International Journal of Molecular Sciences,
Journal Year:
2025,
Volume and Issue:
26(3), P. 1170 - 1170
Published: Jan. 29, 2025
Acidosis,
a
common
feature
of
cerebral
ischemia
and
hypoxia,
results
in
neuronal
damage
death.
This
study
aimed
to
investigate
the
protective
effects
mechanisms
action
melatonin
against
acidosis-induced
damage.
SH-SY5Y
cells
were
exposed
an
acidic
environment
simulate
acidosis,
photothrombotic
(PT)
infarction
model
was
used
establish
animal
male
C57/BL6J
mice.
Both
vivo
vitro
studies
demonstrated
that
acidosis
increased
cytoplasmic
transcription
factor
EB
(TFEB)
levels,
reduced
nuclear
TFEB
suppressed
autophagy,
as
evidenced
by
elevated
p62
higher
LC3-II/LC3-I
ratio,
decreased
synapse-associated
proteins
(PSD-95
synaptophysin),
apoptosis.
In
contrast,
promoted
translocation
TFEB,
enhanced
reversed
Moreover,
role
melatonin’s
neuroprotective
validated
modulating
translocation.
conclusion,
mitigates
promoting
thereby
enhancing
autophagy.
These
findings
offer
new
insights
into
potential
treatments
for
acidosis.
Frontiers in Cellular Neuroscience,
Journal Year:
2025,
Volume and Issue:
19
Published: March 26, 2025
Caenorhabditis
elegans
has
been
widely
used
as
a
model
organism
in
neurodevelopment
for
several
decades
due
to
its
simplicity,
rapid
growth,
short
life
cycle,
transparency,
and
rather
simple
genetics.
It
useful
modeling
neurodegenerative
diseases
by
the
heterologous
expression
of
major
proteins
that
form
neurodegenerative-linked
aggregates
such
amyloid-
β
peptide,
tau
protein,
α
-synuclein,
among
others.
Furthermore,
chemical
treatments
well
existence
interference
RNA
libraries,
transgenic
worm
lines,
possibility
generating
new
strains
create
magnificent
range
possible
tools
study
signaling
pathways
could
confer
protection
against
protein
or,
on
contrary,
are
playing
detrimental
role.
In
this
review,
we
summarize
different
C.
models
with
focus
Alzheimer’s
Parkinson’s
how
genetic
be
dissect
involved
their
pathogenesis
mentioning
examples.
Finally,
discuss
use
pharmacological
agents
help
these
disease-associated
powerful
combinations
experimental
designs
tools.
This
review
highlights
advantages
valuable
intermediary
between
vitro
mammalian
vivo
development
potential
therapies.
