International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(13), P. 7106 - 7106
Published: June 28, 2024
Peroxisome
proliferator-activated
receptors
(PPARs)
may
play
an
important
role
in
the
pathomechanism/pathogenesis
of
Alzheimer's
disease
(AD)
and
several
other
neurological/neuropsychiatric
disorders.
AD
leads
to
progressive
alterations
redox
state,
ion
homeostasis,
lipids,
protein
metabolism.
Significant
molecular
processes
functioning
signaling
pathways
result
degeneration
death
synapses
neuronal
cells,
leading
most
severe
dementia.
receptor
alpha
(PPAR-α)
is
among
affected
by
AD;
it
regulates
transcription
genes
related
metabolism
cholesterol,
fatty
acids,
lipids
neurotransmission,
mitochondria
biogenesis,
function.
PPAR-α
involved
cholesterol
transport
mitochondria,
substrate
for
neurosteroid
biosynthesis.
PPAR-α-coding
enzymes,
such
as
sulfotransferases,
which
are
responsible
sulfation.
The
relation
between
cholesterol/neurosteroids
have
a
significant
impact
on
course
progression
neurodegeneration/neuroprotection
processes.
Unfortunately,
despite
many
years
intensive
studies,
pathogenesis
unknown
therapy
neurodegenerative
diseases
symptomatic,
presenting
goal
challenge
today.
This
review
presents
recent
achievements
therapeutic
approaches
AD,
targeting
its
neurosteroids
neuropsychiatric
Journal of Cellular and Molecular Medicine,
Journal Year:
2024,
Volume and Issue:
28(10)
Published: May 1, 2024
Parkinson's
disease
(PD)
is
a
neurodegenerative
disorder
of
the
brain
and
manifested
by
motor
non-motor
symptoms
because
degenerative
changes
in
dopaminergic
neurons
substantia
nigra.
PD
neuropathology
associated
with
mitochondrial
dysfunction,
oxidative
damage
apoptosis.
Thus,
modulation
apoptosis
growth
factors
could
be
novel
boulevard
management
PD.
Brain-derived
neurotrophic
factor
(BDNF)
its
receptor
tropomyosin
kinase
type
B
(TrkB)
are
chiefly
involved
neuropathology.
BDNF
promotes
survival
nigra
enhances
functional
activity
striatal
neurons.
Deficiency
TrkB
triggers
degeneration
accumulation
α-Syn
As
well,
BDNF/TrkB
signalling
reduced
early
phase
Targeting
specific
activators
may
attenuate
this
review
aimed
to
discuss
potential
role
against
In
conclusion,
decreased
linked
severity
long-term
complications.
Activation
Journal of Cellular and Molecular Medicine,
Journal Year:
2025,
Volume and Issue:
29(5)
Published: March 1, 2025
Alzheimer's
disease
(AD)
is
a
neurodegenerative
caused
by
the
progressive
deposition
of
extracellular
amyloid
beta
(Aβ)
and
intracellular
neurofibrillary
tangles
(NFTs).
Of
note,
metabolic
disorders
such
as
insulin
resistance
(IR)
type
2
diabetes
(T2D)
are
associated
with
development
brain
IR
neurodegeneration.
In
addition,
AD
neuropathology
linked
cognitive
impairment
accelerate
peripheral
progression
T2D.
Therefore,
there
bidirectional
relationship
between
T2D
AD.
It
has
been
demonstrated
that
induce
dysregulation
peroxisome
proliferator-activated
receptor
alpha
(PPAR-α)
leading
to
central
disturbances.
Hence,
dysregulated
PPAR-α
could
be
shared
mechanism
in
both
T2D,
restoration
signalling
agonist
fenofibrate
(FN)
may
alleviate
this
review
aims
shed
light
on
potential
involvement
AD,
how
FN
effective
management
seems
dual
neuroprotective
antidiabetic
effects
can
mitigate
T2D-related
complications
modulating
various
cellular
processes
inflammatory
pathways.
conclusion,
possible
candidate
different
pathways
involved
pathogenesis
these
conditions.
Brain Research Bulletin,
Journal Year:
2025,
Volume and Issue:
unknown, P. 111333 - 111333
Published: April 1, 2025
Liver
X
receptors
(LXRs)
are
nuclear
that
function
as
transcription
factors
regulating
cholesterol
metabolism
and
implicated
in
multiple
sclerosis
(MS)
pathogenesis.
This
mini-review
aims
to
elucidate
the
potential
role
of
LXRs
MS
neuropathology.
is
most
prevalent
inflammatory
demyelinating
disease
central
nervous
system
(CNS),
impacting
both
brain
spinal
cord.
Furthermore,
alterations
can
modify
functional
activity
immune
response
LXRs,
which
Dysregulation
homeostasis
associated
with
pathogenesis
MS.
play
a
critical
myelination
nerve
sheaths,
defects
LXR
may
contribute
progression
have
immunomodulatory
effects,
including
inhibition
proliferation
lymphocytes,
preventing
contact
self-antigens
T
cells,
apoptotic
process
cells.
regulate
microglia,
pro-inflammatory
anti-inflammatory
properties
involved
regulation
clearance
debris
well
remyelination
process.
glial
cells
prevent
cell-mediated
neurodegeneration.
an
important
neuroinflammation
during
by
inhibiting
NF-κB
NLRP3
inflammasome
signaling
pathways.
In
conclusion,
crucial
neuropathology
mitigating
neuroinflammation.
These
findings
proposed
agonists,
through
modulation
response,
could
be
effective
management
Frontiers in Pharmacology,
Journal Year:
2025,
Volume and Issue:
16
Published: April 15, 2025
Vitiligo
is
a
chronic
autoimmune
condition
characterized
by
the
destruction
of
melanocytes,
leading
to
patchy
loss
skin
depigmentation.
