International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(19), P. 14421 - 14421
Published: Sept. 22, 2023
Neurodegeneration
is
an
age-dependent
progressive
phenomenon
with
no
defined
cause.
Aging
the
main
risk
factor
for
neurodegenerative
diseases.
During
aging,
activated
microglia
undergo
phenotypic
alterations
that
can
lead
to
neuroinflammation,
which
a
well-accepted
event
in
pathogenesis
of
Several
common
mechanisms
are
shared
by
genetically
or
pathologically
distinct
diseases,
such
as
excitotoxicity,
mitochondrial
deficits
and
oxidative
stress,
protein
misfolding
translational
dysfunction,
autophagy
activation.
Progressive
loss
neuronal
population
due
increased
stress
leads
mostly
accumulation
dysfunctional
mitochondria.
Mitochondrial
dysfunction
excessive
neuroinflammatory
responses
both
sufficient
induce
pathology
neurodegeneration.
Therefore,
quality
control
key
determinant
health
survival
cells
brain.
Research
has
been
primarily
focused
demonstrate
significance
health,
despite
important
contributions
non-neuronal
constitute
significant
portion
brain
volume.
Moreover,
morphology
function
distinctly
diverse
different
tissues;
however,
little
known
about
their
molecular
diversity
among
cell
types.
dynamics
types
markedly
decide
fate
overall
health;
therefore,
it
not
justifiable
overlook
active
contribution
facilitating
health.
In
this
review
article,
we
aim
discuss
how
remarkable
highly
synchronized
connecting
property
keeping
neurons
healthy
Cells,
Journal Year:
2021,
Volume and Issue:
10(2), P. 352 - 352
Published: Feb. 9, 2021
Substantial
evidence
indicates
that
mitochondrial
impairment
contributes
to
neuronal
dysfunction
and
vulnerability
in
disease
states,
leading
investigators
propose
the
enhancement
of
function
should
be
considered
a
strategy
for
neuroprotection.
However,
multiple
attempts
improve
have
failed
impact
progression,
suggesting
biology
underlying
normal
regulation
pathways
neurons,
its
disease,
is
more
complex
than
initially
thought.
Here,
we
present
proteins
associated
involved
transcriptional
nuclear-encoded
genes
function,
with
focus
on
coactivator
peroxisome
proliferator-activated
receptor
gamma
coactivator-1alpha
(PGC-1α).
We
highlight
PGC-1α's
roles
non-neuronal
cell
types
discuss
dysregulation
PGC-1α-dependent
Huntington's
Disease,
Parkinson's
developmental
disorders,
emphasizing
relationship
between
disease-specific
cellular
cell-type-specific
patterns
PGC-1α
expression.
Finally,
challenges
inherent
therapeutic
targeting
PGC-1α-related
programs,
considering
neuron-enriched
coactivators
co-regulating
synaptic
genes.
This
information
will
provide
novel
insights
into
unique
aspects
neurons
opportunities
Antioxidants,
Journal Year:
2022,
Volume and Issue:
11(9), P. 1780 - 1780
Published: Sept. 9, 2022
Parkinson’s
disease
(PD)
is
the
second
most
common
neurodegenerative
movement
disorder
characterized
by
a
progressive
loss
of
dopaminergic
neurons
in
substantia
nigra
pars
compacta.
Although
complex
interplay
multiple
environmental
and
genetic
factors
has
been
implicated,
etiology
neuronal
death
PD
remains
unresolved.
Various
mechanisms
degeneration
have
proposed,
including
oxidative
stress,
mitochondrial
dysfunction,
neuroinflammation,
α-synuclein
proteostasis,
disruption
calcium
homeostasis,
other
cell
pathways.
While
many
drugs
individually
targeting
these
pathways
shown
promise
preclinical
models,
this
not
yet
translated
into
neuroprotective
therapies
human
PD.
This
consequently
spurred
efforts
to
identify
alternative
targets
with
multipronged
therapeutic
approaches.
A
promising
target
that
could
modulate
etiological
involves
drug-induced
activation
coordinated
program
regulated
transcription
factor,
nuclear
factor
E2-related
2
(Nrf2).
