CNS Neuroscience & Therapeutics,
Journal Year:
2022,
Volume and Issue:
29(1), P. 91 - 103
Published: Oct. 2, 2022
Abstract
Aims
The
peptidyl‐prolyl
cis/trans
isomerase,
Pin1,
has
a
protective
role
in
age‐related
neurodegeneration
by
targeting
different
phosphorylation
sites
of
tau
and
the
key
proteins
required
to
produce
Amyloid‐β,
which
are
well‐known
molecular
signatures
Alzheimer's
disease
(AD)
neuropathology.
direct
interaction
miR‐140‐5p
with
Pin1
mRNA
its
inhibitory
protein
translation
been
identified.
main
purpose
this
study
was
investigate
miRNA‐140‐5p
inhibition
promoting
expression
therapeutic
potential
AntimiR‐140‐5p
Aß
oligomer
(AßO)‐induced
AD
rat
model.
Methods
Spatial
learning
memory
were
assessed
Morris
water
maze.
RT‐PCR,
western
blot,
histological
assays
performed
on
hippocampal
samples
at
various
time
points
after
treatments.
enhanced
ADAM10
expressions
but
little
effect
level.
Results
inhibitor
markedly
ameliorated
spatial
deficits
induced
AßO,
concomitantly
suppressed
inflammatory
mediators
TNFα
IL‐1β,
three
(thr231,
ser396,
ser404)
as
well
increased
phosphorylated
Ser473‐Akt.
Conclusion
According
our
results,
Antimir‐140‐mediated
improvement
AβO‐induced
neuronal
injury
impairment
rats
may
provide
an
appropriate
rationale
for
evaluating
inhibitors
promising
agent
treatment
AD.
Life Sciences,
Journal Year:
2025,
Volume and Issue:
369, P. 123563 - 123563
Published: March 13, 2025
A
decline
in
cellular
quality
control
mechanisms
is
one
of
the
processes
brain
aging.
Autophagy
and
proteostasis
are
two
regulatory
that
maintain
component
turnover
to
preserve
homeostasis,
optimal
function,
neuronal
health
by
eliminating
damaged
aggregated
proteins
preventing
neurodegenerative
disorders
(NDDs).
Impaired
autophagy
significant
hallmarks
aging
many
age-related
NDDs.
MicroRNAs
noncoding
RNA
molecules
have
recently
been
shown
be
essential
for
regulating
several
biological
processes,
such
as
autophagy,
proteostasis,
differentiation,
development
targeting
mRNA's
3'untranslated
region
(3'UTR).
During
aging,
miRNAs
dysregulate
resulting
abnormal
activity
protein
aggregation,
a
characteristic
This
review
highlights
complex
interactions
orchestration
autophagy.
dysregulation
impairs
autophagic
flux
accelerates
disorders,
neuroinflammation,
neurodegeneration.
Understanding
among
miRNAs,
novel
therapeutics
Abstract
Ischemia–reperfusion
(I/R)
injury
describes
the
pathological
process
wherein
tissue
damage,
initially
caused
by
insufficient
blood
supply
(ischemia),
is
exacerbated
upon
restoration
of
flow
(reperfusion).
This
phenomenon
can
lead
to
irreversible
damage
and
commonly
observed
in
contexts
such
as
cardiac
surgery
stroke,
where
temporarily
obstructed.
During
ischemic
conditions,
anaerobic
metabolism
tissues
organs
results
compromised
enzyme
activity.
Subsequent
reperfusion
exacerbates
mitochondrial
dysfunction,
leading
increased
oxidative
stress
accumulation
reactive
oxygen
species
(ROS).
cascade
ultimately
triggers
cell
death
through
mechanisms
autophagy
mitophagy.
Autophagy
constitutes
a
crucial
catabolic
mechanism
within
eukaryotic
cells,
facilitating
degradation
recycling
damaged,
aged,
or
superfluous
organelles
proteins
via
lysosomal
pathway.
essential
for
maintaining
cellular
homeostasis
adapting
diverse
conditions.
