Frontiers in Nutrition,
Journal Year:
2023,
Volume and Issue:
9
Published: Jan. 10, 2023
The
yellow
polyphenolic
pigment
known
as
curcumin,
originating
from
the
rhizome
of
turmeric
plant
Curcuma
longa
L.,
has
been
utilized
for
ages
in
ancient
medicine,
well
cooking
and
food
coloring.
Recently,
biological
activities
curcumin
have
thoroughly
investigated.
studies
mainly
focused
on
their
antioxidant,
antitumor,
anti-inflammatory,
neuroprotective,
hepatoprotective,
cardioprotective
impacts.
This
review
seeks
to
provide
an
in-depth,
detailed
discussion
usage
within
processing
industries
its
effect
health
support
disease
prevention.
Curcumin’s
bioavailability,
bio-efficacy,
bio-safety
characteristics,
side
effects
quality
standards,
are
also
discussed.
Finally,
curcumin’s
multifaceted
uses,
appeal
enhancement,
agro-industrial
techniques
counteracting
instability
low
nanotechnology
drug
delivery
systems
increase
prospective
clinical
use
tactics
all
Nutrients,
Journal Year:
2022,
Volume and Issue:
14(2), P. 256 - 256
Published: Jan. 7, 2022
Despite
the
ongoing
vaccination
efforts,
there
is
still
an
urgent
need
for
safe
and
effective
treatments
to
help
curb
debilitating
effects
of
COVID-19
disease.
This
systematic
review
aimed
investigate
efficacy
supplemental
curcumin
treatment
on
clinical
outcomes
inflammation-related
biomarker
profiles
in
patients.
We
searched
PubMed,
Scopus,
Web
Science,
EMBASE,
ProQuest,
Ovid
databases
up
30
June
2021
find
studies
that
assessed
curcumin-related
compounds
mild
severe
Six
were
identified
which
showed
supplementation
led
a
significant
decrease
common
symptoms,
duration
hospitalization
deaths.
In
addition,
all
these
intervention
amelioration
cytokine
storm
thought
be
driving
force
cases.
was
seen
as
(p
<
0.05)
proinflammatory
cytokines
such
IL1β
IL6,
with
concomitant
increase
anti-inflammatory
cytokines,
including
IL-10,
IL-35
TGF-α.
Taken
together,
findings
suggested
exerts
its
beneficial
through
at
least
partial
restoration
pro-inflammatory/anti-inflammatory
balance.
conclusion,
may
offer
efficacious
option
improving
disease
outcomes.
highlight
point
future
should
employ
larger
cohorts
patients
different
settings
standardized
preparations
compounds.
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.
Ageing Research Reviews,
Journal Year:
2023,
Volume and Issue:
91, P. 102035 - 102035
Published: Aug. 23, 2023
Ferroptosis
is
an
iron-
and
lipid
peroxidation
(LPO)-mediated
programmed
cell
death
type.
Recently,
mounting
evidence
has
indicated
the
involvement
of
ferroptosis
in
neurodegenerative
diseases,
especially
Alzheimer's
disease
(AD),
Parkinson's
(PD),
multiple
sclerosis
(MS),
amyotrophic
lateral
(ALS),
Huntington's
(HD),
so
on.
Treating
presents
opportunities
as
well
challenges
for
diseases.
This
review
provides
a
comprehensive
overview
underlying
mechanisms
that
contribute
to
occurrence
ferroptosis,
their
implications
pathogenesis
advancement
major
disorders.
Meanwhile,
we
summarize
interaction
between
other
types
diseases
contribution
corresponding
drug
development.
In
addition,
specifically
recent
advances
developing
therapeutic
means
targeting
these
which
may
guide
future
approaches
effective
management
devastating
medical
conditions.
Frontiers in Molecular Biosciences,
Journal Year:
2022,
Volume and Issue:
9
Published: Aug. 26, 2022
Alzheimer's
disease
(AD)
accounts
for
two-thirds
of
all
dementia
cases,
affecting
50
million
people
worldwide.
