Nutrients,
Journal Year:
2024,
Volume and Issue:
16(4), P. 507 - 507
Published: Feb. 10, 2024
The
escalating
prevalence
of
metabolic
and
cardiometabolic
disorders,
often
characterized
by
oxidative
stress
chronic
inflammation,
poses
significant
health
challenges
globally.
As
the
traditional
therapeutic
approaches
may
sometimes
fall
short
in
managing
these
conditions,
attention
is
growing
toward
nutraceuticals
worldwide;
with
compounds
being
obtained
from
natural
sources
potential
beneficial
effects
shown
to
potentially
support
and,
some
cases,
replace
pharmacological
treatments,
especially
for
individuals
who
do
not
qualify
conventional
treatments.
This
review
delves
into
burgeoning
field
nutraceutical-based
modulation
as
a
promising
strategy
attenuating
inflammation
disorders.
Drawing
an
extensive
body
research,
showcases
various
nutraceutical
agents,
such
polyphenols,
omega-3
fatty
acids,
antioxidants,
which
exhibit
antioxidative
anti-inflammatory
properties.
All
can
be
classified
novel
drugs
that
are
capable
regulating
pathways
mitigate
oxidative-stress-
inflammation-associated
diseases.
By
exploring
mechanisms
through
interact
immune
responses,
this
highlights
their
restore
redox
balance
temper
inflammation.
Additionally,
prospects
interventions
discussed,
encompassing
bioavailability
enhancement,
personalized
treatment
approaches,
clinical
translation.
Through
comprehensive
analysis
latest
scientific
reports,
article
underscores
avenue
fight
complex
landscape
particularly
accentuating
impact
on
cardiovascular
health.
Cells,
Journal Year:
2025,
Volume and Issue:
14(2), P. 89 - 89
Published: Jan. 10, 2025
Amyloid-β
peptide
(Aβ)
is
a
critical
cause
of
Alzheimer's
disease
(AD).
It
generated
from
amyloid
precursor
protein
(APP)
through
cleavages
by
β-secretase
and
γ-secretase.
γ-Secretase,
which
includes
presenilin,
regulated
several
stimuli.
Tau
has
also
been
identified
as
significant
factor
in
AD.
In
particular,
phosphorylation
crucial
for
neuronal
impairment,
phosphorylated
detaches
microtubules,
leading
to
the
formation
neurofibrillary
tangles
destabilization
microtubule
structure.
This
instability
microtubules
damages
axons
dendrites,
resulting
impairment.
Notably,
Aβ
linked
phosphorylation.
Another
AD
neuroinflammation,
primarily
occurring
microglia.
Microglia
possess
receptors
that
bind
with
Aβ,
triggering
expression
release
an
inflammatory
factor,
although
their
main
physiological
function
phagocytose
debris
pathogens
brain.
NF-κB
activation
plays
major
role
neuroinflammation.
Additionally,
production
reactive
oxygen
species
(ROS)
microglia
contributes
this
microglia,
superoxide
produced
NADPH
oxidase,
specifically
NOX2.
Rho
GTPases
play
essential
regulating
various
cellular
processes,
including
cytoskeletal
rearrangement,
morphology
changes,
migration,
transcription.
The
typical
involves
actin
filament
formation.
Neurons,
complex
processes
synapse
connections,
rely
on
dynamics
structural
support.
Other
brain
cells,
such
astrocytes,
oligodendrocytes,
depend
specific
structures
maintain
unique
architectures.
Thus,
aberrant
regulation
activity
can
disrupt
filaments,
altered
cell
morphology,
changes
synapses,
potentially
contributing
diseases
Frontiers in Neurology,
Journal Year:
2023,
Volume and Issue:
14
Published: Dec. 6, 2023
In
the
realm
of
Alzheimer's
disease,
most
prevalent
form
dementia,
impact
environmental
factors
has
ignited
intense
curiosity
due
to
its
substantial
burden
on
global
health.
