Targeting Cytokine-Mediated Inflammation in Brain Disorders: Developing New Treatment Strategies
Pharmaceuticals,
Год журнала:
2025,
Номер
18(1), С. 104 - 104
Опубликована: Янв. 15, 2025
Cytokine-mediated
inflammation
is
increasingly
recognized
for
playing
a
vital
role
in
the
pathophysiology
of
wide
range
brain
disorders,
including
neurodegenerative,
psychiatric,
and
neurodevelopmental
problems.
Pro-inflammatory
cytokines
such
as
interleukin-1
(IL-1),
tumor
necrosis
factor-alpha
(TNF-α),
interleukin-6
(IL-6)
cause
neuroinflammation,
alter
function,
accelerate
disease
development.
Despite
progress
understanding
these
pathways,
effective
medicines
targeting
are
still
limited.
Traditional
anti-inflammatory
immunomodulatory
drugs
peripheral
inflammatory
illnesses.
Still,
they
face
substantial
hurdles
when
applied
to
central
nervous
system
(CNS),
blood-brain
barrier
(BBB)
unwanted
systemic
effects.
This
review
highlights
developing
treatment
techniques
modifying
cytokine-driven
focusing
on
advances
that
selectively
target
critical
involved
pathology.
Novel
approaches,
cytokine-specific
inhibitors,
antibody-based
therapeutics,
gene-
RNA-based
interventions,
sophisticated
drug
delivery
systems
like
nanoparticles,
show
promise
with
respect
lowering
neuroinflammation
greater
specificity
safety.
Furthermore,
developments
biomarker
discoveries
neuroimaging
improving
our
ability
monitor
responses,
allowing
more
accurate
personalized
regimens.
Preclinical
clinical
trial
data
demonstrate
therapeutic
potential
tailored
techniques.
However,
significant
challenges
remain,
across
BBB
reducing
off-target
As
research
advances,
creation
personalized,
cytokine-centered
therapeutics
has
therapy
landscape
illnesses,
giving
patients
hope
better
results
higher
quality
life.
Язык: Английский
Alzheimer’s Disease: Exploring the Landscape of Cognitive Decline
ACS Chemical Neuroscience,
Год журнала:
2024,
Номер
15(21), С. 3800 - 3827
Опубликована: Окт. 11, 2024
Alzheimer's
disease
(AD)
is
a
progressive
neurodegenerative
disorder
characterized
by
cognitive
decline,
memory
loss,
and
impaired
daily
functioning.
The
pathology
of
AD
marked
the
accumulation
amyloid
beta
plaques
tau
protein
tangles
in
brain,
along
with
neuroinflammation
synaptic
dysfunction.
Genetic
factors,
such
as
mutations
APP,
PSEN1,
PSEN2
genes,
well
APOE
ε4
allele,
contribute
to
increased
risk
acquiring
AD.
Currently
available
treatments
provide
symptomatic
relief
but
do
not
halt
progression.
Research
efforts
are
focused
on
developing
disease-modifying
therapies
that
target
underlying
pathological
mechanisms
Advances
identification
validation
reliable
biomarkers
for
hold
great
promise
enhancing
early
diagnosis,
monitoring
progression,
assessing
treatment
response
clinical
practice
effort
alleviate
burden
this
devastating
disease.
In
paper,
we
analyze
data
from
CAS
Content
Collection
summarize
research
progress
We
examine
publication
landscape
insights
into
current
knowledge
advances
developments.
also
review
most
discussed
emerging
concepts
assess
strategies
combat
explore
genetic
pharmacological
targets,
comorbid
diseases.
Finally,
inspect
applications
products
against
their
development
pipelines
drug
repurposing.
objective
broad
overview
evolving
regarding
AD,
outline
challenges,
evaluate
growth
opportunities
further
combating
Язык: Английский
Deciphering the Functions of Raphe–Hippocampal Serotonergic and Glutamatergic Circuits and their Deficits in Alzheimer’s Disease
International Journal of Molecular Sciences,
Год журнала:
2025,
Номер
26(3), С. 1234 - 1234
Опубликована: Янв. 30, 2025
Subcortical
innervation
of
the
hippocampus
by
raphe
nucleus
is
essential
for
emotional
and
cognitive
control.
The
two
major
afferents
from
to
originate
serotonergic
glutamatergic
neurons,
which
control
hippocampal
inhibitory
network,
theta
activity,
synaptic
plasticity
have
been
extensively
explored
in
growing
body
literature,
whereas
those
circuits
received
little
attention.
Notably,
both
between
are
disrupted
Alzheimer's
disease
(AD),
may
contribute
initiation
progression
behavioral
psychological
symptoms
dementia.
Thus,
deciphering
mechanism
underlying
abnormal
raphe-hippocampal
AD
crucial
prevent
dementia-associated
symptoms.
In
this
review,
we
summarize
anatomical,
neurochemical,
electrophysiological
diversity
nuclei
as
well
architecture
circuitry.
We
then
elucidate
subcortical
activity
their
role
regulation
emotion
cognition.
Additionally,
present
an
overview
pathogenesis
analyze
available
therapies
that
can
potentially
be
used
clinically
alleviate
neuropsychiatric
decline
course.
Язык: Английский
Expression of Neuronal Nicotinic Acetylcholine Receptor and Early Oxidative DNA Damage in Aging Rat Brain—The Effects of Memantine
International Journal of Molecular Sciences,
Год журнала:
2025,
Номер
26(4), С. 1634 - 1634
Опубликована: Фев. 14, 2025
Aging
and
age-related
neurodegenerative
disorders
are
characterized
by
the
dysfunction
or
loss
of
brain
nicotinic
acetylcholine
receptors
(nAChRs),
these
changes
may
be
related
to
other
senescence
markers,
such
as
oxidative
stress
DNA
repair
dysfunction.
However,
mechanism
nAChR
in
aging
modification
this
process
drugs
(e.g.,
memantine,
Mem)
not
yet
fully
understood.
To
study
whether
differences
expression
rat
occur
due
modulated
Mem,
we
analyzed
subunits
(at
RNA
protein
levels)
biomarkers
real-time
quantitative
polymerase
chain
reaction
(RQ-PCR)
Western
blot
validation.
Twenty-one
female
Wistar
rats
were
divided
into
four
groups,
depending
on
age,
oldest
group
received
injections
Mem
water
with
use
intragastric
catheters.
We
studied
cerebral
grey
matter
(CGM),
subcortical
white
(SCWM),
cerebellum
(Ce).
Results
showed
an
decrease
α7
mRNA
level
SCWM.
The
was
accompanied
reduced
8-oxoguanine
glycosylase
1
(OGG1)
increased
tumor
necrosis
factor
alpha
(TNFα)
level.
In
group,
observed
a
higher
SCWM
Ce.
Biomarker
levels
changed,
but
different
extent
area.
Importantly,
antioxidative
status
stopped
even
regressed
under
treatment.
After
two
weeks
treatment,
increase
TP53
8-oxo-2'deoxyguanosine
(8-oxo-2'dG)
observed.
conclude
that
administration
protective
against
mechanisms.
Язык: Английский