Current Issues in Molecular Biology,
Год журнала:
2024,
Номер
47(1), С. 8 - 8
Опубликована: Дек. 26, 2024
Neuroinflammation
is
a
complex
and
dynamic
response
of
the
central
nervous
system
(CNS)
to
injury,
infection,
disease.
While
acute
neuroinflammation
plays
protective
role
by
facilitating
pathogen
clearance
tissue
repair,
chronic
dysregulated
inflammation
contributes
significantly
progression
neurodegenerative
disorders
such
as
Alzheimer's
disease,
Parkinson's
Multiple
Sclerosis.
This
review
explores
cellular
molecular
mechanisms
underlying
neuroinflammation,
focusing
on
roles
microglia,
astrocytes,
peripheral
immune
cells.
Key
signaling
pathways,
including
NF-κB,
JAK-STAT,
NLRP3
inflammasome,
are
discussed
alongside
emerging
regulators
non-coding
RNAs,
epigenetic
modifications,
gut-brain
axis.
The
therapeutic
landscape
evolving,
with
traditional
anti-inflammatory
drugs
like
NSAIDs
corticosteroids
offering
limited
efficacy
in
conditions.
Immunomodulators,
gene
RNA-based
therapeutics,
stem
cell
methods
have
all
shown
promise
for
more
specific
effective
interventions.
Additionally,
modulation
metabolic
states
gut
microbiota
has
emerged
novel
strategy
regulate
neuroinflammation.
Despite
significant
progress,
challenges
remain
translating
these
findings
into
clinically
viable
therapies.
Future
studies
should
concentrate
integrated,
interdisciplinary
reduce
slowing
disorders,
providing
opportunities
revolutionary
advances
CNS
Molecular Biomedicine,
Год журнала:
2023,
Номер
4(1)
Опубликована: Ноя. 8, 2023
Abstract
The
Janus
kinase-signal
transducer
and
transcription
activator
pathway
(JAK-STAT)
serves
as
a
cornerstone
in
cellular
signaling,
regulating
physiological
pathological
processes
such
inflammation
stress.
Dysregulation
this
can
lead
to
severe
immunodeficiencies
malignancies,
its
role
extends
neurotransduction
pro-inflammatory
signaling
mechanisms.
Although
JAK
inhibitors
(Jakinibs)
have
successfully
treated
immunological
inflammatory
disorders,
their
application
has
generally
been
limited
diseases
with
similar
pathogenic
features.
Despite
the
modest
expression
of
JAK-STAT
CNS,
it
is
crucial
for
functions
cortex,
hippocampus,
cerebellum,
making
relevant
conditions
like
Parkinson's
disease
other
neuroinflammatory
disorders.
Furthermore,
influence
on
serotonin
receptors
phospholipase
C
implications
stress
mood
This
review
expands
understanding
JAK-STAT,
moving
beyond
traditional
contexts
explore
stress-related
disorders
CNS
function.
Recent
findings,
effectiveness
Jakinibs
chronic
rheumatoid
arthritis,
expand
therapeutic
applicability.
Advances
isoform-specific
inhibitors,
including
filgotinib
upadacitinib,
promise
greater
specificity
fewer
off-target
effects.
Combination
therapies,
involving
monoclonal
antibodies,
aiming
enhance
efficacy
also
give
great
hope.
Overall,
bridges
gap
between
basic
science
clinical
application,
elucidating
complex
human
health
guiding
future
interventions.
Graphical
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(4), С. 2360 - 2360
Опубликована: Фев. 17, 2024
This
review
explores
the
diverse
applications
of
gold
nanoparticles
(AuNPs)
in
neurological
diseases,
with
a
specific
focus
on
Alzheimer's
disease
(AD),
Parkinson's
(PD),
and
stroke.
The
introduction
highlights
pivotal
role
neuroinflammation
these
disorders
introduces
unique
properties
AuNPs.
review's
core
examines
mechanisms
by
which
AuNPs
exert
neuroprotection
anti-neuro-inflammatory
effects,
elucidating
various
pathways
through
they
manifest
properties.
potential
therapeutic
AD
are
discussed,
shedding
light
promising
avenues
for
therapy.
also
prospects
utilizing
PD
interventions,
presenting
hopeful
outlook
future
treatments.
