Nutrients,
Journal Year:
2023,
Volume and Issue:
15(11), P. 2564 - 2564
Published: May 30, 2023
The
Zingiberaceae
family
possess
various
phenolic
compounds
that
have
significant
systemic
bioactivities
in
the
brain,
including
age-related
neurodegenerative
diseases.
Neurotrophins
are
growth
factors
protect
neurons
from
oxidative
stress,
and
dysregulation
of
neurotrophic
system
may
result
neurocognitive
disease.
Phenolic
been
used
traditional
complementary
medicine
(TCM)
to
improve
cognitive
functions.
These
affect
expression
agents,
but
their
underlying
molecular
mechanisms
require
further
investigation.
Therefore,
goal
this
review
is
determine
functional
roles
brain
disorders
disorders.
While
previous
studies
proposed
for
neuroprotective
activity
these
compounds,
precise
mechanism
action
remains
complex
poorly
understood.
Despite
some
promising
findings,
there
still
shortcomings
therapeutic
use
herbs,
current
interventions
involving
appear
be
clinically
insufficient.
This
article
aims
summarize
recent
discoveries
several
members
as
neuroprotectants
provide
first
evidence-linked
bioactive
ingredients
prominent
family.
Signal Transduction and Targeted Therapy,
Journal Year:
2024,
Volume and Issue:
9(1)
Published: Aug. 23, 2024
Abstract
Alzheimer’s
disease
(AD)
stands
as
the
predominant
form
of
dementia,
presenting
significant
and
escalating
global
challenges.
Its
etiology
is
intricate
diverse,
stemming
from
a
combination
factors
such
aging,
genetics,
environment.
Our
current
understanding
AD
pathologies
involves
various
hypotheses,
cholinergic,
amyloid,
tau
protein,
inflammatory,
oxidative
stress,
metal
ion,
glutamate
excitotoxicity,
microbiota-gut-brain
axis,
abnormal
autophagy.
Nonetheless,
unraveling
interplay
among
these
pathological
aspects
pinpointing
primary
initiators
require
further
elucidation
validation.
In
past
decades,
most
clinical
drugs
have
been
discontinued
due
to
limited
effectiveness
or
adverse
effects.
Presently,
available
primarily
offer
symptomatic
relief
often
accompanied
by
undesirable
side
However,
recent
approvals
aducanumab
(
1
)
lecanemab
2
Food
Drug
Administration
(FDA)
present
potential
in
disrease-modifying
Nevertheless,
long-term
efficacy
safety
need
Consequently,
quest
for
safer
more
effective
persists
formidable
pressing
task.
This
review
discusses
pathogenesis,
advances
diagnostic
biomarkers,
latest
updates
trials,
emerging
technologies
drug
development.
We
highlight
progress
discovery
selective
inhibitors,
dual-target
allosteric
modulators,
covalent
proteolysis-targeting
chimeras
(PROTACs),
protein-protein
interaction
(PPI)
modulators.
goal
provide
insights
into
prospective
development
application
novel
drugs.
International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(9), P. 8434 - 8434
Published: May 8, 2023
In
the
central
nervous
system
(CNS)
there
are
a
greater
number
of
glial
cells
than
neurons
(between
five
and
ten
times
more).
Furthermore,
they
have
functions
(more
eight
functions).
Glia
comprises
different
types
cells,
those
neural
origin
(astrocytes,
radial
glia,
oligodendroglia)
differentiated
blood
monocytes
(microglia).
During
ontogeny,
develop
earlier
(at
fetal
day
15
in
rat)
astrocytes
later
21
rat),
which
could
indicate
their
important
crucial
role
CNS.
Analysis
phylogeny
reveals
that
reptiles
lower
compared
to
humans
this
is
reversed,
as
neurons.
These
data
perhaps
imply
special
involved
many
vital
functions,
including
memory,
learning
processes.
addition,
mechanisms
protect
CNS
through
production
antioxidant
anti-inflammatory
proteins
clean
extracellular
environment
help
communicate
correctly
with
each
other.
The
inflammatory
mediators
prevent
changes
brain
homeostasis.
On
contrary,
excessive,
or
continued
appears
characteristic
element
diseases,
such
Alzheimer’s
disease
(AD),
amyotrophic
lateral
sclerosis
(ALS),
multiple
(MS),
neurodevelopmental
bipolar
disorder,
schizophrenia,
autism.
drugs
techniques
been
developed
reverse
oxidative
stress
and/or
excess
inflammation
occurs
but
much
remains
be
investigated.
This
review
attempts
highlight
functional
relevance
normal
neuropathological
conditions
by
showing
molecular
cellular
Cells,
Journal Year:
2023,
Volume and Issue:
12(3), P. 417 - 417
Published: Jan. 26, 2023
Increasing
evidence
suggests
a
pivotal
role
of
receptor-interacting
protein
kinase
1
(RIPK1),
an
initiator
necroptosis,
in
neuroinflammation.
However,
the
precise
RIPK1
microglial
activation
remains
unclear.