As
self-degradation
clearance
mechanism,
exhibits
dualistic
function:
it
confer
protection
during
initial
phases
injury,
yet
potentially
exacerbate
later
stages.
paper
aims
elucidate
fundamental
I/R
highlighting
its
dual
role
regulation
effects
on
both
organ-specific
systemic
responses.
By
comprehending
their
implications
organ
function,
this
study
seeks
explore
potential
therapeutic
interventions
modulation
clinical
settings.
Abstract
Multiple
sclerosis
(MS),
the
most
prevalent
myelinopathy
with
unclear
etiology,
involves
mitochondrial
dysfunction
that
critically
contributes
to
oligodendrocyte
damage
and
neurodegeneration.
Recent
interest
has
surged
around
role
of
inflammatory
ncRNAs
in
function,
particularly
context
neurodegenerative
diseases
(NDs)
where
neuroinflammationis
a
hallmark
feature.
This
review
emphasizes
collection
characterization
mitochondrial-related
(MR)
non-coding
RNAs
(ncRNAs)
(MRncRNAs),
have
been
extensively
studied
NDs.
Through
literature
review,
we
identified
36
upregulated
MRncRNAs
Parkinson's
disease
(PD),
Amyotrophic
lateral
(ALS),
Alzheimer's
(ALZ),
Huntington's
(HD).
Notably,
miR-34
was
most
dominantly
dysregulated
miR
PD,
ALS,
ALZ
while
HD,
two
other
miRNAs
(miR-10b-5p
miR-196a)
identified.
Further
bioinformatic
analysis
revealed
miR-124-5p,
-146a-3p,
-15b-3p
target
genes
more
than
others,
mRNA
pro-apoptotic
protein
BCL2L11
is
targeted.
link
between
these
function
MS
remains
unidentified.
Among
81
detected
patients,
nine
(miR-15b,
miR-21,
miR-27b,
miR-34a,
miR-124,
miR-137,
miR-146a,
miR-155,
miR-92a)
shared
lncRNAs
(MALAT1
HOTAIR).
autophagy
pathway
involved.
Six
are
significantly
involved
MR
diseases.
miR-34a-5p
showed
connection
mitochondria,
miR-15b
targeted
hub
genes,
SDHC
BCL2.
Moreover,
several
proteins
(HIF1A,
STAT3,
MAPK1,
GSK3B)
by
well-known
regulators
pathways
homeostasis:
These
findings
highlight
critical
roles
neurodegeneration,
emphasizing
urgent
need
for
experimental
studies
on
MRmiRNAs,
myelinopathies.
Frontiers in Aging Neuroscience,
Journal Year:
2025,
Volume and Issue:
17
Published: May 7, 2025
Alzheimer’s
disease
(AD)
is
a
neurodegenerative
condition
associated
with
aging.
As
the
population
ages,
incidence
of
AD
has
risen
annually,
making
it
fourth
leading
cause
death,
following
cardiovascular
disease,
cancer,
and
stroke.
The
main
pathological
features
are
now
thought
to
include
accumulation
extracellular
amyloid-β
(Aβ)
plaques,
formation
intracellular
neurofibrillary
tangles,
reduction
in
synaptic
connections
cerebral
cortex
hippocampus.
Polyphenols
help
protect
against
by
influencing
Aβ
metabolism.
Research
shown
that
polyphenols
particularly
effective
reducing
inflammation
inhibiting
tumor
necrosis
factor-activated
TNF-κB
activity,
indicating
their
significant
pharmacological
activity.
MicroRNAs
(miRNAs)
play
role
regulating
miRNA
stability
protein
expression
after
transcription.
They
prevalent
brain
tissue
can
specifically
influence
neuronal
growth
synapses.
levels
miRNAs
brains
patients
significantly
differ
from
those
healthy
individuals
same
age.
have
been
recognized
as
potential
biological
markers
therapeutic
targets
for
early
diagnosis
AD.
It
important
note
gene
regulation
affecting
various
miRNAs,
suggesting
link
between
polyphenols,
AD,
miRNAs.