Additionally,
delves
into
providing
after
strokes,
emphasizing
their
significance
mitigating
cerebrovascular
accidents'
aftermath.
Experimental
findings
from
cellular
animal
models
consolidated
to
provide
comprehensive
overview
AuNPs'
effectiveness,
offering
insights
impact
at
both
vivo
levels.
enhances
our
understanding
diseases
lays
groundwork
innovative
strategies
neurology.
Antioxidants,
Год журнала:
2024,
Номер
13(4), С. 395 - 395
Опубликована: Март 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 Cellular and Infection Microbiology,
Год журнала:
2024,
Номер
14
Опубликована: Фев. 16, 2024
Abnormal
behavior
of
α-synuclein
and
prion
proteins
is
the
hallmark
Parkinson’s
disease
(PD)
illnesses,
respectively,
being
complex
neurological
disorders.
A
primary
cause
protein
aggregation,
brain
injury,
cognitive
loss
in
illnesses
misfolding
normal
cellular
(PrP
C
)
into
an
infectious
form
Sc
).
Aggregation
causes
disruptions
processes
(PD),
leading
to
dopamine-producing
neurons
motor
symptoms.
Alteration
composition
or
activity
gut
microbes
may
weaken
intestinal
barrier
make
it
possible
for
prions
go
from
brain.
The
gut-brain
axis
linked
neuroinflammation;
metabolites
produced
by
microbiota
affect
aggregation
α-synuclein,
regulate
inflammation
immunological
responses,
influence
course
neurotoxicity
proteins,
even
if
their
targets
are
distinct
proteins.
This
thorough
analysis
explores
interactions
that
exist
between
neurodegenerative
particularly
involvement
microbiota,
a
collection
bacteria,
archaea,
fungi,
viruses
etc.,
various
becoming
increasingly
recognized.
microbiome
influences
neuroinflammation,
neurotransmitter
synthesis,
mitochondrial
function,
integrity
through
axis,
which
contributes
development
progression
disease.
review
delves
molecular
mechanisms
underlie
these
relationships,
emphasizing
effects
microbial
such
as
bacterial
lipopolysaccharides
(LPS),
short-chain
fatty
acids
(SCFAs)
regulating
functioning.
Additionally,
looks
at
how
environmental
dietary
decisions
whether
they
could
be
risk
factors
illnesses.
study
concludes
highlighting
critical
role
plays
It
also
provides
promising
direction
future
research
treatment
approaches.
People
afflicted
difficult
ailments
find
hope
new
preventive
therapeutic
approaches
diseases
better
understood.
Journal of Neuroinflammation,
Год журнала:
2023,
Номер
20(1)
Опубликована: Июль 23, 2023
Abstract
Neuroinflammation
has
been
implicated
in
the
initiation
and
progression
of
several
central
nervous
system
(CNS)
disorders,
including
Alzheimer’s
disease,
Parkinson’s
amyotrophic
lateral
sclerosis,
multiple
ischemic
stroke,
traumatic
brain
injury,
spinal
cord
viral
encephalitis,
bacterial
encephalitis.
Microglia
astrocytes
are
essential
neural
development,
maintenance
synaptic
connections,
homeostasis
a
healthy
brain.
The
activation
microglia
is
defense
mechanism
against
damaged
tissues
harmful
pathogens.
However,
their
triggers
neuroinflammation,
which
can
exacerbate
or
induce
CNS
injury.
Non-coding
RNAs
(ncRNAs)
functional
RNA
molecules
that
lack
coding
capabilities
but
actively
regulate
mRNA
expression
function
through
various
mechanisms.
ncRNAs
highly
expressed
potential
mediators
neuroinflammation.
We
reviewed
recent
research
progress
on
role
miRNAs,
lncRNAs,
circRNAs
regulating
neuroinflammation
diseases.
