Saudi Pharmaceutical Journal,
Journal Year:
2023,
Volume and Issue:
31(9), P. 101729 - 101729
Published: Aug. 7, 2023
This
review
highlights
the
potential
role
of
cyclooxygenase-2
enzyme
(COX-2)
in
pathogenesis
Alzheimer's
disease
(AD)
and
therapeutic
use
non-steroidal
anti-inflammatory
drugs
(NSAIDs)
management
AD.
In
addition
to
COX-2
enzymes
inflammation,
formation
amyloid
plaques
neurofibrillary
tangles
brain,
emphasizes
that
COXs-2
have
a
crucial
normal
synaptic
activity
plasticity,
relationship
with
acetylcholine,
tau
protein,
beta-amyloid
(Aβ)
which
are
main
causes
disease.
Furthermore,
points
out
kinase
enzymes,
including
Cyclin
Dependent
Kinase
5
(CDK5)
Glycogen
Synthase
3β
(GSK3β),
known
play
phosphorylation
strongly
associated
Therefore,
like
NSAIDs
may
be
hopeful
approach
for
managing
However,
results
from
studies
examining
effectiveness
treating
AD
been
mixed
further
research
is
needed
fully
understand
mechanisms
by
involved
development
progression
identify
new
strategies.
Signal Transduction and Targeted Therapy,
Journal Year:
2023,
Volume and Issue:
8(1)
Published: July 12, 2023
Abstract
Studies
in
neurodegenerative
diseases,
including
Alzheimer’s
disease,
Parkinson’s
disease
and
Amyotrophic
lateral
sclerosis,
Huntington’s
so
on,
have
suggested
that
inflammation
is
not
only
a
result
of
neurodegeneration
but
also
crucial
player
this
process.
Protein
aggregates
which
are
very
common
pathological
phenomenon
can
induce
neuroinflammation
further
aggravates
protein
aggregation
neurodegeneration.
Actually,
even
happens
earlier
than
aggregation.
Neuroinflammation
induced
by
genetic
variations
CNS
cells
or
peripheral
immune
may
deposition
some
susceptible
population.
Numerous
signaling
pathways
range
been
to
be
involved
the
pathogenesis
neurodegeneration,
although
they
still
far
from
being
completely
understood.
Due
limited
success
traditional
treatment
methods,
blocking
enhancing
inflammatory
considered
promising
strategies
for
therapy
many
them
got
exciting
results
animal
models
clinical
trials.
Some
them,
few,
approved
FDA
usage.
Here
we
comprehensively
review
factors
affecting
major
pathogenicity
sclerosis.
We
summarize
current
strategies,
both
clinic,
diseases.
Nutrients,
Journal Year:
2021,
Volume and Issue:
13(8), P. 2764 - 2764
Published: Aug. 12, 2021
Malnutrition
in
older
adults
has
been
recognised
as
a
challenging
health
concern
associated
with
not
only
increased
mortality
and
morbidity,
but
also
physical
decline,
which
wide
ranging
acute
implications
for
activities
of
daily
living
quality
life
general.
is
common
may
contribute
to
the
development
geriatric
syndromes
adults.
old
reflected
by
either
involuntary
weight
loss
or
low
body
mass
index,
hidden
deficiencies
such
micronutrient
are
more
difficult
assess
therefore
frequently
overlooked
community-dwelling
old.
In
developed
countries,
most
cited
cause
malnutrition
disease,
both
chronic
disorders
have
potential
result
aggravate
malnutrition.
Therefore,
higher
age
one
risk
factor
developing
highest
being
at
nutritional
becoming
malnourished.
However,
aetiology
complex
multifactorial,
likely
facilitated
ageing
processes.
This
comprehensive
narrative
review
summarizes
current
evidence
on
prevalence
determinants
spanning
from
age-related
changes
disease-associated
factors,
outlines
remaining
challenges
understanding,
identification
well
treatment
malnutrition,
some
cases
include
targeted
supplementation
macro-
and/or
micronutrients,
when
diet
alone
sufficient
meet
age-specific
requirements.
International Journal of Molecular Sciences,
Journal Year:
2021,
Volume and Issue:
22(21), P. 11338 - 11338
Published: Oct. 20, 2021
Mitochondria
are
the
energy
center
of
cell.
They
found
in
cell
cytoplasm
as
dynamic
networks
where
they
adapt
production
based
on
cell’s
needs.
also
at
proinflammatory
response
and
have
essential
roles
against
pathogenic
infections.
a
major
site
for
Reactive
Oxygen
Species
(ROS;
or
free
radicals),
which
to
fight
infection.
However,
excessive
uncontrolled
can
become
deleterious
cell,
leading
mitochondrial
tissue
damage.