Nrf2
regulates
over
250
genes,
creating
multifaceted
network
integrates
cellular
activities
expressing
cytoprotective
promoting
resolution
inflammation,
restoring
redox
protein
stimulating
energy
metabolism,
facilitating
repair.
However,
FDA-approved
electrophilic
activators
cause
irreversible
alkylation
cysteine
residues
various
proteins
resulting
side
effects.
We
propose
transcriptional
repressor
BTB
CNC
homology
1
(Bach1),
which
antagonizes
Nrf2,
serve
as
complementary
for
both
Nrf2-dependent
Nrf2-independent
review
presents
current
knowledge
on
Nrf2/Bach1
signaling
pathway,
its
role
processes,
benefits
simultaneously
inhibiting
Bach1
stabilizing
using
non-electrophilic
small
molecules
novel
approach
Oxidative Medicine and Cellular Longevity,
Journal Year:
2022,
Volume and Issue:
2022, P. 1 - 13
Published: Oct. 5, 2022
Parkinson’s
disease
(PD)
is
a
neurodegenerative
second
only
to
Alzheimer’s
in
terms
of
prevalence.
Previous
studies
have
indicated
that
the
occurrence
and
progression
PD
are
associated
with
mitochondrial
dysfunction.
Mitochondrial
dysfunction
one
most
important
causes
for
apoptosis
dopaminergic
neurons.
Therefore,
maintaining
stability
functioning
potential
strategy
treatment
PD.
Voltage-dependent
anion
channel
(VDAC)
main
component
outer
membrane,
it
participates
variety
biological
processes.
In
this
review,
we
focus
on
roles
VDACs
We
found
involved
by
regulating
apoptosis,
autophagy,
ferroptosis.
VDAC1
oligomerization,
ubiquitination,
regulation
permeability
transition
pore
(mPTP)
VDACs,
interaction
between
α-synuclein
(α-syn)
all
promising
methods
proposed
inhibition
oligomerization
promotion
ubiquitination
as
an
effective
approach
proven
expression
has
significant
change
models.
The
levels
decreased
substantia
nigra
(SN)
patients
suffering
from
compared
control
group
consisting
normal
individuals
using
bioinformatics
tools.
VDAC2
mainly
through
apoptosis.
VDAC3
may
similar
function
VDAC1.
It
can
be
concluded
functional
contribute
therapeutic
International Journal of Molecular Sciences,
Journal Year:
2023,
Volume and Issue:
24(19), P. 14421 - 14421
Published: Sept. 22, 2023
Neurodegeneration
is
an
age-dependent
progressive
phenomenon
with
no
defined
cause.
Aging
the
main
risk
factor
for
neurodegenerative
diseases.
During
aging,
activated
microglia
undergo
phenotypic
alterations
that
can
lead
to
neuroinflammation,
which
a
well-accepted
event
in
pathogenesis
of
Several
common
mechanisms
are
shared
by
genetically
or
pathologically
distinct
diseases,
such
as
excitotoxicity,
mitochondrial
deficits
and
oxidative
stress,
protein
misfolding
translational
dysfunction,
autophagy
activation.
Progressive
loss
neuronal
population
due
increased
stress
leads
mostly
accumulation
dysfunctional
mitochondria.
Mitochondrial
dysfunction
excessive
neuroinflammatory
responses
both
sufficient
induce
pathology
neurodegeneration.
Therefore,
quality
control
key
determinant
health
survival
cells
brain.
Research
has
been
primarily
focused
demonstrate
significance
health,
despite
important
contributions
non-neuronal
constitute
significant
portion
brain
volume.
Moreover,
morphology
function
distinctly
diverse
different
tissues;
however,
little
known
about
their
molecular
diversity
among
cell
types.
dynamics
types
markedly
decide
fate
overall
health;
therefore,
it
not
justifiable
overlook
active
contribution
facilitating
health.
In
this
review
article,
we
aim
discuss
how
remarkable
highly
synchronized
connecting
property
keeping
neurons
healthy
