Frontiers in Endocrinology,
Journal Year:
2025,
Volume and Issue:
15
Published: Jan. 17, 2025
Obesity
is
a
major
modifiable
risk
factor
leading
to
neuroinflammation
and
neurodegeneration.
Excessive
fat
storage
in
obesity
promotes
the
progressive
infiltration
of
immune
cells
into
adipose
tissue,
resulting
release
pro-inflammatory
factors
such
as
cytokines
adipokines.
These
inflammatory
mediators
circulate
through
bloodstream,
propagating
inflammation
both
periphery
central
nervous
system.
Gut
dysbiosis,
which
results
leaky
intestinal
barrier,
exacerbates
plays
significant
role
linking
pathogenesis
neurodegeneration
gut-brain/gut-brain-liver
axis.
Inflammatory
states
within
brain
can
lead
insulin
resistance,
mitochondrial
dysfunction,
autolysosomal
increased
oxidative
stress.
disruptions
impair
normal
neuronal
function
subsequently
cognitive
decline
motor
deficits,
similar
pathologies
observed
neurodegenerative
diseases,
including
Alzheimer's
disease,
multiple
sclerosis,
Parkinson's
disease.
Understanding
underlying
disease
mechanisms
crucial
for
developing
therapeutic
strategies
address
defects
these
metabolic
pathways.
In
this
review,
we
summarize
provide
insights
different
strategies,
methods
alter
gut
lifestyle
changes,
dietary
supplementation,
well
pharmacological
agents
derived
from
natural
sources,
that
target
obesity-induced
Bone Research,
Journal Year:
2025,
Volume and Issue:
13(1)
Published: March 17, 2025
Abstract
Following
the
discovery
of
bone
as
an
endocrine
organ
with
systemic
influence,
bone-brain
interaction
has
emerged
a
research
hotspot,
unveiling
complex
bidirectional
communication
between
and
brain.
Studies
indicate
that
brain
can
influence
each
other’s
homeostasis
via
multiple
pathways,
yet
there
is
dearth
systematic
reviews
in
this
area.
This
review
comprehensively
examines
interactions
across
three
key
areas:
bone-derived
factors
on
function,
effects
brain-related
diseases
or
injuries
(BRDI)
health,
concept
skeletal
interoception.
Additionally,
discusses
innovative
approaches
biomaterial
design
inspired
by
mechanisms,
aiming
to
facilitate
through
materiobiological
aid
treatment
neurodegenerative
bone-related
diseases.
Notably,
integration
artificial
intelligence
(AI)
highlighted,
showcasing
AI’s
role
expediting
formulation
effective
targeted
strategies.
In
conclusion,
offers
vital
insights
into
mechanisms
suggests
advanced
harness
these
clinical
practice.
These
offer
promising
avenues
for
preventing
treating
impacting
skeleton
brain,
underscoring
potential
interdisciplinary
enhancing
human
health.
Journal of Nanobiotechnology,
Journal Year:
2024,
Volume and Issue:
22(1)
Published: Oct. 12, 2024
Endothelial
cells
(ECs)
are
pivotal
in
maintaining
vascular
health,
regulating
hemodynamics,
and
modulating
inflammatory
responses.
Nanocarriers
hold
transformative
potential
for
precise
drug
delivery
within
the
system,
particularly
targeting
ECs
therapeutic
purposes.
However,
complex
interactions
between
nanocarriers
present
significant
challenges
development
clinical
translation
of
nanotherapeutics.
This
review
assesses
recent
advancements
key
strategies
employing
to
ECs.
It
suggested
that
through
physicochemical
design
surface
modifications,
can
enhance
specificity
improve
internalization
efficiency
Additionally,
we
elaborated
on
applications
specifically
designed
treatment
cardiovascular
diseases,
cancer
metastasis,
disorders.
Despite
these
advancements,
safety
concerns,
complexity
vivo
processes,
challenge
achieving
subcellular
remain
obstacles
effective
with
nanocarriers.
A
comprehensive
understanding
endothelial
cell
biology
its
interaction
is
crucial
realizing
full
targeted
systems.
Pharmaceuticals,
Journal Year:
2025,
Volume and Issue:
18(1), P. 104 - 104
Published: Jan. 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.
Pharmaceutics,
Journal Year:
2025,
Volume and Issue:
17(3), P. 281 - 281
Published: Feb. 20, 2025
The
blood–brain
barrier
(BBB)
is
a
critical
structure
that
maintains
brain
homeostasis
by
selectively
regulating
nutrient
influx
and
waste
efflux.
Not
surprisingly,
it
often
compromised
in
neurodegenerative
diseases.
In
addition
to
its
involvement
these
pathologies,
the
BBB
also
represents
significant
challenge
for
drug
delivery
into
central
nervous
system.
Nanoparticles
(NPs)
have
been
widely
explored
as
carriers
capable
of
overcoming
this
effectively
transporting
therapies
brain.
However,
their
potential
directly
address
ameliorate
dysfunction
has
received
limited
attention.
review,
we
examine
how
NPs
enhance
across
treat
diseases
explore
emerging
strategies
restore
integrity
vital
structure.