Pathogens
exploit
role
mitochondria
during
infection
by
affecting
oxidative
phosphorylation
mechanism
(OXPHOS),
network
disrupting
communication
between
nucleus
mitochondria.
The
these
biological
processes
makes
organelle
good
targets
development
therapeutic
strategies.
In
this
review,
we
presented
summary
endosymbiotic
origin
their
involvement
pathogen
response,
well
potential
promising
infectious
diseases
chronic
inflammatory
diseases.
Molecular Neurodegeneration,
Journal Year:
2022,
Volume and Issue:
17(1)
Published: March 21, 2022
Across
neurodegenerative
diseases,
common
mechanisms
may
reveal
novel
therapeutic
targets
based
on
neuronal
protection,
repair,
or
regeneration,
independent
of
etiology
site
disease
pathology.
To
address
these
and
discuss
emerging
treatments,
in
April,
2021,
Glaucoma
Research
Foundation,
BrightFocus
the
Melza
M.
Frank
Theodore
Barr
Foundation
collaborated
to
bring
together
key
opinion
leaders
experts
field
for
a
virtual
meeting
titled
"Solving
Neurodegeneration".
This
"think-tank"
style
focused
uncovering
mechanistic
roots
promising
new
catalyzed
by
goal
finding
treatments
glaucoma,
world's
leading
cause
irreversible
blindness
interest
three
hosting
foundations.
Glaucoma,
which
causes
vision
loss
through
degeneration
optic
nerve,
likely
shares
early
cellular
molecular
events
with
other
diseases
central
nervous
system.
Here
we
major
areas
overlap
between
system:
neuroinflammation,
bioenergetics
metabolism,
genetic
contributions,
neurovascular
interactions.
We
summarize
important
discussion
points
emphasis
research
that
are
most
innovative
treatment
neurodegeneration
yet
require
further
development.
The
is
highlighted
provides
unique
opportunities
collaboration
will
lead
efforts
preventing
ultimately
loss.
International Journal of Biological Sciences,
Journal Year:
2022,
Volume and Issue:
18(5), P. 2075 - 2090
Published: Jan. 1, 2022
Ferroptosis
and
neuroinflammation
play
crucial
roles
in
Alzheimer's
disease
(AD)
pathophysiology.
Forsythoside
A
(FA),
the
main
constituent
of
Forsythia
suspensa
(Thunb.)
Vahl.,
possesses
anti-inflammatory,
antibacterial,
antioxidant,
neuroprotective
properties.
The
present
study
aimed
to
investigate
potential
role
FA
AD
neuropathology
using
male
APP/PS1
double
transgenic
mice,
Aβ1-42-exposed
N2a
cells,
erastin-stimulated
HT22
LPS-induced
BV2
cells.
treatment
significantly
improved
mitochondrial
function
inhibited
lipid
peroxidation
In
LPS-stimulated
decreased
formation
pro-inflammatory
factors
IL-6,
IL-1β,
NO.
ameliorated
memory
cognitive
impairments
suppressed
Aβ
deposition
p-tau
levels
brain.
Analyses
proteomics,
immunohistochemistry,
ELISA,
western
blot
revealed
that
augmented
dopaminergic
signaling,
iron
peroxidation,
prevented
activation
IKK/IκB/NF-κB
reduced
secretion
factors,
promoted
production
anti-inflammatory
exerted
anti-ferroptosis
anti-neuroinflammatory
effects
Nrf2/GPX4
axis
played
a
key
these
effects.
Collectively,
results
demonstrate
protective
highlight
its
therapeutic
as
drug
component
for
treatment.
Cells,
Journal Year:
2022,
Volume and Issue:
11(12), P. 1885 - 1885
Published: June 10, 2022
Alzheimer’s
disease
(AD)
is
a
neurodegenerative
disorder
molecularly
characterized
by
the
formation
of
amyloid
β
(Aβ)
plaques
and
type
2
microtubule-associated
protein
(Tau)
abnormalities.
Multiple
studies
have
shown
that
many
brain’s
immunological
cells,
specifically
microglia
astrocytes,
are
involved
in
AD
pathogenesis.
Cells
innate
immune
system
play
an
essential
role
eliminating
pathogens
but
also
regulate
brain
homeostasis
AD.
When
activated,
cells
can
cause
programmed
cell
death
through
multiple
pathways,
including
pyroptosis,
apoptosis,
necroptosis,
PANoptosis.
The
often
results
release
proinflammatory
cytokines
propagate
response
eliminate
Aβ
aggregated
Tau
proteins.
However,
chronic
neuroinflammation,
which
result
from
death,
has
been
linked
to
diseases
worsen
Therefore,
must
be
tightly
balanced
appropriately
clear
these
AD-related
structural
abnormalities
without
inducing
neuroinflammation.
