Journal of Controlled Release,
Год журнала:
2024,
Номер
376, С. 470 - 487
Опубликована: Окт. 23, 2024
Alzheimer's
disease
(AD)
is
one
kind
of
devasting
neurodegenerative
disorders
affecting
over
50
million
people
worldwide.
Multi-targeted
therapy
has
emerged
as
a
new
treatment
for
diagnosing
and
alleviating
the
pathogenesis
process
AD;
however,
current
strategy
limited
by
its
unsatisfactory
efficiency.
In
our
study,
engineered
activated
neutrophil-derived
exosomes
(MP@Cur-MExo)
were
developed
to
improve
mitochondrial
function
in
neurons
targeting
Aβ-induced
neurotoxicity.
MP@Cur-MExo
are
derived
from
IL-8-stimulated
neutrophils
decorated
with
mitochondria
ligand
Aβ
targeted
modified
SPION.
Engineered
can
be
cleaved
matrix
metallopeptidase-2,
which
overexpressed
AD
brain.
Consequently,
released
SPION
Curcumin-loaded
collaboratively
protected
neuron
cells
against
deficiency.
addition,
effectively
accumulated
inflamed
region
brain
at
an
early
stage,
allowing
diagnosis
through
bimodal
(MRI/IVIS)
imaging.
Importantly,
mouse
model
stage
AD,
intravenously
injected
restored
reduced
damage,
thereby
attenuating
progression.
conclusion,
designed
demonstrated
that
omnidirectional
improvement
serve
novel
practical
approach
diseases.
This
study
also
reveals
promising
therapeutic
agent
impeding
progression
future
clinical
applications.
International Journal of Molecular Sciences,
Год журнала:
2024,
Номер
25(4), С. 2320 - 2320
Опубликована: Фев. 15, 2024
Genetic
abnormalities
play
a
crucial
role
in
the
development
of
neurodegenerative
disorders
(NDDs).
exploration
has
indeed
contributed
to
unraveling
molecular
complexities
responsible
for
etiology
and
progression
various
NDDs.
The
intricate
nature
rare
common
variants
NDDs
contributes
limited
understanding
genetic
risk
factors
associated
with
them.
Advancements
next-generation
sequencing
have
made
whole-genome
whole-exome
possible,
allowing
identification
substantial
effects,
improving
both
Mendelian
complex
neurological
conditions.
resurgence
gene
therapy
holds
promise
targeting
diseases
ensuring
sustained
correction.
This
approach
is
particularly
enticing
diseases,
where
traditional
pharmacological
methods
fallen
short.
In
context
our
epidemiology
three
most
prevalent
NDDs—amyotrophic
lateral
sclerosis,
Alzheimer’s
disease,
Parkinson’s
primary
goal
underscore
progress
sequencing.
aims
enhance
disease
mechanisms
explore
gene-based
therapies
Throughout
this
review,
we
focus
on
variations,
methodologies
their
identification,
pathophysiology,
promising
potential
therapy.
Ultimately,
objective
provide
comprehensive
forward-looking
perspective
emerging
research
arena
Neuroglia,
Год журнала:
2024,
Номер
5(4), С. 410 - 444
Опубликована: Окт. 21, 2024
Microglia,
the
unique
and
motile
immune
cells
of
central
nervous
system
(CNS),
function
as
a
security
guard
in
maintaining
CNS
homeostasis,
primarily
through
calcium
signaling.
The
dynamics
microglia
control
important
functions
such
phagocytosis,
cytokine
release,
migration.
Calcium
dysregulation
has
been
linked
to
several
disorders,
like
Alzheimer’s
disease
(AD),
Parkinson’s
(PD),
multiple
sclerosis
(MS),
ischemic
stroke
(IS).
entering
channels
voltage-gated
(VGCCs),
store-operated
entry
(SOCE),
transient
receptor
potential
(TRP)
is
essential
for
microglial
activation
pro-inflammatory
responses.
Under
pathological
conditions,
formation
amyloid-β
plaques
AD,
aggregation
α-synuclein
PD,
oxidative
stress
MS,
exacerbates
neuroinflammation,
mitochondrial
dysfunction,
neurodegeneration.
Therapeutic
strategies
targeting
signaling
pathways,
using
channel
blockers
antioxidant
interventions,
show
promise
alleviating
slowing
down
progression.
This
review
summarizes
underlying
mechanisms
therapeutic
benefits
restoring
balance
disorders.
