PLoS ONE,
Journal Year:
2025,
Volume and Issue:
20(5), P. e0323264 - e0323264
Published: May 7, 2025
Background
Ageing
is
a
significant
risk
factor
for
age-related
diseases,
accounting
51%
of
global
total
disease
burden.
As
thus,
promoting
healthy
ageing
crucial.
Although
several
potential
anti-ageing
drugs
show
promise,
none
have
been
approved
purpose.
The
World
Health
Organization
(WHO)
recommends
physical
exercise
exceeding
600
metabolic
equivalent
task
(MET)
minutes
per
week
adults.
However,
whether
positively
impacts
biological
remains
unclear.
Objective
This
study
aimed
to
investigate
the
joint
correlation
between
MET
level,
caffeine
consumption,
and
ageing.
Methods
We
analyzed
data
from
seven
survey
cycles
(2007–2020)
National
Nutrition
Examination
Survey
(NHANES),
involving
23,739
participants.
Physical
activity
levels
were
measured
in
week,
was
assessed
using
both
PhenoAge
ENABL
Age
algorithms.
Generalized
linear
regression
employed
test
correlations,
adjusting
confounding
factors.
A
cubic
spline
model
used
detect
non-linear
relationships.
Pre-specified
subgroup
analyses
explored
effect
modifications,
while
predefined
sensitivity
confirmed
robustness
results.
Results
Each
100-MET
increase
weekly
associated
with
0.2-year
delay
(p
<
0.001
Age).
Individuals
less
than
had
higher
accelerated
compared
those
(mean
difference
[MD]:
2.2
years,
95%
CI
[1.5–2.8],
p
0.001;
MD:
2.1
[1.1–3.1],
0.001).
L-shaped
association
observed,
diminishing
benefits
delayed
beyond
292
259
Age.
Daily
intake
did
not
modify
interaction
>
0.05).
Stronger
effects
observed
non-Hispanic
Black
individuals,
obesity,
low-income
populations,
but
no
benefit
found
cancer
patients.
Conclusions
Our
findings
highlight
positive
plateau
specific
thresholds.
Caffeine
does
influence
this
relationship.
These
results
underscore
importance
at
appropriate
as
strategy
management
general
population.
Angiogenesis,
Journal Year:
2024,
Volume and Issue:
27(2), P. 129 - 145
Published: Feb. 7, 2024
Vascular
endothelial
cell
(EC)
aging
has
a
strong
impact
on
tissue
perfusion
and
overall
cardiovascular
health.
While
studies
confined
to
the
investigation
of
aging-associated
vascular
readouts
in
one
or
few
tissues
have
already
drastically
expanded
our
understanding
EC
aging,
single-cell
omics
other
high-resolution
profiling
technologies
started
illuminate
intricate
molecular
changes
underlying
across
diverse
beds
at
scale.
In
this
review,
we
provide
an
overview
recent
insights
into
heterogeneous
adaptations
endothelium.
We
address
critical
questions
regarding
tissue-specific
universal
responses
endothelium
process,
turnover
dynamics
throughout
lifespan,
differential
susceptibility
ECs
acquiring
traits.
doing
so,
underscore
transformative
potential
approaches
advancing
comprehension
essential
foster
development
future
innovative
therapeutic
strategies
for
conditions.
FEBS Letters,
Journal Year:
2024,
Volume and Issue:
598(22), P. 2776 - 2787
Published: April 11, 2024
Aging
is
associated
with
a
global
decline
in
stem
cell
function.
To
date,
several
strategies
have
been
proposed
to
rejuvenate
aged
cells:
most
of
these
result
functional
improvement
the
tissue
where
cells
reside,
but
impact
on
lifespan
whole
organism
has
less
clearly
established.
Here,
we
review
some
recent
work
dealing
interventions
that
improve
regenerative
capacity
somatic
mammals
and
might
important
translational
possibilities.