In
this
review,
we
discuss
responses,
inflammatory
cytokine
secretion
as
they
relate
Therapeutic
strategies
targeting
mechanisms
will
critical
consider
for
future
preventive
or
palliative
treatments
International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(7), P. 6518 - 6518
Published: March 30, 2023
Alzheimer’s
disease
is
one
of
the
most
commonly
diagnosed
cases
senile
dementia
in
world.
It
an
incurable
process,
often
leading
to
death.
This
multifactorial,
and
factor
this
inflammation.
Numerous
mediators
secreted
by
inflammatory
cells
can
cause
neuronal
degeneration.
Neuritis
may
coexist
with
other
mechanisms
disease,
contributing
progression,
also
directly
underlie
AD.
Although
much
has
been
established
about
processes
pathogenesis
AD,
many
aspects
remain
unexplained.
The
work
devoted
particular
pathomechanism
inflammation
its
role
diagnosis
treatment.
An
in-depth
detailed
understanding
neuroinflammation
help
development
diagnostic
methods
for
early
contribute
new
therapeutic
strategies
disease.
Frontiers in Aging Neuroscience,
Journal Year:
2024,
Volume and Issue:
16
Published: April 12, 2024
Neuroinflammation
refers
to
a
highly
complicated
reaction
of
the
central
nervous
system
(CNS)
certain
stimuli
such
as
trauma,
infection,
and
neurodegenerative
diseases.
This
is
cellular
immune
response
whereby
glial
cells
are
activated,
inflammatory
mediators
liberated
reactive
oxygen
nitrogen
species
synthesized.
key
process
that
helps
protect
brain
from
pathogens,
but
inappropriate,
or
protracted
inflammation
yields
pathological
states
Parkinson’s
disease,
Alzheimer’s,
Multiple
Sclerosis,
other
disorders
showcase
various
pathways
neurodegeneration
distributed
in
parts
CNS.
review
reveals
major
neuroinflammatory
signaling
associated
with
neurodegeneration.
Additionally,
it
explores
promising
therapeutic
avenues,
stem
cell
therapy,
genetic
intervention,
nanoparticles,
aiming
regulate
neuroinflammation
potentially
impede
decelerate
advancement
these
conditions.
A
comprehensive
understanding
intricate
connection
between
diseases
pivotal
for
development
future
treatment
strategies
can
alleviate
burden
imposed
by
devastating
disorders.
International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(3), P. 1869 - 1869
Published: Jan. 18, 2023
Aging
is
the
most
prominent
risk
factor
for
late-onset
Alzheimer’s
disease.
associates
with
a
chronic
inflammatory
state
both
in
periphery
and
central
nervous
system,
evidence
thereof
mechanisms
leading
to
neuroinflammation
being
discussed.
Nonetheless,
significantly
enhanced
by
accumulation
of
amyloid
beta
accelerates
progression
disease
through
various
pathways
discussed
present
review.
Decades
clinical
trials
targeting
2
abnormal
proteins
disease,
tau,
led
many
failures.
As
such,
via
different
strategies
could
prove
valuable
therapeutic
strategy,
although
much
research
still
needed
identify
appropriate
time
window.
Active
focusing
on
identifying
early
biomarkers
help
translating
these
novel
from
bench
bedside.
Cells,
Journal Year:
2022,
Volume and Issue:
11(17), P. 2728 - 2728
Published: Sept. 1, 2022
Alzheimer’s
disease
(AD)
is
the
most
common
form
of
dementia
worldwide,
with
a
complex,
poorly
understood
pathogenesis.
Cerebral
atrophy,
amyloid-β
(Aβ)
plaques,
and
neurofibrillary
tangles
represent
main
pathological
hallmarks
AD
brain.
Recently,
neuroinflammation
has
been
recognized
as
prominent
feature
brain
substantial
evidence
suggests
that
inflammatory
response
modulates
progression.
Additionally,
dysregulation
calcium
(Ca2+)
homeostasis
represents
another
early
factor
involved
in
pathogenesis,
intracellular
Ca2+
concentration
essential
to
ensure
proper
cellular
neuronal
functions.
Although
growing
supports
involvement
mechanisms
neurodegeneration-related
processes,
scant
data
are
available
on
its
contribution
microglia
astrocytes
functioning,
both
health
throughout
continuum.
Nevertheless,
AD-related
aberrant
signalling
crucially
underpinning
neuroinflammatory
processes
that,
turn,
impact
function.
In
this
light,
we
attempted
provide
an
overview
current
understanding
interactions
between
glia
cells-mediated
responses
molecular
AD.