Organic Chemistry Frontiers,
Год журнала:
2024,
Номер
11(6), С. 1824 - 1842
Опубликована: Янв. 1, 2024
In
this
review,
we
briefly
summarize
the
recent
research
progress
in
enantioselective
higher-order
cycloadditions,
focusing
on
preparation
of
medium-sized
and
multicyclic
chiral
molecules
by
metal-free
catalysis.
Cells,
Год журнала:
2025,
Номер
14(3), С. 168 - 168
Опубликована: Янв. 22, 2025
The
recent
approval
of
lecanemab
highlights
that
the
amyloid
beta
(Aβ)
protein
is
an
important
pathological
target
in
Alzheimer’s
disease
(AD)
and
further
emphasizes
significance
neuroinflammatory
pathways
regulating
Aβ
accumulation.
Indeed,
accumulation
triggers
microglia
activation,
which
are
key
mediators
neuroinflammation.
inflammatory
responses
this
process
can
lead
to
neuronal
damage
functional
decline.
Microglia
secrete
proinflammatory
cytokines
accelerate
death
release
anti-inflammatory
growth
factors
contributing
recovery
protection.
Thus,
play
a
dual
role
neurodegeneration
neuroprotection,
complicating
their
function
AD.
Therefore,
elucidating
complex
interactions
between
protein,
microglia,
neuroinflammation
essential
for
developing
new
strategies
treating
This
review
investigates
receptors
involved
activating
aims
enhance
understanding
how
these
processes
impact
AD,
as
well
they
be
regulated.
also
analyzed
studies
reported
existing
literature
ongoing
clinical
trials.
Overall,
will
contribute
regulatory
mechanisms
therapies
slow
progression
Diseases,
Год журнала:
2025,
Номер
13(2), С. 60 - 60
Опубликована: Фев. 16, 2025
Inflammation
is
a
pivotal
characteristic
of
neurodegenerative
diseases.
The
triggering
receptor
expressed
on
the
myeloid
cells
2
(TREM2)
gene
has
previously
been
shown
to
suppress
inflammation
by
directly
inhibiting
inflammation-related
pathways.
Mitochondrial
dysfunction
recently
emerged
as
another
critical
pathological
manifestation
Although
TREM2
involved
in
regulation
cellular
energy
metabolism
and
mitochondrial
autophagy,
its
role
relationship
between
autophagy
remains
unclear.
In
this
study,
we
generated
TREM2-overexpressing
BV-2
established
neuroinflammatory
model
with
LPS.
We
compared
these
wild-type
terms
inflammation,
metabolism,
mitochondria
using
methods
such
RT-qPCR,
Western
blotting,
immunocytochemistry,
transmission
electron
microscopy,
flow
cytometry.
Microglia
overexpressing
exhibited
increased
resistance
inflammation.
Additionally,
inhibited
metabolic
reprogramming
that
occurs
early
LPS-induced
reduced
ROS
release,
mitigated
damage,
maintained
certain
level
autophagic
activity,
cleared
damaged
mitochondria.
Consequently,
they
alleviated
caused
barrier.
ur
results
suggest
can
alleviate
maintaining
homeostasis
activity.
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
Biomarker Research,
Год журнала:
2024,
Номер
12(1)
Опубликована: Ноя. 4, 2024
Abstract
Atherosclerosis
is
a
chronic
lipid-driven
inflammatory
disease
characterized
by
infiltration
of
large
numbers
macrophages.
The
progression
the
closely
related
to
status
macrophages
in
atherosclerotic
plaques.
Recent
advances
plaque
analysis
have
revealed
subpopulation
that
express
high
levels
triggering
receptor
expressed
on
myeloid
cells
2
(TREM2).
Although
TREM2
known
play
critical
role
inflammation,
lipid
metabolism,
and
tissue
repair,
its
atherosclerosis
still
not
fully
understood.
studies
shown
promotes
macrophage
cholesterol
uptake
efflux,
enhances
efferocytosis
function,
regulates
inflammation
cell
survival,
all
which
are
significant
functions
atherosclerosis.
In
early
plaques
increases
lesion
size.
advanced
survival
stability.
dualistic
nature
atherosclerosis,
where
it
can
exert
both
protective
effect
side
increased
size,
presents
complex
but
crucial
area
study.
Understanding
these
dual
roles
could
help
development
new
therapeutic
strategies
modulate
activity
utilize
atheroprotective
function
while
mitigating
deleterious
effects.
this
review,
we
discuss
mechanisms
during
different
stages
plaques,
as
well
potential
applications
diagnosis
treatment
