Nörodejeneratif
Hastalıklarda
Sirtuinler
ve
Mitokondriyal
Aktivite
Yasemin
ATICI
Zeynep
ÖKTEN
Sara
KASEBİ
Lipit
Metabolizmasının
Apolipoproteinlerin
Alzheimer
Hastalığına
Etkisi
Buse
SEMERCİ
ARIKAN
Mehmet
ERDEM
Tuğba
Raika
KIRAN
Hastalığının
Patofizyolojisi
Oksidatif
Stres
Abdullah
Kaan
YAĞIZ
Berat
AKTOLUN
İnme
Biyobelirteçleri
Yeşim
GÜVENÇ
DEMİRAĞCI
Kanserde
Terapötik
Hedef
Olarak
Axl
Reseptörü
İnhibitörleri
Hatibe
KARA
Prostat
Kanseri
Gamze
GÖK
Otoimmün
Tiroid
Hastalıkları
Fonksiyon
Testleri
Yavuz
ELBAŞ
Eylem
ÇAĞILTAY
Paraoksonaz
Enzim
Ailesi
Enzimlerinden
Homosistein
Tiyolaktonaz,
Aril
Esteraz
Aktivitelerine
Genel
Bir
Bakış
Neslihan
CİHAN
ÇALIŞGAN
Gül
KIRTIL
ŞENEŞ
Doğan
YÜCEL
International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(17), P. 13033 - 13033
Published: Aug. 22, 2023
Neurodegenerative
diseases
(NDs)
are
a
diverse
group
of
disorders
characterized
by
the
progressive
degeneration
and
death
neurons,
leading
to
range
neurological
symptoms.
Despite
heterogeneity
these
conditions,
common
denominator
is
implication
mitochondrial
dysfunction
in
their
pathogenesis.
Mitochondria
play
crucial
role
creating
biomolecules,
providing
energy
through
adenosine
triphosphate
(ATP)
generated
oxidative
phosphorylation
(OXPHOS),
producing
reactive
oxygen
species
(ROS).
When
they’re
not
functioning
correctly,
becoming
fragmented
losing
membrane
potential,
they
contribute
diseases.
In
this
review,
we
explore
how
mitochondria
fuse
undergo
fission,
especially
context
NDs.
We
discuss
genetic
protein
mutations
linked
impact
dynamics.
also
look
at
key
regulatory
proteins
fusion
(MFN1,
MFN2,
OPA1)
fission
(DRP1
FIS1),
including
post-translational
modifications.
Furthermore,
highlight
potential
drugs
that
can
influence
By
unpacking
complex
processes,
aim
direct
research
towards
treatments
improve
life
quality
for
people
with
challenging
conditions.
Antioxidants,
Journal Year:
2025,
Volume and Issue:
14(1), P. 108 - 108
Published: Jan. 18, 2025
The
study
of
mitochondrial
dysfunction
has
become
increasingly
pivotal
in
elucidating
the
pathophysiology
various
cerebral
pathologies,
particularly
neurodegenerative
disorders.
Mitochondria
are
essential
for
cellular
energy
metabolism,
regulation
reactive
oxygen
species
(ROS),
calcium
homeostasis,
and
execution
apoptotic
processes.
Disruptions
function,
driven
by
factors
such
as
oxidative
stress,
excitotoxicity,
altered
ion
balance,
lead
to
neuronal
death
contribute
cognitive
impairments
several
brain
diseases.
Mitochondrial
can
arise
from
genetic
mutations,
ischemic
events,
hypoxia,
other
environmental
factors.
This
article
highlights
critical
role
progression
diseases
discusses
need
targeted
therapeutic
strategies
attenuate
damage,
restore
enhance
neuroprotection.
Nutrients,
Journal Year:
2023,
Volume and Issue:
15(19), P. 4236 - 4236
Published: Sept. 30, 2023
Taurine,
a
naturally
occurring
sulfur-containing
amino
acid,
has
attracted
significant
attention
in
recent
years
due
to
its
potential
health
benefits.
Found
various
foods
and
often
used
energy
drinks
supplements,
taurine
been
studied
extensively
understand
impact
on
human
physiology.
Determining
exact
functional
roles
represents
complex
multifaceted
topic.
We
provide
an
overview
of
the
scientific
literature
present
analysis
effects
aspects
health,
focusing
aging
cardiovascular
pathophysiology,
but
also
including
athletic
performance,
metabolic
regulation,
neurological
function.
Additionally,
our
report
summarizes
current
recommendations
for
intake
addresses
safety
concerns.
Evidence
from
both
animal
studies
indicates
that
may
have
beneficial
effects,
blood
pressure
improved
cardiac
fitness,
enhanced
vascular
health.
Its
mechanisms
action
antioxidant
properties
make
it
intriguing
candidate
anti-aging
strategies.
Frontiers in Pharmacology,
Journal Year:
2024,
Volume and Issue:
14
Published: Jan. 11, 2024
Mitochondria
are
critical
for
cellular
energetic
metabolism,
intracellular
signaling
orchestration
and
programmed
death
regulation.