Only
four
the
more
than
100
AD
drugs
developed
thus
far
have
successfully
improved
symptoms.
Furthermore,
these
improvements
are
only
temporary,
as
no
treatment
can
stop
or
reverse
progression.
A
growing
number
recent
studies
demonstrated
that
iron-dependent
programmed
cell
death,
known
ferroptosis,
contributes
to
AD-mediated
nerve
death.
The
ferroptosis
pathways
within
cells
include
iron
homeostasis
regulation,
cystine/glutamate
(Glu)
transporter
(system
xc-),
glutathione
(GSH)/glutathione
peroxidase
4
(GPX4),
and
lipid
peroxidation.
In
regulation
pathway
homeostasis,
abnormal
uptake,
excretion
storage
in
lead
increased
intracellular
free
Fenton
reactions.
decreased
Glu
expression
leads
accumulation
outside
cells,
resulting
inhibition
system
xc-
pathway.
GSH
depletion
causes
abnormalities
GPX4,
leading
excessive
peroxides.
Alterations
specific
amino
acid
metabolism
eventually
ferroptosis.
This
review
explores
connection
between
signaling
metabolism,
potentially
informing
future
diagnosis
methodologies.
Antioxidants,
Journal Year:
2022,
Volume and Issue:
11(11), P. 2167 - 2167
Published: Oct. 31, 2022
Alzheimer’s
disease
(AD),
the
most
common
form
of
dementia,
has
increasing
incidence,
mortality
rates,
and
poses
a
huge
burden
on
healthcare.
None
currently
approved
drugs
for
treatment
AD
influence
progression.
Many
clinical
trials
aiming
at
inhibiting
amyloid
plaque
formation,
beta
clearance,
or
neurofibrillary
tangle
pathology
yielded
inconclusive
results
failed.
Meanwhile,
research
identified
many
interlinked
vicious
cascades
implicating
oxidative
stress,
mitochondrial
dysfunction,
chronic
neuroinflammation,
pointed
to
novel
therapeutic
targets
such
as
improving
bioenergetics
quality
control,
diminishing
modulating
neuroinflammatory
pathways.
molecules
tested
in
vitro
animal
models
have
proven
efficient,
but
their
translation
into
clinic
needs
further
regarding
appropriate
doses,
delivery
routes,
possible
side
effects.
Cell-based
therapies
extracellular
vesicle-mediated
messenger
RNAs
microRNAs
seem
also
promising
strategies
allowing
target
specific
signaling
pathways,
need
harvesting
culture
methods
well
control
tumorigenic
The
rapidly
developing
area
nanotechnology
could
improve
drug
be
used
early
diagnosis.
Ageing and Neurodegenerative Diseases,
Journal Year:
2022,
Volume and Issue:
2(3), P. 11 - 11
Published: Jan. 1, 2022
Alzheimer’s
disease
(AD)
is
a
progressive
neurodegenerative
disorder
characterized
by
two
pathological
hallmark
lesions:
extracellular
plaques
composed
of
β-amyloid
(Aβ)
peptide
and
intracellular
neurofibrillary
tangles
made
up
highly
phosphorylated
tau
protein.
Over
the
past
decades,
most
disease-modifying
therapies
against
AD
have
been
developed
mainly
on
basis
amyloid
cascade
hypothesis
with
focus
Aβ.
However,
these
agents
yielded
only
limited
benefits
progression,
which
prompts
us
to
revitalize
long-neglected
hypothesis.
Tau
protein
microtubule-associated
protein,
can
stabilize
microtubules,
regulate
microtubule
assembly,
affect
morphology
growth
neuronal
axons.
Much
more
importantly,
degree
pathology
closely
related
cognitive
decline
in
patients
than
that
Aβ
pathology.
Therefore,
tau-targeting
therapy
seems
be
promising
approach
combat
AD.
