International Journal of Molecular Sciences,
Год журнала:
2023,
Номер
24(19), С. 14421 - 14421
Опубликована: Сен. 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
Journal of Parkinson s Disease,
Год журнала:
2020,
Номер
11(1), С. 45 - 60
Опубликована: Окт. 13, 2020
Mitochondrial
dysfunction
represents
a
well-established
player
in
the
pathogenesis
of
both
monogenic
and
idiopathic
Parkinson’s
disease
(PD).
Initially
originating
from
observation
that
mitochondrial
toxins
cause
PD,
findings
genetic
PD
supported
contribution
to
disease.
Here,
proteins
encoded
by
autosomal
recessively
inherited
genes
Parkin,
PTEN-induced
kinase
1
(PINK1),
DJ-1
are
involved
pathways.
Additional
evidence
for
stems
models
autosomal-dominant
due
mutations
alpha-synuclein
(SNCA)
leucine-rich
repeat
2
(LRRK2).
Moreover,
patients
harboring
alterations
polymerase
gamma
(POLG)
often
exhibit
signs
parkinsonism.
While
some
molecular
studies
suggest
is
primary
event
others
speculate
it
result
impaired
clearance.
Most
recent
research
even
implicated
damage-associated
patterns
released
non-degraded
mitochondria
neuroinflammatory
processes
PD.
we
summarize
manifold
literature
dealing
with
context
light
advances
field
personalized
medicine,
patient
stratification
according
degree
impairment
followed
enhancement
therapy
may
hold
potential
at
least
subset
cases.
Thus,
second
part
this
review,
discuss
therapeutic
approaches
targeting
aim
prevent
or
delay
neurodegeneration
The Journal of Cell Biology,
Год журнала:
2021,
Номер
220(4)
Опубликована: Март 22, 2021
Parkinson’s
disease
(PD)
is
a
progressive
neurodegenerative
disorder
resulting
from
the
death
of
dopamine
neurons
in
substantia
nigra
pars
compacta.
Our
understanding
PD
biology
has
been
enriched
by
identification
genes
involved
its
rare,
inheritable
forms,
termed
PARK
genes.
These
encode
proteins
including
α-syn,
LRRK2,
VPS35,
parkin,
PINK1,
and
DJ1,
which
can
cause
monogenetic
when
mutated.
Investigating
cellular
functions
these
instrumental
identifying
signaling
pathways
that
mediate
pathology
neuroprotective
mechanisms
active
during
homeostatic
pathological
conditions.
It
now
evident
many
PD-associated
perform
multiple
neurons.
Furthermore,
several
contribute
to
non–cell-autonomous
neuron
death,
such
as
neuroinflammation.
A
comprehensive
cell-autonomous
essential
for
developing
therapeutics
may
slow
or
halt
progression.
Journal of Biomedical Science,
Год журнала:
2023,
Номер
30(1)
Опубликована: Окт. 12, 2023
Mitochondrial
mass
and
quality
are
tightly
regulated
by
two
essential
opposing
mechanisms,
mitochondrial
biogenesis
(mitobiogenesis)
mitophagy,
in
response
to
cellular
energy
needs
other
environmental
cues.
Great
strides
have
been
made
uncover
key
regulators
of
these
complex
processes.
Emerging
evidence
has
shown
that
there
exists
a
tight
coordination
between
mitophagy
mitobiogenesis,
their
defects
may
cause
many
human
diseases.
In
this
review,
we
will
first
summarize
the
recent
advances
discovery
molecular
regulations
mitobiogenesis
then
focus
on
mechanism
signaling
pathways
involved
simultaneous
regulation
tissue
or
cultured
cells
needs,
stress,
pathophysiological
conditions.
Further
studies
crosstalk
processes
at
level
provide
better
understanding
how
cell
maintains
optimal
fitness
function
under
physiological
conditions,
which
holds
promise
for
fighting
aging
aging-related
Frontiers in Aging Neuroscience,
Год журнала:
2022,
Номер
14
Опубликована: Июнь 20, 2022
Parkinson's
disease
(PD)
is
one
of
the
most
common
neurodegenerative
movement
disorders
worldwide.
There
are
currently
no
cures
or
preventative
treatments
for
PD.
Emerging
evidence
indicates
that
mitochondrial
dysfunction
closely
associated
with
pathogenesis
sporadic
and
familial
Because
dopaminergic
neurons
have
high
energy
demand,
cells
affected
by
PD
exhibit
promotes
disease-defining
loss
in
substantia
nigra
pars
compacta
(SNpc).
The
mitochondrion
has
a
particularly
important
role
as
cellular
"powerhouse"
neurons.
Therefore,
mitochondria
become
promising
therapeutic
target
treatments.
This
review
aims
to
describe
pathology
PD,
outline
genes
factors
related
summarize
current
knowledge
on
quality
control
give
an
overview
strategies
targeting
neuroprotective
interventions