Although
its
precise
cause
remains
unclear,
recent
evidence
suggests
that
metabolic
disturbances,
particularly
oxidative
stress
and
mitochondrial
dysfunction,
may
play
significant
role
in
pathogenesis
disease.
Oxidative
thought
damage
melanocytes
trigger
inflammatory
responses,
culminating
melanocyte
immune-mediate
destruction.
Additionally,
patients
with
vitiligo
often
exhibit
extra-cutaneous
abnormalities
such
as
abnormal
glucose
metabolism,
dyslipidemia,
high
fasting
plasma
levels,
blood
pressure,
out
range
C-peptide
low
biological
antioxidant
capacity,
suggesting
potential
link
between
impairment
development.
This
implies
functional
mirrors
more
general
systemic
targetable
dysfunction.
Notably,
therapies
targeting
pathways,
those
involving
peroxisome
proliferator-activated
nuclear
receptor
γ
(PPARγ)
agonists,
are
currently
being
investigated
treatments
for
vitiligo.
PPARγ
activation
restores
membrane
potential,
DNA
copy
number
and,
consequently,
ATP
production.
Moreover,
agonists
counteract
stress,
reduce
inflammation,
inhibit
apoptosis,
maintain
fatty
acid
addition
well-known
capability
enhance
insulin
sensitivity.
increasing
strong
relationship
alterations
other
approved
anti-diabetic
treatments,
like
metformin
fibrates,
treatment.
Taken
together,
these
data
support
use
approaches
alternative
traditional
immune-suppressive
treatment
Clinical and Preventive Medicine,
Journal Year:
2025,
Volume and Issue:
2, P. 152 - 161
Published: April 17, 2025
Aim.
To
conduct
a
generalization
of
scientific
research
on
the
history
use
medications
for
correction
dyslipidemia
in
clinical
practice.
Materials
and
methods.
The
analysis
articles,
guidelines
recommendations
justification
implementation
appointment
hypolipidemic
drugs
treatment
prevention
cardiovascular
diseases
(CVD)
was
carried
out.
methods
used
were:
systematic
approach,
bibliosemantic,
analytical.
Results.
Hypotheses
regarding
role
hypercholesterolemia
development
atherosclerotic
lesions
system
were
proposed
as
early
second
half
19th
century,
approaches
need
to
correct
substantiated
only
with
introduction
concept
risk
factors
20th
century.
However,
it
took
almost
two
decades
CVD
into
first
pharmacological
drug
that
began
be
practice
nicotinic
acid
(niacin).
Bile
sequestrants
(cholestyramine,
colestipol,
colesevelam)
became
group,
fibrates
(fenofibrate,
bezafibrate,
gemfibrozil,
ciprofibrate)
third
group
therapy
drugs.
Later,
these
gave
way
statins,
whose
effectiveness
higher
safety
profile
better.
Statin
is
generally
well
tolerated
adverse
reactions
occur
less
than
5%
randomized
trials.
At
current
stage,
statins
remain
first-line
lipid
metabolism.
evidence
base
significant,
results
trials
have
demonstrated
this
secondary
primary
CVD.
Since
end
90s
there
has
been
steady
increase
prescription
Сonclusions.
Medications
since
Niacin,
fibrates,
bile
now
replaced
by
which
European Journal of Pharmacology,
Journal Year:
2025,
Volume and Issue:
unknown, P. 177646 - 177646
Published: April 1, 2025
Neurogenesis
is
a
complex
process
by
which
the
neurons
and
supporting
cells
of
central
nervous
system
(CNS)
are
generated
neural
stem
cells.
Adult
hippocampal
neurogenesis
(AHN)
in
human
brain
an
active
during
life
plays
critical
role
regulation
memory,
cognition,
mood.
It
has
been
shown
that
epilepsy
linked
with
dysregulation
AHN.
Of
note,
AHN
very
sensitive
to
pathological
electrical
stimuli
epileptic
seizures,
result
induction
acute
inhibition
chronic
epilepsy.
Epileptic
seizure-induced
neurodegeneration
activates
mobilization
substitute
for
loss
temporal
lobe
(TLE),
most
refractory
type
Moreover,
recurrent
seizures
TLE
trigger
certain
regions.
However,
transient
seizure
terminated
1-4
weeks
following
status
epilepticus
(SE).
Nevertheless,
adult
dramatically
reduced
associated
development
cognitive
impairment
TLE.
These
findings
indicate
severity
seizures.
Hence,
activators
may
attenuate
pathogenesis
Therefore,
this
review
aims
discuss
explain
beneficial
how
could
be
effective
management
Autophagy,
Journal Year:
2025,
Volume and Issue:
unknown
Published: May 15, 2025
Epilepsy
is
a
neurological
disease
characterized
by
repeated
unprovoked
seizure.
controlled
anti-epileptic
drugs
(AEDs);
however,
one
third
of
epileptic
patients
have
symptoms
that
are
not
AEDs
in
condition
called
refractory
epilepsy.
Dysregulation
macroautophagy/autophagy
involved
the
pathogenesis
Autophagy
prevents
development
and
progression
epilepsy
through
regulating
balance
between
inhibitory
excitatory
neurotransmitters.
Induction
autophagy
autophagy-related
proteins
could
be
novel
therapeutic
strategy
management
Despite
protective
role
against
epileptogenesis
epilepsy,
its
status
epilepticus
perplexing
might
reflect
nature
as
double-edged
sword.
inducers
play
critical
reducing
seizure
frequency
severity,
an
adjuvant
treatment
However,
inhibitors
also
anticonvulsant
effect.
Therefore,
aim
present
mini-review
to
discuss
potential
how
modulators
affect
