
review
focuses
on
regulation
cues
discusses
interventions
therapy
targeting
Frontiers in Neuroscience,
Journal Year:
2022,
Volume and Issue:
16
Published: Feb. 7, 2022
Introduction
Alzheimer’s
disease
(AD)
is
the
most
prevalent
cause
of
dementia,
and
emerging
evidence
suggests
that
ferroptosis
involved
in
pathological
process
AD.
Materials
Methods
Three
microarray
datasets
(GSE122063,
GSE37263,
GSE140829)
about
AD
were
collected
from
GEO
database.
AD-related
module
genes
identified
through
a
weighted
gene
co-expression
network
analysis
(WGCNA).
The
ferroptosis-related
extracted
FerrDb.
apoptosis-related
downloaded
UniProt
as
control
to
show
specificity
ferroptosis.
overlap
was
performed
obtain
associated
with
apoptosis.
Then
Gene
Ontology
(GO)
Kyoto
Encyclopedia
Genes
Genomes
(KEGG)
pathway
enrichment
analyses
protein-protein
interaction
(PPI)
conducted.
Cytoscape
CytoHubba
used
identify
hub
genes,
Logistic
regression
distinguish
patients
controls.
Results
53
obtained.
GO
revealed
response
oxidative
stress
starvation,
multicellular
organismal
homeostasis
highly
enriched
terms.
KEGG
showed
these
overlapped
not
only
renal
cell
carcinoma
pathways
central
carbon
metabolism
cancer,
but
also
autophagy-related
Ferroptosis-related
(JUN,
SLC2A1,
TFRC,
ALB,
NFE2L2)
finally
identified,
which
could
controls
(P
<
0.05).
area
under
ROC
curve
(AUC)
0.643.
Apoptosis-related
(STAT1,
MCL1,
BCL2L11)
AUC
0.608,
less
than
former
value,
suggesting
more
special
apoptosis
Conclusion
We
five
are
closely
can
differentiate
JUN,
NFE2L2
thus
potential
biomarkers
for
diagnosis
therapeutic
monitoring.
Antioxidants,
Journal Year:
2023,
Volume and Issue:
12(6), P. 1289 - 1289
Published: June 16, 2023
The
incidence
of
neurological
diseases,
such
as
Parkinson’s
disease,
Alzheimer’s
disease
and
stroke,
is
increasing.
An
increasing
number
studies
have
correlated
these
diseases
with
brain
iron
overload
the
resulting
oxidative
damage.
Brain
deficiency
has
also
been
closely
linked
to
neurodevelopment.
These
disorders
seriously
affect
physical
mental
health
patients
bring
heavy
economic
burdens
families
society.
Therefore,
it
important
maintain
homeostasis
understand
mechanism
affecting
reactive
oxygen
species
(ROS)
balance,
in
neural
damage,
cell
death
and,
ultimately,
leading
development
disease.
Evidence
shown
that
many
therapies
targeting
ROS
imbalances
good
preventive
therapeutic
effects
on
diseases.
This
review
highlights
molecular
mechanisms,
pathogenesis
treatment
strategies
metabolism
Critical Reviews in Microbiology,
Journal Year:
2023,
Volume and Issue:
50(2), P. 127 - 137
Published: Jan. 4, 2023
The
cause
of
Alzheimer's
disease
(AD),
and
the
pathophysiological
mechanisms
involved,
remain
major
unanswered
questions
in
medical
science.
Oral
bacteria,
especially
those
species
associated
with
chronic
periodontitis
particularly
Porphyromonas
gingivalis,
are
being
linked
causally
to
AD
pathophysiology
a
subpopulation
susceptible
individuals.
P.
gingivalis
produces
large
amounts
proteolytic
enzymes,
haem
iron
capture
proteins,
adhesins
internalins
that
secreted
attached
cell
surface
concentrated
onto
outer
membrane
vesicles
(OMVs).
These
enzymes
adhesive
proteins
have
been
shown
host
tissue
damage
stimulate
inflammatory
responses.
ecological
roles
OMVs,
their
ability
disperse
widely
throughout
deliver
functional
lead
proposal
they
may
be
link
between
focal
infection
subgingivae
during
neurodegeneration
AD.
OMVs
can
cross
blood
brain
barrier
accelerate
AD-specific
neuropathology
by
increasing
neuroinflammation,
plaque/tangle
formation
dysregulation
homeostasis,
thereby
inducing
ferroptosis
leading
neuronal
death
neurodegeneration.
Antioxidants,
Journal Year:
2023,
Volume and Issue:
12(10), P. 1811 - 1811
Published: Sept. 29, 2023
In
diseases
of
the
central
nervous
system,
such
as
Alzheimer's
disease
(AD),
Parkinson's
(PD),
stroke,
amyotrophic
lateral
sclerosis
(ALS),
Huntington's
(HD),
and
even
epilepsy
migraine,
oxidative
stress
load
commonly
surpasses
endogenous
antioxidative
capacity.
While
processes
have
been
robustly
implicated
in
pathogenesis
these
diseases,
significance
particular
antioxidants,
both
especially
exogenous,
maintaining
redox
homeostasis
requires
further
research.
Among
enzymes
catalase,
superoxide
dismutase,
glutathione
peroxidase
are
to
disabling
free
radicals,
thereby
preventing
damage
cellular
lipids,
proteins,
nucleic
acids.
Whether
supplementation
with
endogenously
occurring
antioxidant
compounds
melatonin
carries
any
benefit,
however,
remains
equivocal.
Similarly,
while
health
benefits
certain
exogenous
including
ascorbic
acid
(vitamin
C),
carotenoids,
polyphenols,
sulforaphanes,
anthocyanins
touted,
their
clinical
efficacy
effectiveness
neurological
contexts
need
be
more
defined.
Here,
we
review
current
literature
on
mechanisms
mitigating
comment
possible
benefit
most
common
antioxidants
AD,
PD,
ALS,
HD,
epilepsy,
migraine.
We
selected
a
basically
neurodegenerative
nature.