Therefore,
mitochondrial
dysfunction
is
associated
with
various
pathogeneses.
The
maintenance
of
homeostasis
functional
recovery
after
injury
coordinated
by
biogenesis,
dynamics
autophagy,
which
collectively
referred
to
as
quality
control.
There
increasing
evidence
that
mitochondria
important
targets
melatonin
exert
protective
effects
under
pathological
conditions.
Melatonin,
an
evolutionarily
conserved
tryptophan
metabolite,
can
be
synthesized,
transported
metabolized
in
mitochondria.
In
this
review,
we
summarize
the
role
damaged
elimination
energy
supply
regulating
control,
may
provide
new
strategies
clinical
treatment
mitochondria-related
diseases.
Biomedicine & Pharmacotherapy,
Journal Year:
2024,
Volume and Issue:
175, P. 116673 - 116673
Published: May 6, 2024
Multiple
sclerosis
(MS)
is
a
complex
autoimmune
disorder
that
impacts
the
central
nervous
system
(CNS),
resulting
in
inflammation,
demyelination,
and
neurodegeneration.
The
NOD-like
receptor
(NLR)
family
pyrin
domain-containing
3
(NLRP3)
inflammasome,
multiprotein
of
innate
immune
system,
serves
an
essential
role
pathogenesis
MS
by
regulating
production
pro-inflammatory
cytokines
(IL-1β
&
IL-18)
induction
pyroptotic
cell
death.
Mitochondrial
dysfunction
one
main
potential
factors
can
trigger
NLRP3
inflammasome
activation
lead
to
inflammation
axonal
damage
MS.
This
highlights
importance
understanding
how
mitochondrial
dynamics
modulate
activity
contribute
inflammatory
neurodegenerative
features
lack
comprehensive
urge
for
introduction
new
therapeutic
strategies
led
us
review
targeting
interplay
between
paper
also
evaluates
natural
synthetic
compounds
improve
function
and/or
inhibit
thereby
providing
neuroprotection.
Moreover,
it
summarizes
evidence
from
animal
models
demonstrate
beneficial
effects
these
on
reducing
Finally,
this
advocates
deeper
investigation
into
molecular
crosstalk
as
means
refine
targets
Free Radical Biology and Medicine,
Journal Year:
2023,
Volume and Issue:
208, P. 657 - 671
Published: Sept. 20, 2023
Aging
is
a
complex
biological
process
characterized
by
progressive
decline
in
cellular
and
tissue
function,
ultimately
leading
to
organismal
aging.
Stem
cells,
with
their
regenerative
potential,
play
crucial
role
maintaining
homeostasis
repair
throughout
an
organism's
lifespan.
Mitochondria,
the
powerhouses
of
cell,
have
emerged
as
key
players
aging
process,
impacting
stem
cell
function
contributing
age-related
dysfunction.
Here
are
discuss
mechanisms
through
which
mitochondria
influence
fate
decisions,
including
energy
production,
metabolic
regulation,
ROS
signalling,
epigenetic
modifications.
Therefore,
this
review
highlights
driving
senescence
subsequent
impact
on
overall
diseases.
Finally,
we
explore
potential
anti-aging
therapies
targeting
mitochondrial
health
implications
for
promoting
healthy
This
comprehensive
sheds
light
critical
interplay
between
senescence,
aging,
offering
insights
into
strategies
attenuating
longevity.
Nutrients,
Journal Year:
2023,
Volume and Issue:
15(13), P. 2851 - 2851
Published: June 23, 2023
Oral
niacinamide
mononucleotide
(NMN)
and
aerobic
exercise
have
been
shown
to
enhance
adenine
dinucleotide
(NAD+)
in
the
body.
NAD+
plays
a
critical
role
body
can
directly
indirectly
affect
many
key
cellular
functions,
including
metabolic
pathways,
DNA
repair,
chromatin
remodeling,
cell
aging,
immune
function.
It
is
noteworthy
that
level
of
decreases
gradually
with
increasing
age.
Decreased
levels
causally
associated
number
diseases
cognitive
decline,
cancer,
diseases,
sarcopenia,
frailty.
Many
related
aging
be
slowed
down
or
even
reversed
by
restoring
levels.
For
example,
oral
NMN
increase
APP/PS1
mice
proven
improve
mitochondrial
autophagy,
but
currently,
there
no
regimen
combining
exercise.
This
review
summarizes
recent
studies
on
effect
enhancement
vivo
improvements
autophagy
abnormalities
AD
through
exercise,
focusing
(1)
how
improves
internal
level;
(2)
regulates
content
body;
(3)
relationship
between
activation
AMPK;
(4)
SIRT1
regulated
AMPK
activates
PGC-1α
mediate
changes
dynamics.
By
summarizing
results
above
four
aspects,
combined
synthesis
vivo,
we
infer
elevates
so
as
propose
new
hypothesis
interferes
Alzheimer's
disease
(AD).