Journal of Alzheimer s Disease,
Journal Year:
2024,
Volume and Issue:
98(2), P. 699 - 713
Published: Feb. 27, 2024
Alzheimer's
disease
(AD)
is
a
progressive
neurodegenerative
and
symptoms
develop
gradually
over
many
years.
The
current
direction
for
medication
development
in
AD
focused
on
neuro-inflammation
oxidative
stress.
Amyloid-β
(Aβ)
deposition
activates
microglia
leading
to
neurodegeneration
induced
by
activation
of
COX-2
via
NFκB
p50
glioblastoma
cells.
Antioxidants,
Journal Year:
2024,
Volume and Issue:
13(4), P. 395 - 395
Published: March 26, 2024
Central
neurological
disorders
are
significant
contributors
to
morbidity,
mortality,
and
long-term
disability
globally
in
modern
society.
These
encompass
neurodegenerative
diseases,
ischemic
brain
traumatic
injury,
epilepsy,
depression,
more.
The
involved
pathogenesis
is
notably
intricate
diverse.
Ferroptosis
neuroinflammation
play
pivotal
roles
elucidating
the
causes
of
cognitive
impairment
stemming
from
these
diseases.
Given
concurrent
occurrence
ferroptosis
due
metabolic
shifts
such
as
iron
ROS,
well
their
critical
central
nervous
disorders,
investigation
into
co-regulatory
mechanism
has
emerged
a
prominent
area
research.
This
paper
delves
mechanisms
along
with
interrelationship.
It
specifically
emphasizes
core
molecules
within
shared
pathways
governing
neuroinflammation,
including
SIRT1,
Nrf2,
NF-κB,
Cox-2,
iNOS/NO·,
how
different
immune
cells
structures
contribute
dysfunction
through
mechanisms.
Researchers’
findings
suggest
that
mutually
promote
each
other
may
represent
key
factors
progression
disorders.
A
deeper
comprehension
common
pathway
between
cellular
holds
promise
for
improving
symptoms
prognosis
related
Frontiers in Aging Neuroscience,
Journal Year:
2024,
Volume and Issue:
16
Published: July 3, 2024
As
the
most
common
cause
of
dementia,
Alzheimer’s
disease
(AD)
is
characterized
by
neurodegeneration
and
synaptic
loss
with
an
increasing
prevalence
in
elderly.
Increased
inflammatory
responses
triggers
brain
cells
to
produce
pro-inflammatory
cytokines
accelerates
Aβ
accumulation,
tau
protein
hyper-phosphorylation
leading
neurodegeneration.
Therefore,
this
paper,
we
discuss
current
understanding
how
inflammation
affects
activity
induce
AD
pathology,
biomarkers
possible
therapies
that
combat
for
AD.
Molecules,
Journal Year:
2025,
Volume and Issue:
30(2), P. 266 - 266
Published: Jan. 11, 2025
Dual
inhibition
of
cyclooxygenase-2
(COX-2)
and
lipoxygenase
(LOX)
is
a
recognized
strategy
for
enhanced
anti-inflammatory
effects
in
small
molecules,
offering
potential
therapeutic
benefits
individuals
at
risk
dementia,
particularly
those
with
neurodegenerative
diseases,
common
cancers,
diabetes
type.
Alzheimer’s
disease
(AD)
the
most
cause
acetylcholinesterase
(AChE)
key
approach
treating
AD.
Meanwhile,
Caspase-3
catalyzes
early
events
apoptosis,
contributing
to
neurodegeneration
subsequently
Structure-based
virtual
screening
US-FDA-approved
molecules
from
ZINC15
database
identified
clozapine
(CLOZ)
as
dual
inhibitor
COX-2
AChE,
significant
binding
affinity.
Further
molecular
docking
CLOZ
active
site
LOX
also
showed
potential.
Further,
results
were
validated
using
dynamics
simulation
(MDS)
studies,
confirming
docking.
The
MDS
good
interactions
residues.
was
further
assessed
lipopolysaccharide
(LPS)-challenged
rats
treated
thirty
days
doses
5
10
mg/kg,
p.o.
demonstrated
modulation
COX-2,
5-LOX,
Caspase-3,
MDA
LPS-induced
brains.
Additionally,
expression
level
IL-10
measured.
Our
decrease
levels
MDA.
decrement
pro-inflammatory
markers
NF-κB,
TNF-α,
IL-6
an
improvement
TGF-β1.
Overall,
findings
indicate
that
has
neuroprotective
against
LPS-treated
can
be
explored.
Abstract
Introduction
Alzheimer's
disease
(AD),
the
main
cause
of
dementia,
is
characterized
by
synaptic
loss
and
neurodegeneration.
Amyloid‐β
(Aβ)
accumulation,
hyperphosphorylation
tau
protein,
neurofibrillary
tangles
(NFTs)
in
brain
are
considered
to
be
initiating
factors
AD.