Recent
investigations
have
unveiled
these
as
key
contributors,
shedding
new
light
their
profound
influence.
Notably,
emerging
evidence
highlights
detrimental
role
various
contaminants
in
incidence
and
progression
disease.
These
encompass
a
broad
spectrum,
including
air
pollutants
laden
with
ozone,
neurotoxic
metals
like
lead,
aluminum,
manganese,
cadmium,
pesticides
insidious
effects,
ubiquitous
presence
plastics
microplastics.
By
meticulously
delving
into
intricate
web
connecting
this
devastating
neurological
disorder,
comprehensive
chapter
takes
deep
dive
involvement
significant
risk
for
Furthermore,
it
explores
underlying
molecular
mechanisms
through
which
exert
influence,
aiming
unravel
complex
interactions
that
drive
pathogenesis
Additionally,
proposes
potential
strategies
mitigate
effects
brain
health,
ultimate
goal
restoring
preserving
typical
cognitive
function.
Through
exploration,
we
aim
enhance
our
understanding
multifaceted
relationship
between
neurotoxins
providing
solid
foundation
developing
innovative
in-vivo
models
advancing
knowledge
pathological
processes
debilitating
condition.
Brain Sciences,
Journal Year:
2023,
Volume and Issue:
14(1), P. 19 - 19
Published: Dec. 23, 2023
The
term
“neuroinflammation”
defines
the
typical
inflammatory
response
of
brain
closely
related
to
onset
many
neurodegenerative
diseases
(NDs).
Neuroinflammation
is
well
known,
but
its
mechanisms
and
pathways
are
not
entirely
comprehended.
Some
progresses
have
been
achieved
through
efforts
research.
Consequently,
new
cellular
molecular
mechanisms,
diverse
conventional,
emerging.
In
listing
some
those
that
will
be
subject
our
description
discussion,
essential
important
roles
peripheral
infiltrated
monocytes
clonotypic
cells,
alterations
in
gut–brain
axis,
dysregulation
apelinergic
system,
endothelial
glycocalyx
component
neuronal
vascular
units,
variations
expression
genes
levels
encoding
molecules
by
action
microRNAs
(miRNAs),
or
other
epigenetic
factors
distinctive
transcriptional
factors,
as
role
autophagy,
ferroptosis,
sex
differences,
modifications
circadian
cycle.
Such
can
add
significantly
understanding
complex
etiological
puzzle
neuroinflammation
ND.
addition,
they
could
represent
biomarkers
targets
ND,
which
increasing
elderly.
Journal of Neuroinflammation,
Journal Year:
2024,
Volume and Issue:
21(1)
Published: July 27, 2024
Abstract
Neuroinflammation
contributes
to
impaired
cognitive
function
in
brain
aging
and
neurodegenerative
disorders
like
Alzheimer’s
disease,
which
is
characterized
by
the
aggregation
of
pathological
tau.
One
major
driver
both
age-
tau-associated
neuroinflammation
NF-κB
NLRP3
signaling
axis.
However,
current
treatments
targeting
or
may
have
adverse/systemic
effects,
most
not
been
clinically
translatable.
In
this
study,
we
tested
efficacy
a
novel,
nucleic
acid
therapeutic
(Nanoligomer)
cocktail
specifically
for
reducing
improving
old
(aged
19
months)
wildtype
mice,
rTg4510
tau
pathology
mice
2
months).
We
found
that
4
weeks
NF-κB/NLRP3-targeting
Nanoligomer
treatment
strongly
reduced
neuro-inflammatory
cytokine
profiles
improved
cognitive-behavioral
mice.
These
effects
Nanoligomers
were
also
associated
with
glial
cell
activation
pathology,
favorable
changes
transcriptome
signatures
glia-associated
inflammation
(reduced)
neuronal
health
(increased),
positive
systemic
effects.
Collectively,
our
results
provide
basis
future
translational
studies
brain,
perhaps
using
Nanoligomers,
inhibit
improve
neurodegeneration.
