GeroScience,
Journal Year:
2020,
Volume and Issue:
43(3), P. 1135 - 1158
Published: Oct. 10, 2020
Abstract
In
2009,
rapamycin
was
reported
to
increase
the
lifespan
of
mice
when
implemented
later
in
life.
This
observation
resulted
a
sea-change
how
researchers
viewed
aging.
first
evidence
that
pharmacological
agent
could
have
an
impact
on
aging
administered
life,
i.e.,
intervention
did
not
be
early
life
before
negative
Over
past
decade,
there
has
been
explosion
number
reports
studying
effect
various
diseases,
physiological
functions,
and
biochemical
processes
mice.
this
review,
we
focus
those
areas
which
is
strong
for
rapamycin’s
age-related
diseases
mice,
e.g.,
lifespan,
cardiac
disease/function,
central
nervous
system,
immune
cell
senescence.
We
conclude
it
time
pre-clinical
studies
focused
taking
clinic,
as
potential
treatment
Alzheimer’s
disease.
Frontiers in Bioscience-Scholar,
Journal Year:
2012,
Volume and Issue:
S4(3), P. 941 - 952
Published: Jan. 1, 2012
The
buildup
of
Abeta
and
tau
is
believed
to
directly
cause
or
contribute
the
progressive
cognitive
deficits
characteristic
Alzheimer
disease.
However,
molecular
pathways
linking
accumulation
learning
memory
remain
elusive.
There
growing
evidence
that
soluble
forms
can
obstruct
by
interfering
with
several
signaling
cascades.
In
this
review,
I
will
present
data
showing
mammalian
target
rapamycin
(mTOR)
may
play
a
role
in
induced
neurodegeneration.
Frontiers in Molecular Neuroscience,
Journal Year:
2015,
Volume and Issue:
8
Published: Dec. 16, 2015
Since
the
discovery
of
phosphorylation
40S
ribosomal
protein
S6
(rpS6)
about
four
decades
ago,
much
effort
has
been
made
to
uncover
molecular
mechanisms
underlying
regulation
this
post-translational
modification.
In
field
neuroscience,
rpS6
is
commonly
used
as
a
readout
mammalian
target
rapamycin
complex
1
signaling
activation
or
marker
for
neuronal
activity.
Nevertheless,
its
biological
role
in
neurons
still
remains
puzzling.
Here
we
review
pharmacological
and
physiological
stimuli
regulating
modification
nervous
system
well
pathways
that
transduce
these
signals
into
phosphorylation.
Altered
observed
various
genetic
pathophysiological
mouse
models
also
discussed.
Finally,
examine
current
state
knowledge
on
highlight
questions
remain
be
addressed.
GeroScience,
Journal Year:
2020,
Volume and Issue:
43(3), P. 1135 - 1158
Published: Oct. 10, 2020
Abstract
In
2009,
rapamycin
was
reported
to
increase
the
lifespan
of
mice
when
implemented
later
in
life.
This
observation
resulted
a
sea-change
how
researchers
viewed
aging.
first
evidence
that
pharmacological
agent
could
have
an
impact
on
aging
administered
life,
i.e.,
intervention
did
not
be
early
life
before
negative
Over
past
decade,
there
has
been
explosion
number
reports
studying
effect
various
diseases,
physiological
functions,
and
biochemical
processes
mice.
this
review,
we
focus
those
areas
which
is
strong
for
rapamycin’s
age-related
diseases
mice,
e.g.,
lifespan,
cardiac
disease/function,
central
nervous
system,
immune
cell
senescence.
We
conclude
it
time
pre-clinical
studies
focused
taking
clinic,
as
potential
treatment
Alzheimer’s
disease.