However,
this
hypothesis
falls
short
explaining
many
aspects
AD
pathogenesis.
Recently,
there
has
been
mounting
evidence
that
neuroinflammation
plays
a
key
role
pathophysiology
causes
neurodegeneration
over‐activating
microglia
releasing
inflammatory
mediators.
Methods
PubMed,
Web
Science,
EMBASE,
MEDLINE
were
used
for
searching
summarizing
all
recent
publications
related
inflammation
its
association
with
disease.
Results
Our
review
shows
how
dysregulation
influences
pathology
as
well
roles
neuroinflammation,
possible
microglia‐associated
therapeutic
targets,
top
neuroinflammatory
biomarkers,
anti‐inflammatory
drugs
combat
inflammation.
Conclusion
In
conclusion,
microglial
reactions
important
pathogenesis
need
discussed
more
detail
promising
strategies.
Life,
Journal Year:
2024,
Volume and Issue:
14(7), P. 839 - 839
Published: July 1, 2024
Background:
Despite
the
important
clinical
issue
of
cognitive
impairment
after
moderate
traumatic
brain
injury
(TBI),
there
is
currently
no
suitable
treatment.
Here,
we
used
in
vitro
and
vivo
models
to
investigate
effect
Donepezil—an
acetylcholinesterase
(AChE)
inhibitor—on
acute
period
following
injury,
while
focusing
on
neuroinflammation
autophagy-
mitophagy-related
markers.
Methods:
The
purpose
study
was
potential
neuroprotective
effects
TBI-induced
cells
donepezil
treatment,
study,
therapeutic
by
analyzing
TBI
model
involved
injuring
SH-SY5Y
using
a
cell-injury
controller
then
investigating
at
concentration
80
μM.
made
stereotaxic
impactor
for
male
C57BL/6J
mice.
Immuno-histochemical
markers
functions
were
compared
7
days
treatment
(1
mg/kg/day).
Mice
divided
into
four
groups:
sham
operation
with
saline
(18
mice
each
group).
Donepezil
administered
within
4
h
post-TBI.
Results:
In
vitro,
found
lead
increased
cell
viability
5,5′,6,6′-tetrachloro-1,1′,3,3′-tetraethylbenzimi-dazolylcarbocyanine
iodide
(JC-1),
along
decreased
reactive
oxygen
species
(ROS),
lactate-dehydrogenase
(LDH),
2′-7′-dichlorodihydrofluorescein
diacetate
(DCFH-DA)-positive
cells,
terminal
deoxynucleotidyl
transferase
dUTP
nick
end
labeling
(TUNEL)-positive
cells.
mRNA
protein
expressions
(Cyclooxygenase-2,
COX-2;
NOD-like
receptor
3,
NLRP3;
Caspase-1;
Interleukin-1
beta,
IL-1β),
as
well
(death-associated
kinase
1,
DAPK1;
PTEN-induced
PINK1;
BCL2/adenovirus
E1B
19
kDa
protein-interacting
3-like,
BNIP3L;
Beclin-1,
BECN1;
BCL2-associated
X
protein,
BAX;
microtubule-associated
1A/1B-light
chain
3B
(LC3B);
Sequestosome-1;
p62)
all
decrease
also
showed
that
resulted
levels
cortical
tissue
losses
swelling
group
without
shown
Western
blotting
markers,
especially
COX-2
BNIP3L,
which
most
significant
decreases.
Moreover,
an
escape
latency,
alteration
rate,
improved
preference
index,
altogether
pointing
better
performance
Conclusions:
may
be
beneficial
improving
early
phase
ameliorating
neuroinflammation,
autophagy
mitophagy.
Current Behavioral Neuroscience Reports,
Journal Year:
2025,
Volume and Issue:
12(1)
Published: Jan. 23, 2025
Abstract
Purpose
of
Review
Autism
Spectrum
Disorder
(ASD)
is
a
neurodevelopmental
disorder
with
multifaceted
etiologies.
Emerging
evidence
implicates
dysregulation
prostaglandins
and
cyclooxygenase
(COX)
enzymes
in
ASD
pathophysiology.
This
review
aims
to
explore
key
mechanisms
through
which
COX
may
influence
ASD.
Recent
Findings
research
highlights
significant
roles
for
modulating
Wnt
(Wingless
Int-1)
signalling
pathways,
are
known
autism
susceptibility
as
well
regulating
dendritic
arborisation
cerebellar
function.
Polymorphisms
genes
have
also
been
linked
ASD,
indicating
genetic
component
this
dysregulation.
Furthermore,
show
potential
biomarkers
Summary
The
accumulated
underscores
the
involvement
insight
offers
deeper
understanding
pave
way
more
effective
diagnostic
treatment
strategies.