Journal of Clinical Investigation,
Journal Year:
2018,
Volume and Issue:
128(4), P. 1208 - 1216
Published: Feb. 18, 2018
Along
with
a
general
decline
in
overall
health,
most
chronic
degenerative
human
diseases
are
inherently
associated
increasing
age.
Age-associated
cognitive
impairments
and
neurodegenerative
diseases,
such
as
Parkinson’s
Alzheimer’s
potentially
debilitating
conditions
that
lack
viable
options
for
treatment,
resulting
tremendous
economic
societal
cost.
Most
high-profile
clinical
trials
have
led
to
inefficacious
results,
suggesting
novel
approaches
treating
these
pathologies
needed.
Numerous
recent
studies
demonstrated
senescent
cells,
which
characterized
by
sustained
cell
cycle
arrest
production
of
distinct
senescence-associated
secretory
phenotype,
accumulate
age
at
sites
age-related
throughout
the
body,
where
they
actively
promote
tissue
deterioration.
Cells
features
senescence
been
detected
context
brain
aging
disease,
may
also
dysfunction.
Here,
we
discuss
evidence
implicating
cells
mechanistic
contribution
drive
neurodegeneration,
how
or
their
effects
be
targeted
therapeutically.
International Journal of Molecular Sciences,
Journal Year:
2019,
Volume and Issue:
20(9), P. 2293 - 2293
Published: May 9, 2019
A
large
body
of
experimental
evidence
suggests
that
neuroinflammation
is
a
key
pathological
event
triggering
and
perpetuating
the
neurodegenerative
process
associated
with
many
neurological
diseases.
Therefore,
different
stimuli,
such
as
lipopolysaccharide
(LPS),
are
used
to
model
neurodegeneration.
By
acting
at
its
receptors,
LPS
activates
various
intracellular
molecules,
which
alter
expression
plethora
inflammatory
mediators.
These
factors,
in
turn,
initiate
or
contribute
development
processes.
an
important
tool
for
study
However,
serotype,
route
administration,
number
injections
this
toxin
induce
varied
responses.
Thus,
here,
we
review
use
models
neurodegeneration
well
discuss
neuroinflammatory
mechanisms
induced
by
could
underpin
events
linked
process.
Molecular Brain,
Journal Year:
2017,
Volume and Issue:
10(1)
Published: Nov. 28, 2017
Parkinson's
disease
(PD)
is
a
chronic
and
progressive
neurodegeneration
of
dopamine
neurons
in
the
substantia
nigra.
The
reason
for
death
these
unclear;
however,
studies
have
demonstrated
potential
involvement
mitochondria,
endoplasmic
reticulum,
α-synuclein
or
levels
contributing
to
cellular
oxidative
stress
as
well
PD
symptoms.
Even
though
those
papers
had
separately
described
individual
roles
each
element
leading
neurodegeneration,
recent
publications
suggest
that
product
various
interactions.
This
review
discusses
role
mediating
separate
pathological
events
together,
ultimately
result
cell
PD.
Understanding
multi-faceted
relationships
between
events,
with
common
denominator
underlying
processes,
needed
developing
better
therapeutic
strategies.
Journal of Clinical Investigation,
Journal Year:
2018,
Volume and Issue:
128(4), P. 1208 - 1216
Published: Feb. 18, 2018
Along
with
a
general
decline
in
overall
health,
most
chronic
degenerative
human
diseases
are
inherently
associated
increasing
age.
Age-associated
cognitive
impairments
and
neurodegenerative
diseases,
such
as
Parkinson’s
Alzheimer’s
potentially
debilitating
conditions
that
lack
viable
options
for
treatment,
resulting
tremendous
economic
societal
cost.
Most
high-profile
clinical
trials
have
led
to
inefficacious
results,
suggesting
novel
approaches
treating
these
pathologies
needed.
Numerous
recent
studies
demonstrated
senescent
cells,
which
characterized
by
sustained
cell
cycle
arrest
production
of
distinct
senescence-associated
secretory
phenotype,
accumulate
age
at
sites
age-related
throughout
the
body,
where
they
actively
promote
tissue
deterioration.
Cells
features
senescence
been
detected
context
brain
aging
disease,
may
also
dysfunction.
Here,
we
discuss
evidence
implicating
cells
mechanistic
contribution
drive
neurodegeneration,
how
or
their
effects
be
targeted
therapeutically.