This
review
describes
research
progress
AD,
an
emphasis
immunotherapy.
The
current
challenges
future
perspectives
this
field
are
also
discussed.
Cells,
Journal Year:
2023,
Volume and Issue:
12(16), P. 2019 - 2019
Published: Aug. 8, 2023
The
brain
is
a
highly
dynamic
organ
that
requires
constant
energy
source
to
function
normally.
This
mostly
supplied
by
glucose,
simple
sugar
serves
as
the
brain’s
principal
fuel
source.
Glucose
transport
across
blood–brain
barrier
(BBB)
primarily
controlled
via
sodium-independent
facilitated
glucose
transport,
such
transporter
1
(GLUT1)
and
3
(GLUT3).
However,
other
transporters,
including
GLUT4
sodium-dependent
transporters
SGLT1
SGLT6,
have
been
reported
in
vitro
vivo.
When
BBB
endothelial
layer
crossed,
neurons
astrocytes
can
absorb
using
their
GLUT1
GLUT3
transporters.
then
enters
glycolytic
pathway
metabolized
into
adenosine
triphosphate
(ATP),
which
supplies
support
cellular
functions.
metabolism
of
are
impacted
several
medical
conditions,
cause
neurological
neuropsychiatric
symptoms.
Alzheimer’s
disease
(AD),
Parkinson’s
(PD),
epilepsy,
traumatic
injury
(TBI),
schizophrenia,
etc.,
few
most
prevalent
disorders,
characterized
decline
or
hypometabolism
early
course
disease.
Indeed,
AD
considered
metabolic
disorder
related
decreased
metabolism,
involving
insulin
resistance
age-dependent
mitochondrial
dysfunction.
Although
conventional
view
reduced
cerebral
an
effect
neuronal
loss
consequent
atrophy,
growing
body
evidence
points
opposite,
where
prodromal
at
least
precedes
onset
atrophy
manifestation
clinical
underlying
processes
responsible
for
these
abnormalities
complicated
remain
poorly
understood.
review
article
provides
comprehensive
overview
current
understanding
potential
therapeutic
targets.
Frontiers in Immunology,
Journal Year:
2024,
Volume and Issue:
15
Published: May 16, 2024
Importance
Research
is
beginning
to
elucidate
the
sophisticated
mechanisms
underlying
microbiota-gut-brain-immune
interface,
moving
from
primarily
animal
models
human
studies.
Findings
support
dynamic
relationships
between
gut
microbiota
as
an
ecosystem
(microbiome)
within
(host)
and
its
intersection
with
host
immune
nervous
systems.
Adding
this
effects
on
epigenetic
regulation
of
gene
expression
further
complicates
strengthens
response.
At
heart
inflammation,
which
manifests
in
a
variety
pathologies
including
neurodegenerative
diseases
such
Alzheimer’s
disease,
Parkinson’s
Multiple
Sclerosis
(MS).
Observations
Generally,
research
date
limited
has
focused
bacteria,
likely
due
simplicity
cost-effectiveness
16s
rRNA
sequencing,
despite
lower
resolution
inability
determine
functional
ability/alterations.
However,
omits
all
other
fungi,
viruses,
phages,
are
emerging
key
members
microbiome.
Much
been
done
pre-clinical
and/or
small
studies
more
developed
parts
world.
The
observed
promising
but
cannot
be
considered
reliable
or
generalizable
at
time.
Specifically,
causal
determined
currently.
More
followed
by
then
little
MS.
data
for
MS
encouraging
this.
Conclusions
relevance
While
still
nascent,
interface
may
missing
link,
hampered
our
progress
understanding,
let
alone
preventing,
managing,
putting
into
remission
diseases.
Relationships
must
first
established
humans,
have
shown
poorly
translate
complex
physiology
environments,
especially
when
investigating
microbiome
where
often
overly
simplistic.
Only
can
robust
conducted
humans
using
mechanistic
model