Understanding
how
these
affect
will
provide
important
therapeutic
insights
for
preventing
managing
dysfunction.
International Journal of Molecular Sciences,
Год журнала:
2023,
Номер
24(19), С. 14582 - 14582
Опубликована: Сен. 26, 2023
Parkinson’s
disease
is
a
neurodegenerative
exhibiting
the
fastest
growth
in
incidence
recent
years.
As
with
most
diseases,
pathophysiology
incompletely
elucidated,
but
compelling
evidence
implicates
inflammation,
both
central
nervous
system
and
periphery,
initiation
progression
of
disease,
although
it
not
yet
clear
what
triggers
this
inflammatory
response
where
begins.
Gut
dysbiosis
seems
to
be
likely
candidate
for
systemic
inflammation.
The
therapies
current
use
provide
only
symptomatic
relief,
do
interfere
progression.
Nonetheless,
animal
models
have
shown
promising
results
that
target
various
vicious
neuroinflammatory
cascades.
Translating
these
therapeutic
strategies
into
clinical
trials
still
its
infancy,
series
issues,
such
as
exact
timing,
identifying
biomarkers
able
identify
early
pre-symptomatic
stages,
or
proper
indications
genetic
testing
population
at
large,
will
need
settled
future
guidelines.
Frontiers in Pharmacology,
Год журнала:
2024,
Номер
15
Опубликована: Июль 25, 2024
Neurodegenerative
diseases
constitute
a
global
health
issue
and
major
economic
burden.
They
significantly
impair
both
cognitive
motor
functions,
their
prevalence
is
expected
to
rise
due
ageing
societies
continuous
population
growth.
Conventional
therapies
provide
symptomatic
relief,
nevertheless,
disease-modifying
treatments
that
reduce
or
halt
neuron
death
malfunction
are
still
largely
unavailable.
Amongst
the
common
hallmarks
of
neurodegenerative
protein
aggregation,
oxidative
stress,
neuroinflammation
mitochondrial
dysfunction.
Transcription
factor
nuclear
factor-erythroid
2-related
2
(NRF2)
constitutes
central
regulator
cellular
defense
mechanisms,
including
regulation
antioxidant,
anti-inflammatory
pathways,
making
it
highly
attractive
therapeutic
target
for
disease
modification
in
disorders.
Here,
we
describe
role
NRF2
neurodegeneration,
review
current
pharmacological
interventions
challenges
activating
pathway,
present
alternative
approaches
modification.
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(2), С. 1071 - 1071
Опубликована: Янв. 15, 2024
As
the
global
population
ages,
prevalence
of
Parkinson’s
disease
(PD)
is
steadily
on
rise.
PD
demonstrates
chronic
and
progressive
characteristics,
many
cases
can
transition
into
dementia.
This
increases
societal
economic
burdens,
emphasizing
need
to
find
effective
treatments.
Among
widely
recognized
causes
abnormal
accumulation
proteins,
autophagy
dysfunction
accelerates
this
accumulation.
The
resultant
Lewy
bodies
are
also
commonly
found
in
Alzheimer’s
patients,
suggesting
an
increased
potential
for
onset
Additionally,
production
free
radicals
due
mitochondrial
contributes
neuronal
damage
degeneration.
activation
astrocytes
M1
phenotype
microglia
promote
dopamine
neurons.
drugs
currently
used
only
delay
clinical
progression
exacerbation
without
targeting
its
root
cause,
come
with
various
side
effects.
Thus,
there
a
demand
treatments
fewer
effects,
much
offered
by
natural
products.
In
study,
we
reviewed
total
14
articles
related
herbal
medicines
products
investigated
their
relevance
possible
treatment.
results
showed
that
against
lysosomal
disorder,
dysfunction,
inflammation,
key
mechanisms
underlying
PD.
Therefore,
reduce
neurotoxicity
might
improve
both
motor
non-motor
symptoms
associated
Furthermore,
these
products,
multi-target
enhance
bioavailability,
inhibit
antibiotic
resistance,
additionally
eliminate
making
them
good
alternative
therapies