In
present
study,
we
explored
lipopolysaccharide
(LPS)-induced
neuroinflammation
and
1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine
(MPTP)-induced
PD
model
mice
by
using
RIPK1-specific
inhibitors
necrostatin-1
(Nec-1)
stable
(Nec-1s).
Nec-1/Nec-1s
or
siRNA
inhibited
production
proinflammatory
molecules
phosphorylation
RIPK1-RIPK3-MLKL
cell
death
LPS-induced
inflammatory
LPS/QVD/BV6-induced
necroptotic
conditions
BV2
cells.
Detailed
mechanistic
studies
showed
that
exerted
anti-inflammatory
effects
modulating
AMPK,
PI3K/Akt,
MAPKs,
NF-κB
signaling
pathways
LPS-stimulated
Subsequent
vivo
gene
expression
inhibiting
brains
LPS-injected
mice.
Furthermore,
exert
neuroprotective
MPTP-induced
We
found
p-RIPK1
is
mainly
expressed
microglia,
thus
may
contribute
to
subsequent
dopaminergic
neurons
These
data
suggest
key
regulator
Acta Pharmaceutica Sinica B,
Journal Year:
2024,
Volume and Issue:
14(8), P. 3327 - 3361
Published: May 13, 2024
Mitophagy,
essential
for
mitochondrial
health,
selectively
degrades
damaged
mitochondria.
It
is
intricately
linked
to
the
cGAS–STING
pathway,
crucial
innate
immunity.
This
pathway
responds
DNA
and
associated
with
cellular
stress.
Our
review
explores
molecular
details
regulatory
mechanisms
of
mitophagy
pathway.
We
critically
evaluated
literature
demonstrating
how
dysfunctional
leads
neuroinflammatory
conditions,
primarily
through
accumulation
mitochondria,
activating
activation
prompts
production
proinflammatory
cytokines,
exacerbating
neuroinflammation.
emphasizes
interaction
between
Effective
might
suppress
offering
protection
against
Conversely,
impaired
may
activate
potentially
leading
chronic
Additionally,
we
explored
this
influences
neurodegenerative
disorders,
suggesting
a
common
mechanism
in
such
diseases.
In
conclusion,
there
need
additional
targeted
research
unravel
complexities
mitophagy–cGAS–STING
interactions
their
role
neurodegeneration.
highlights
potential
therapies
targeting
these
pathways,
which
could
lead
new
treatments
conditions.
synthesis
enhances
our
understanding
foundations
neuroinflammation
opens
therapeutic
avenues
disease
research.
Aging and Disease,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Jan. 1, 2024
Aging
in
the
healthy
brain
is
characterized
by
a
low-grade,
chronic,
and
sterile
inflammatory
process
known
as
neuroinflammaging.
This
condition,
mainly
consisting
an
up-regulation
of
response
at
level,
contributes
to
pathogenesis
age-related
neurodegenerative
disorders.
Development
this
proinflammatory
state
involves
interaction
between
genetic
environmental
factors,
able
induce
epigenetic
modifications.
Indeed,
exposure
compounds,
drugs,
infections,
can
contribute
modifications
DNA
methylome,
histone
fold
proteins,
nucleosome
positioning,
leading
modulation
neuroinflammatory
responses.
Furthermore,
some
modifiers,
which
combine
interact
during
life
course,
modeling
epigenome
dynamics
sustain,
or
dampen
phenotype.
The
aim
review
summarize
current
knowledge
about
neuroinflammaging
with
particular
focus
on
mechanisms
underlying
onset
progression
cascades
central
nervous
system;
furthermore,
we
describe
diagnostic
biomarkers
that
may
increase
accuracy
help
tailor
therapeutic
strategies
patients
diseases.
Journal of Neuroinflammation,
Journal Year:
2024,
Volume and Issue:
21(1)
Published: Feb. 26, 2024
Abstract
Neuroinflammation
is
highly
influenced
by
microglia,
particularly
through
activation
of
the
NLRP3
inflammasome
and
subsequent
release
IL-1β.
Extracellular
ATP
a
strong
activator
inducing
K
+
efflux
as
key
signaling
event,
suggesting
that
-permeable
ion
channels
could
have
high
therapeutic
potential.
In
these
include
ATP-gated
THIK-1
P2X7
receptors,
but
their
interactions
potential
role
in
human
brain
are
unknown.
Using
novel
specific
inhibitor
combination
with
patch-clamp
electrophysiology
slices
neocortex,
we
found
generated
main
tonic
conductance
microglia
sets
resting
membrane
stimulated
concentration-dependent
manner
only
via
metabotropic
potentiation
THIK-1.
We
further
demonstrated
was
mandatory
for
ATP-evoked
IL-1β
release,
which
strongly
suppressed
blocking
Surprisingly,
contributed
marginally
to
total
presence
ATP,
dominated
P2X7.
This
suggests
previously
unknown,
-independent
mechanism
activation.
Nuclear
sequencing
revealed
almost
selective
expression
while
had
much
broader
expression.
Thus,
inhibition
be
an
effective
and,
contrast
P2X7,
microglia-specific
strategy
contain
neuroinflammation.
Graphical