Overall,
underscore
rejuvenation
represents
strategy
homeostasis
upon
aging
present
approaches
potential
affect
health
span
organism.
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(8), P. 4452 - 4452
Published: April 18, 2024
Schizophrenia
is
a
significant
worldwide
health
concern,
affecting
over
20
million
individuals
and
contributing
to
potential
reduction
in
life
expectancy
by
up
14.5
years.
Despite
its
profound
impact,
the
precise
pathological
mechanisms
underlying
schizophrenia
continue
remain
enigmatic,
with
previous
research
yielding
diverse
occasionally
conflicting
findings.
Nonetheless,
one
consistently
observed
phenomenon
brain
imaging
studies
of
patients
disruption
white
matter,
bundles
myelinated
axons
that
provide
connectivity
rapid
signalling
between
regions.
Myelin
produced
specialised
glial
cells
known
as
oligodendrocytes,
which
have
been
shown
be
disrupted
post-mortem
analyses
patients.
Oligodendrocytes
are
generated
throughout
major
population
oligodendrocyte
progenitor
(OPC),
essential
for
matter
plasticity.
Notably,
decline
specific
subpopulation
OPC
has
identified
principal
factor
loss
aging
brain,
suggesting
this
may
also
schizophrenia.
In
review,
we
analysed
genomic
databases
pinpoint
intersections
identify
shared
cognitive
dysfunction.
Nature,
Journal Year:
2024,
Volume and Issue:
unknown
Published: Dec. 18, 2024
Old
age
is
associated
with
a
decline
in
cognitive
function
and
an
increase
neurodegenerative
disease
risk1.
Brain
ageing
complex
accompanied
by
many
cellular
changes2.
Furthermore,
the
influence
that
aged
cells
have
on
neighbouring
how
this
contributes
to
tissue
unknown.
More
generally,
tools
systematically
address
question
tissues
not
yet
been
developed.
Here
we
generate
spatially
resolved
single-cell
transcriptomics
brain
atlas
of
4.2
million
from
20
distinct
ages
across
adult
lifespan
two
rejuvenating
interventions—exercise
partial
reprogramming.
We
build
spatial
clocks,
machine
learning
models
trained
atlas,
identify
cell-type-specific
transcriptomic
fingerprints
ageing,
rejuvenation
disease,
including
for
rare
cell
types.
Using
clocks
deep
learning,
find
T
cells,
which
increasingly
infiltrate
age,
marked
pro-ageing
proximity
effect
cells.
Surprisingly,
neural
stem
strong
pro-rejuvenating
also
potential
mediators
their
neighbours.
These
results
suggest
types
can
potent
neighbours
could
be
targeted
counter
ageing.
Spatial
represent
useful
tool
studying
cell–cell
interactions
contexts
should
allow
scalable
assessment
efficacy
interventions
disease.
A
map
mouse
at
different
reveals
signatures
effects
Nature Aging,
Journal Year:
2023,
Volume and Issue:
3(7), P. 866 - 893
Published: July 13, 2023
The
regenerative
potential
of
brain
stem
cell
niches
deteriorates
during
aging.
Yet
the
mechanisms
underlying
this
decline
are
largely
unknown.
Here
we
characterize
genome-wide
chromatin
accessibility
neurogenic
niche
cells
in
vivo
Interestingly,
at
adhesion
and
migration
genes
decreases
with
age
quiescent
neural
(NSCs)
but
increases
activated
(proliferative)
NSCs.
Quiescent
NSCs
exhibit
opposing
behaviors
aging:
become
less
adhesive,
whereas
more
adhesive.
Old
also
show
decreased
vitro
diminished
mobilization
out
for
neurogenesis
vivo.
Using
tension
sensors,
find
that
aging
force-producing
adhesions
Inhibiting
cytoskeletal-regulating
kinase
ROCK
reduces
these
adhesions,
restores
old
vitro,
boosts
These
results
have
implications
restoring
migratory
improving
aged
brain.