This
review
examines
whether
impact
APP
Aβ.
Additionally,
we
explored
effects
on
related
Frontiers in Aging,
Journal Year:
2025,
Volume and Issue:
6
Published: May 13, 2025
MicroRNAs
(miRNAs)
are
small
non-coding
RNA
molecules
that
known
to
regulate
gene
expression
in
their
target
locations
thereby
contributing
epigenetic
mechanisms
associated
with
disease
pathologies.
Dysregulation
of
miRNA
activity
has
been
implicated
the
pathology
Alzheimer’s
(AD),
offering
insights
into
potential
biomarkers
for
early
diagnosis
and
therapeutic
targets.
Mitochondrial
dysfunction
its
effects
(such
as
oxidative
stress)
can
be
seen
early-onset
AD.
This
review
critically
examines
recent
findings
on
mitochondrial-associated
miRNAs—including
miR-34a,
miR-140,
miR-455-3p,
miR-1273g-3p—highlighting
roles
mitochondrial
bioenergetics,
stress,
synaptic
function.
We
discuss
targeting
specific
miRNAs
restore
health
explore
utility
AD
diagnosis.
A
better
understanding
miRNA-mediated
regulation
may
open
new
avenues
intervention
Frontiers in Cell and Developmental Biology,
Journal Year:
2022,
Volume and Issue:
9
Published: Jan. 4, 2022
As
a
primary
cause
of
dementia
and
death
in
older
people,
Alzheimer's
disease
(AD)
has
become
common
problem
challenge
worldwide.
Abnormal
accumulation
tau
proteins
the
brain
is
hallmark
pathology
AD
closely
related
to
clinical
progression
severity
cognitive
deficits.
Here,
we
found
that
overexpression
phosphatase
tensin
homolog
(PTEN)-induced
kinase
1
(PINK1)
effectively
promoted
degradation
tau,
thereby
rescuing
neuron
loss,
synaptic
damage,
impairments
mouse
model
tauopathy
with
AAV-full-length
human
Tau
(hTau)
injected
into
hippocampal
CA1
area
(hTau
mice).
Overexpression
PINK1
activated
autophagy,
chloroquine
but
not
MG132
reversed
PINK1-induced
decrease
levels
improvement
hTau
mice.
Furthermore,
also
ameliorated
mitochondrial
dysfunction
induced
by
hTau.
Taken
together,
our
data
revealed
abnormal
accumulated
via
autophagy-lysosome
pathway,
indicating
may
be
potential
target
for
treatment.
International Journal of Molecular Sciences,
Journal Year:
2022,
Volume and Issue:
23(14), P. 7789 - 7789
Published: July 14, 2022
As
a
neurodegenerative
disease,
Alzheimer’s
disease
(AD)
shows
higher
incidence
during
the
aging
process,
mainly
revealing
characteristics
of
significant
decrease
in
cognition,
uncontrolled
emotion,
and
reduced
learning
memory
capacity,
even
leading
to
death.
In
prevention
treatment
AD,
some
pharmacological
therapy
has
been
applied
clinical
practice.
Unfortunately,
there
are
still
limited
effective
treatments
for
AD
due
absence
clear
defined
targets.
Currently,
it
is
recognized
that
causes
include
amyloid-β
peptide
(Aβ)
deposition,
hyperphosphorylation
tau
protein,
neurofibrillary
tangles,
mitochondrial
dysfunction,
inflammation.
With
in-depth
mechanistic
exploration,
found
these
highly
correlated
with
dysfunctional
status
autophagy.
Numerous
experimental
results
have
also
confirmed
development
progression
accompanied
by
an
abnormal
functional
autophagy;
therefore,
regulating
autophagy
become
one
important
strategies
alleviating
or
arresting
AD.
increasing
attention
given
microRNAs
(miRNAs),
more
studies
series
miRNAs
involved
through
indirect
regulation
Therefore,
targeting
may
be
essential
breakthrough
This
article
summarizes
autophagy,
aim
providing
new
theoretical
reference
point
miRNA-mediated