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Lipid oxidation and peroxidation in CNS health and disease: from molecular mechanisms to therapeutic opportunities.
[zellweger syndrome]
Reactive
oxygen
species
(
ROS
)
are
produced
at
low
levels
in
mammalian
cells
by
various
metabolic
processes
,
such
as
oxidative
phosphorylation
by
the
mitochondrial
respiratory
chain
,
NAD
(
P
)
H
oxidases
,
and
arachidonic
acid
oxidative
metabolism
.
To
maintain
physiological
redox
balance
,
cells
have
endogenous
antioxidant
defenses
regulated
at
the
transcriptional
level
by
Nrf
2
/
ARE
.
Oxidative
stress
results
when
ROS
production
exceeds
the
cell
's
ability
to
detoxify
ROS
.
Overproduction
of
ROS
damages
cellular
components
,
including
lipids
,
leading
to
decline
in
physiological
function
and
cell
death
.
Reaction
of
ROS
with
lipids
produces
oxidized
phospholipids
,
which
give
rise
to
4
-
hydroxynonenal
,
4
-
oxo-
2
-
nonenal
,
and
acrolein
.
The
brain
is
susceptible
to
oxidative
damage
due
to
its
high
lipid
content
and
oxygen
consumption
.
Neurodegenerative
diseases
(
AD
,
ALS
,
bipolar
disorder
,
epilepsy
,
Friedreich
's
ataxia
,
HD
,
MS
,
NBIA
,
NPC
,
PD
,
peroxisomal
disorders
,
schizophrenia
,
Wallerian
degeneration
,
Zellweger
syndrome
)
and
CNS
traumas
(
stroke
,
TBI
,
SCI
)
are
problems
of
vast
clinical
importance
.
Free
iron
can
react
with
H
(
2
)
O
(
2
)
via
the
Fenton
reaction
,
a
primary
cause
of
lipid
peroxidation
,
and
may
be
of
particular
importance
for
these
CNS
injuries
and
disorders
.
Cholesterol
is
an
important
regulator
of
lipid
organization
and
the
precursor
for
neurosteroid
biosynthesis
.
Atherosclerosis
,
the
major
risk
factor
for
ischemic
stroke
,
involves
accumulation
of
oxidized
LDL
in
the
arteries
,
leading
to
foam
cell
formation
and
plaque
development
.
This
review
will
discuss
the
role
of
lipid
oxidation
/
peroxidation
in
various
CNS
injuries
/
disorders
.
Diseases
Validation
Diseases presenting
"plaque development"
symptom
zellweger syndrome
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