Translational Neurodegeneration,
Journal Year:
2024,
Volume and Issue:
13(1)
Published: Feb. 20, 2024
Abstract
Brain
aging
is
a
recognized
risk
factor
for
neurodegenerative
diseases
like
Alzheimer's
disease,
Parkinson's
and
amyotrophic
lateral
sclerosis
(ALS,
Lou
Gehrig's
disease),
but
the
intricate
interplay
between
brain
pathogenesis
of
these
conditions
remains
inadequately
understood.
Cellular
senescence
considered
to
contribute
cellular
dysfunction
inflammaging.
According
threshold
theory
senescent
cell
accumulation,
vulnerability
associated
with
rates
generation
clearance
within
brain.
Given
role
microglia
in
eliminating
cells,
accumulation
may
lead
acceleration
aging,
contributing
inflammaging
increased
diseases.
In
this
review,
we
propose
idea
that
microglia,
which
notably
vulnerable
could
potentially
serve
as
central
catalyst
progression
The
are
emerging
promising
target
mitigating
Molecular Metabolism,
Journal Year:
2023,
Volume and Issue:
74, P. 101755 - 101755
Published: June 16, 2023
Recently,
the
hallmarks
of
aging
were
updated
to
include
dysbiosis,
disabled
macroautophagy,
and
chronic
inflammation.
In
particular,
low-grade
inflammation
during
aging,
without
overt
infection,
is
defined
as
"inflammaging,"
which
associated
with
increased
morbidity
mortality
in
population.
Emerging
evidence
suggests
a
bidirectional
cyclical
relationship
between
development
age-related
conditions,
such
cardiovascular
diseases,
neurodegeneration,
cancer,
frailty.
How
crosstalk
other
underlies
biological
mechanisms
disease
thus
particular
interest
current
geroscience
research.
BMC Medicine,
Journal Year:
2022,
Volume and Issue:
20(1)
Published: Dec. 27, 2022
Abstract
Obesity
usually
is
accompanied
by
inflammation
of
fat
tissue,
with
a
prominent
role
visceral
fat.
Chronic
in
obese
tissue
lower
grade
than
acute
immune
activation
for
clearing
the
from
an
infectious
agent.
It
loss
adipocyte
metabolic
homeostasis
that
causes
resident
cells
supporting
functions
and
regaining
homeostasis.
Initially,
excess
influx
lipids
glucose
context
overnutrition
met
growth
proliferation.
Eventual
lipid
overload
hypertrophic
adipocytes
leads
to
endoplasmic
reticulum
stress
secretion
variety
signals
causing
increased
sympathetic
tone,
lipolysis
adipocytes,
uptake
macrophages,
matrix
remodeling,
angiogenesis,
cell
activation.
Pro-inflammatory
signaling
system
release
amounts
pro-inflammatory
other
mediators
resulting
enhanced
tissue-protective
responses.
With
chronic
overnutrition,
these
protective
actions
are
insufficient,
death
as
well
senescence
several
types
seen.
This
structural
damage
expression
or
immunostimulatory
components
monocytes
many
types,
contribution
stromal
cells.
Matrix
remodeling
angiogenesis
further
intensified
possibly
detrimental
fibrosis.
The
accumulation
senescent
also
may
be
via
eventual
spread
state
affected
neighboring
microRNA-containing
vesicles.
Obese
can
viewed
initially
response
order
cope
ambient
nutrients
restore
but
contribute
at
later
stage.
Life,
Journal Year:
2022,
Volume and Issue:
12(9), P. 1332 - 1332
Published: Aug. 28, 2022
Aging
is
a
biological
feature
that
characterized
by
gradual
degeneration
of
function
in
cells,
tissues,
organs,
or
an
intact
organism
due
to
the
accumulation
environmental
factors
and
stresses
with
time.
Several
have
been
attributed
aging
such
as
oxidative
stress
augmented
production
exposure
reactive
oxygen
species,
inflammatory
cytokines
production,
telomere
shortening,
DNA
damage,
and,
importantly,
deposit
senescent
cells.
These
are
irreversibly
mitotically
inactive,
yet
metabolically
active
The
reason
underlying
their
senescence
lies
within
extrinsic
intrinsic
arms.
arm
mainly
expression
secretory
profile
known
senescence-associated
phenotype
(SASP).
results
from
impact
several
genes
meant
regulate
cell
cycle,
tumor
suppressor
genes.
P16
Signal Transduction and Targeted Therapy,
Journal Year:
2023,
Volume and Issue:
8(1)
Published: March 14, 2023
Abstract
The
ageing
process
is
a
systemic
decline
from
cellular
dysfunction
to
organ
degeneration,
with
more
predisposition
deteriorated
disorders.
Rejuvenation
refers
giving
aged
cells
or
organisms
youthful
characteristics
through
various
techniques,
such
as
reprogramming
and
epigenetic
regulation.
great
leaps
in
rejuvenation
prove
that
not
one-way
street,
many
rejuvenative
interventions
have
emerged
delay
even
reverse
the
process.
Defining
mechanism
by
which
roadblocks
signaling
inputs
influence
complex
programs
essential
for
understanding
developing
strategies.
Here,
we
discuss
intrinsic
extrinsic
factors
counteract
cell
rejuvenation,
targeted
core
mechanisms
involved
this
Then,
critically
summarize
latest
advances
state-of-art
strategies
of
rejuvenation.
Various
methods
also
provide
insights
treating
specific
ageing-related
diseases,
including
reprogramming,
removal
senescence
(SCs)
suppression
senescence-associated
secretory
phenotype
(SASP),
metabolic
manipulation,
stem
cells-associated
therapy,
dietary
restriction,
immune
heterochronic
transplantation,
etc.
potential
applications
therapy
extend
cancer
treatment.
Finally,
analyze
detail
therapeutic
opportunities
challenges
technology.
Deciphering
will
further
into
anti-ageing
disease
treatment
clinical
settings.
Cell,
Journal Year:
2024,
Volume and Issue:
187(16), P. 4150 - 4175
Published: Aug. 1, 2024
Cellular
senescence
is
a
cell
fate
triggered
in
response
to
stress
and
characterized
by
stable
cell-cycle
arrest
hypersecretory
state.
It
has
diverse
biological
roles,
ranging
from
tissue
repair
chronic
disease.
The
development
of
new
tools
study
vivo
paved
the
way
for
uncovering
its
physiological
pathological
roles
testing
senescent
cells
as
therapeutic
target.
However,
lack
specific
broadly
applicable
markers
makes
it
difficult
identify
characterize
tissues
living
organisms.
To
address
this,
we
provide
practical
guidelines
called
"minimum
information
cellular
experimentation
vivo"
(MICSE).
presents
an
overview
rodent
tissues,
transgenic
models,
non-mammalian
systems,
human
tumors
their
use
identification
specification
cells.
These
uniform,
state-of-the-art,
accessible
toolset
improve
our
understanding
vivo.
