Some
of
neurodegenerative
diseases
may
be
characterized
by
continuing
behavioral
and
cognitive
dysfunction
that
contains
memory
loss
and/or
apathy.
Alzheimer's
disease
is
the
most
typical
type
such
deficit
cognition
alteration
behavior.
Despite
huge
efforts
against
disease,
there
has
been
yet
no
successful
treatment
for
this
disease.
Interestingly,
several
possible
risk
genes
to
are
frequently
expressed
within
brain
cells,
which
also
linked
cholesterol
metabolism,
lipid
transport,
exosomes
caveolae
formation,
suggesting
a
therapeutic
target
consider
dysfunctions.
modulation
autophagy/mitophagy
with
glucagon-like
peptide-1
(GLP-1)
N-methyl-d-aspartate
(NMDA)
receptors
signaling
offer
novel
approach
prevent
alleviate
dysfunction.
A
paradigm
both
GLP-1
NMDA
at
sites
promising
crucial
dysfunctions
presented
here,
might
able
modify
progression
This
research
direction
open
potential
move
clinical
care
toward
disease-modifying
strategies
maximal
benefits
patients
without
detrimental
adverse
events
diseases.
International Immunopharmacology,
Journal Year:
2024,
Volume and Issue:
141, P. 112934 - 112934
Published: Aug. 23, 2024
Hepatic
fibrosis
is
a
common
pathology
present
in
most
chronic
liver
diseases.
Autophagy
lysosome-mediated
intracellular
catabolic
and
recycling
process
that
plays
an
essential
role
maintaining
normal
hepatic
functions.
Nuclear
factor
erythroid
2-like
2
(Nrf2)
transcription
responsible
for
the
regulation
of
cellular
anti-oxidative
stress
response.
This
study
was
designed
to
assess
cytoprotective
effect
mesenchymal
stem
cell-derived
exosomes
(MSC-exos)
on
endothelial-mesenchymal
transition
(EMT)
Carbon
Tetrachloride
(CCL4)
induced
fibrosis.
Rats
were
treated
with
0.1
ml
CCL4
twice
weekly
8
weeks,
followed
by
administration
single
dose
MSC-exos.
then
sacrificed
after
4
samples
collected
gene
expression
analyses,
Western
blot,
histological
studies,
immunohistochemistry,
transmission
electron
microscopy.
Our
results
showed
MSC-exos
decreased
collagen
deposition,
apoptosis,
inflammation.
Exosomes
modulate
Nrf2/Keap1/p62
pathway,
restoring
autophagy
Nrf2
levels
through
modulation
non-canonical
pathway
Nrf2/Keap1/p62.
Additionally,
regulated
miR-153-3p,
miR-27a,
miR-144
miRNA-34a
expression.
In
conclusion,
shed
light
as
agent
against
EMT
tumorigenesis
Molecules,
Journal Year:
2024,
Volume and Issue:
29(16), P. 3922 - 3922
Published: Aug. 20, 2024
Some
neurodegenerative
diseases
may
be
characterized
by
continuing
behavioral
and
cognitive
dysfunction
that
encompasses
memory
loss
and/or
apathy.
Alzheimer’s
disease
is
the
most
typical
type
of
such
are
deficits
cognition
alterations
behavior.
Despite
huge
efforts
against
disease,
there
has
yet
been
no
successful
treatment
for
this
disease.
Interestingly,
several
possible
risk
genes
frequently
expressed
within
brain
cells,
which
also
linked
to
cholesterol
metabolism,
lipid
transport,
exosomes,
caveolae
formation,
suggesting
a
therapeutic
target
dysfunctions.
modulation
autophagy/mitophagy
with
alteration
glucagon-like
peptide-1
(GLP-1)
N-methyl-d-aspartate
(NMDA)
receptor
signaling
offer
novel
approach
preventing
alleviating
dysfunction.
A
paradigm
showing
both
GLP-1
NMDA
receptors
at
sites
promising
crucial
targets
dysfunctions
presented
here,
able
modify
progression
This
research
direction
create
potential
move
clinical
care
toward
disease-modifying
strategies
maximal
benefits
patients
without
detrimental
adverse
events
diseases.
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(22), P. 12378 - 12378
Published: Nov. 18, 2024
Alzheimer's
disease
is
a
progressive
neurodegenerative
disorder
characterized
by
mitochondria
dysfunction,
accumulation
of
beta-amyloid
plaques,
and
hyperphosphorylated
tau
tangles
in
the
brain
leading
to
memory
loss
cognitive
deficits.
There
currently
no
cure
for
this
condition,
but
potential
stem
cells
therapy
pathologies
actively
being
researched.
This
review
discusses
preclinical
clinical
studies
that
have
used
mouse
models
human
patients
investigate
use
novel
types
cell
treatment
approaches.
The
findings
provide
valuable
insights
into
applications
cell-based
therapies
include
neural,
glial,
mesenchymal,
embryonic,
induced
pluripotent
cells.
We
cover
current
on
replacement
where
can
functionally
integrate
neural
networks,
replace
damaged
neurons,
strengthen
impaired
synaptic
circuits
brain.
address
paracrine
action
acting
via
secreted
factors
induce
neuroregeneration
modify
inflammatory
responses.
focus
neuroprotective
functions
exosomes
as
well
their
neurogenic
synaptogenic
effects.
look
shuttling
through
tunneling
nanotubes
enables
transfer
healthy
restoring
normal
functioning
cells,
improving
metabolism,
reducing
level
apoptosis.