Journal of Advanced Research,
Journal Year:
2024,
Volume and Issue:
unknown
Published: May 1, 2024
Tissues
maintain
their
function
through
interaction
with
microenvironment.
During
aging,
both
hair
follicles
and
blood
vessels
(BV)
in
skin
undergo
degenerative
changes.
However,
it
is
elusive
whether
the
changes
are
due
to
intrinsic
aging
or
respectively,
interactions.
To
explore
how
interact
regulate
angiogenesis
regeneration
during
aging.
Single-cell
RNA-sequencing
(scRNA-seq)
analyses
were
used
identify
declined
ability
of
dermal
papilla
(DP)
endothelial
cells
(ECs)
CellChat
CellCall
performed
investigate
between
DP
ECs.
metabolism
(scMetabolism)
analysis
iPATH
applied
analyze
downstream
metabolites
Hair-plucking
model
mouse
cell
organoid
for
functional
studies.
distance
ECs
decreased.
interacts
ECs,
decreased
EDN1-EDNRA
signaling
from
CTF1-IL6ST
ECs-secreted
EDN1
binds
DP-expressed
EDNRA
which
enhances
Taurine
(TA)
promote
regeneration.
DP-emitted
CTF1
ECs-expressed
IL6ST
activates
alpha-linolenic
acid
(ALA)
angiogenesis.
Activated
EDN1-EDNRA-TA
promotes
aged
cultures,
increased
CTF1-IL6ST-ALA
also
cultures.
Our
finding
reveals
reciprocal
interactions
DP.
releases
sensed
by
activate
TA
induces
regeneration,
while
emits
signal
received
enhance
ALA
study
provides
new
insights
into
mutualistic
cellular
crosstalk
vessels,
identifies
novel
contributing
normal
skin.
Neuron,
Journal Year:
2025,
Volume and Issue:
113(1), P. 82 - 108
Published: Jan. 1, 2025
SummaryBrain
aging
leads
to
a
decline
in
cognitive
function
and
concomitant
increase
the
susceptibility
neurodegenerative
diseases
such
as
Alzheimer's
Parkinson's
diseases.
A
key
question
is
how
changes
within
individual
cells
of
brain
give
rise
age-related
dysfunction.
Developments
single-cell
"omics"
technologies,
transcriptomics,
have
facilitated
high-dimensional
profiling
cells.
These
technologies
led
new
comprehensive
characterizations
at
resolution.
Here,
we
review
insights
gleaned
from
omics
studies
aging,
starting
with
cell-type-centric
overview
age-associated
followed
by
discussion
cell-cell
interactions
during
aging.
We
highlight
provide
an
unbiased
view
different
rejuvenation
interventions
comment
on
promise
combinatorial
approaches
for
brain.
Finally,
propose
directions,
including
models
neural
stem
focal
point
rejuvenation.
bioRxiv (Cold Spring Harbor Laboratory),
Journal Year:
2025,
Volume and Issue:
unknown
Published: Jan. 14, 2025
Abstract
Sarcopenia,
which
diminishes
lifespan
and
healthspan
in
the
elderly,
is
commonly
exacerbated
by
viral
pneumonia,
including
influenza
COVID-19.
In
a
study
of
A
pneumonia
mice,
young
mice
fully
recovered
from
sarcopenia,
while
older
did
not.
We
identified
population
tissue-resident
skeletal
muscle
macrophages
that
form
spatial
niche
with
satellite
cells
myofibers
but
are
lost
age.
Mice
gain-of-function
mutation
Mertk
receptor
maintained
this
macrophage-myofiber
interaction
during
aging
influenza-induced
sarcopenia.
contrast,
deletion
or
loss
Cx3cr1
disrupted
niche,
preventing
regeneration.
Heterochronic
parabiosis
not
restore
old
mice.
These
findings
suggest
age-related
disrupts
cellular
signaling
necessary
for
regeneration
after
offering
potential
target
to
mitigate
sarcopenia
aging.