Benha Journal of Applied Sciences,
Journal Year:
2023,
Volume and Issue:
8(8), P. 29 - 37
Published: Aug. 29, 2023
Background:
Vitiligo
is
an
acquired
autoimmune
disorder
characterized
by
patchy
depigmentation
in
the
skin
and
hair.Dysregulation
of
lipid
metabolism
immune
dysregulation
are
key
factors
pathogenesis
vitiligo.Apolipoprotein
E4
(ApoE4),
a
protein
involved
metabolism,
has
been
implicated
various
health
conditions.Assessing
serum
levels
ApoE4
patients
with
vitiligo
may
provide
insights
into
disease
process
clinical
implications.Objective:
The
review
aims
to
explore
potential
role
pathogenesis,
its
association
dysregulation,
implications
altered
levels.Conclusions:
In
conclusion,
assessment
Apolipoprotein
(ApoE4)
holds
promise
as
avenue
for
understanding
implications.
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(2), P. 967 - 967
Published: Jan. 12, 2024
Neurodegenerative
diseases
are
a
heterogeneous
group
of
age-related
disorders
characterised
by
the
progressive
degeneration
or
death
neurons
in
central
peripheral
nervous
system
[...].
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(3), P. 1795 - 1795
Published: Feb. 1, 2024
In
this
narrative
review,
we
delved
into
the
intricate
interplay
between
Apolipoprotein
E
(APOE)
alleles
(typically
associated
with
Alzheimer's
disease-AD)
and
alpha-synucleinopathies
(aS-pathies),
involving
Parkinson's
disease
(PD),
dementia
(PDD),
Lewy
bodies
(DLB),
multiple-system
atrophy
(MSA).
First,
in-vitro,
animal,
human-based
data
on
exacerbating
effect
of
APOE4
LB
pathology
were
summarized.
We
found
robust
evidence
that
carriage
constitutes
a
risk
factor
for
PDD-APOE2,
APOE3
may
not
alter
developing
PDD.
confirmed
copies
confer
an
increased
hazard
towards
DLB,
as
well.
Again
APOE2
appear
unrelated
to
conversion.
Of
note,
in
individuals
DLB
APOE4,
appears
be
intermediately
prevalent
AD
PDD-PD
(AD
>
PDD
PD).
Less
consistency
existed
when
it
came
PD;
APOE-PD
associations
tended
markedly
modified
by
ethnicity.
Finally,
failed
establish
association
APOE
gene
MSA.
Phenotypic
(age
onset,
survival,
cognitive-neuropsychiatric-
motor-,
sleep-related
manifestations)
alleles,
each
aforementioned
conditions
also
outlined.
synopsis
literature
gaps
was
provided
followed
suggestions
future
research.
International Journal of Molecular Sciences,
Journal Year:
2025,
Volume and Issue:
26(3), P. 1260 - 1260
Published: Jan. 31, 2025
Alzheimer’s
disease
(AD)
is
a
significant
health
challenge
in
the
21st
century.
In
spite
of
approval
many
new
disease-modifying
therapies
for
AD,
clinical
advantages
these
treatments
are
less
certain.
Aim:
This
investigation
was
intended
to
determine
potential
neuroprotective
impact
morin
hydrate
(MH),
zeolite
clinoptilolite
(ZC),
and/or
physical
and
mental
activities
(PhM)
on
an
aluminum
chloride
(AlCl3)-induced
AD
rat
model.
Methods:
Male
Sprague
Dawley
rats
were
randomly
allocated
into
seven
groups.
Group
I
control
group.
Groups
II–VII
treated
with
AlCl3
5
weeks.
III–VII
tested
effects
MH,
ZC,
PhM.
Biochemical,
brain
histopathological,
behavioral
studies
performed.
Results:
PhM,
ZC
combined
therapy
exhibited
effect
demonstrated
by
corrected
catecholamines
tau
β-amyloid
levels,
as
well
antioxidant
anti-ferroptotic
probably
through
Nrf2/HO-1/GPX4
ACSL4
signaling
pathways.
addition,
counteracted
inflammatory
responses
modulating
TLR4/NF-κβ/NLRP3
inflammasome
expression.
Moreover,
groups
showed
maximum
improvement
both
APOE4/LRP1
Wnt3/β-catenin/GSK-3β
expressions.
Conclusion:
research
highlights
MH
plus
PhM
against
AlCl3-induced
via
modulation
Nrf2/HO-1/GPX4,
TLR4/NF-κβ/NLRP3,
APOE4/LRP1,
It
first
point
out
inclusion
ferroptosis-Nrf2/inflammasomes
cross-talk
neuroprotection
mechanism
MH/ZC
AlCl3-mediated
Alzheimer s Research & Therapy,
Journal Year:
2023,
Volume and Issue:
15(1)
Published: Oct. 19, 2023
Abstract
Background
APOE
genotype
is
the
greatest
genetic
risk
factor
for
sporadic
Alzheimer’s
disease
(AD).
APOE4
increases
AD
up
to
12-fold
compared
APOE3
,
an
effect
that
greater
in
females.
Evidence
suggests
one-way
could
modulate
and
progression
through
neuroinflammation.
Indeed,
associated
with
higher
glial
activation
cytokine
levels
patients
mice.
Therefore,
identifying
pathways
contribute
-associated
neuroinflammation
important
approach
understanding
treating
AD.
Human
vivo
evidence
TLR4,
one
of
key
receptors
involved
innate
immune
system,
be
-modulated
Consistent
idea,
we
previously
demonstrated
TLR4
antagonist
IAXO-101
can
reduce
LPS-
Aβ-induced
secretion
cultures.
goal
this
study
was
advance
these
findings
determine
whether
neuroinflammation,
Aβ
pathology,
behavior
mice
express
.
Methods
We
used
five
familial
mutations
human
(E3FAD)
or
(E4FAD).
Female
male
E4FAD
female
E3FAD
were
treated
vehicle
two
treatment
paradigms:
prevention
from
4
6
months
age
reversal
7
age.
Learning
memory
assessed
by
modified
Morris
water
maze.
deposition,
fibrillar
amyloid
astrogliosis,
microgliosis
immunohistochemistry.
Soluble
apoE,
insoluble
apoE
Aβ,
IL-1β
measured
ELISA.
Results
resulted
lower
Iba-1
coverage,
number
reactive
microglia,
improved
both
paradigms.
IAXO-101-treated
also
had
coverage
reactivity
RVS
paradigm,
but
there
no
on
behavior.
There
Conclusion
Our
data
supports
a
potential
mechanistic
therapeutic
target
modulating
cognition
