Human Genomics,
Journal Year:
2024,
Volume and Issue:
18(1)
Published: June 3, 2024
Several
lines
of
evidence
suggest
that
leukocyte
telomere
length
(LTL)
can
affect
the
development
prostate
cancer
(PC).
Here,
we
employed
single
nucleoside
polymorphisms
(SNPs)
as
instrumental
variables
(IVs)
for
LTL
(n
=
472,174)
and
conducted
Mendelian
randomization
analysis
to
estimate
their
causal
impact
on
PCs
(79,148
patients/61,106
controls
6311
patients/88,902
controls).
Every
1-s.d
extension
increased
risk
by
34%.
Additionally,
candidate
mediators
between
via
two-step
revealed
among
23
candidates,
Alzheimer's
disease,
liver
iron
content,
sex
hormone
binding
global
levels,
naive
CD4-CD8-T
cell%
T
cell,
circulating
leptin
levels
played
substantial
mediating
roles.
There
is
no
robust
support
reverse
relationship
selected
PCs.
Adjusting
former
four
mediators,
rather
than
adjusting
decreased
This
study
provides
potential
intervention
measures
preventing
LTL-induced
Frontiers in Bioscience-Landmark,
Journal Year:
2025,
Volume and Issue:
30(2)
Published: Feb. 18, 2025
Alzheimer’s
disease
(AD)
is
the
most
prevalent
cause
of
dementia
and
a
significant
contributor
to
health
issues
mortality
among
older
individuals.
This
condition
involves
progressive
deterioration
in
cognitive
function
onset
dementia.
Recent
advancements
suggest
that
development
AD
more
intricate
than
its
underlying
brain
abnormalities
alone.
In
addition,
disease,
metabolic
syndrome,
oxidative
stress
are
all
intricately
linked
one
another.
Increased
concentrations
circulating
lipids
disturbances
glucose
homeostasis
contribute
intensification
lipid
oxidation,
leading
gradual
depletion
body’s
antioxidant
defenses.
heightened
metabolism
adversely
impacts
cell
integrity,
resulting
neuronal
damage.
Pathways
commonly
acknowledged
as
contributors
pathogenesis
include
alterations
synaptic
plasticity,
disorganization
neurons,
death.
Abnormal
some
membrane
proteins
thought
creation
amyloid
(Aβ)
oligomers,
which
extremely
hazardous
neurotransmission
pathways,
especially
those
involving
acetylcholine.
The
interaction
between
Aβ
oligomers
these
neurotransmitter
systems
induce
cellular
dysfunction,
an
imbalance
signaling,
and,
ultimately,
manifestation
neurological
symptoms.
Antioxidants
have
impact
on
human
since
they
may
improve
aging
process
by
combating
free
radicals.
Neurodegenerative
diseases
currently
incurable;
however,
be
effectively
managed.
An
appealing
alternative
utilization
natural
antioxidants,
such
polyphenols,
through
diet
or
dietary
supplements,
offer
numerous
advantages.
Within
this
framework,
we
extensively
examined
importance
advancement
well
potential
influence
antioxidants
mitigating
effects.
Cancers,
Journal Year:
2025,
Volume and Issue:
17(2), P. 257 - 257
Published: Jan. 14, 2025
As
cells
divide,
telomeres
shorten
through
a
phenomenon
known
as
telomere
attrition,
which
leads
to
unavoidable
senescence
of
cells.
Unprotected
DNA
exponentially
increases
the
odds
mutations,
can
evolve
into
premature
aging
disorders
and
tumorigenesis.
There
has
been
growing
academic
clinical
interest
in
exploring
this
duality
developing
optimal
therapeutic
strategies
combat
attrition
cellular
immortality
cancer.
The
purpose
review
is
provide
an
updated
overview
biology
tactics
address
We
used
Rayyan
platform
PubMed
database
examined
ClinicalTrial.gov
registry
gain
insight
trials
their
results.
Cancer
activate
telomerase
or
utilize
alternative
lengthening
escape
shortening,
leading
near
immortality.
Contrarily,
normal
experience
telomeric
erosion,
contributing
disorders,
such
Werner
syndrome
Hutchinson-Gilford
Progeria,
(2)
aging-related
diseases,
neurodegenerative
cardiovascular
diseases.
literature
presents
several
promising
approaches
potentially
balance
maintenance
shortening
This
highlights
gaps
knowledge
points
potential
these
interventions
preclinical
studies
inform
future
research
cancer
aging.
Frontiers in Immunology,
Journal Year:
2023,
Volume and Issue:
14
Published: Nov. 8, 2023
Life
expectancy
is
increasing
throughout
the
world
and
coincides
with
a
rise
in
non-communicable
diseases
(NCDs),
especially
for
metabolic
disease
that
includes
diabetes
mellitus
(DM)
neurodegenerative
disorders.
The
debilitating
effects
of
disorders
influence
entire
body
significantly
affect
nervous
system
impacting
greater
than
one
billion
people
disability
peripheral
as
well
cognitive
loss,
now
seventh
leading
cause
death
worldwide.
Metabolic
disorders,
such
DM,
neurologic
remain
significant
challenge
treatment
care
individuals
since
present
therapies
may
limit
symptoms
but
do
not
halt
overall
progression.
These
clinical
challenges
to
address
interplay
between
warrant
innovative
strategies
can
focus
upon
underlying
mechanisms
aging-related
oxidative
stress,
cell
senescence,
death.
Programmed
pathways
involve
autophagy,
apoptosis,
ferroptosis,
pyroptosis
play
critical
role
oversee
processes
include
insulin
resistance,
β-cell
function,
mitochondrial
integrity,
reactive
oxygen
species
release,
inflammatory
activation.
silent
mating
type
information
regulation
2
homolog
1
Bioengineering,
Journal Year:
2023,
Volume and Issue:
10(7), P. 871 - 871
Published: July 23, 2023
Almost
three
million
individuals
suffer
from
multiple
sclerosis
(MS)
throughout
the
world,
a
demyelinating
disease
in
nervous
system
with
increased
prevalence
over
last
five
decades,
and
is
now
being
recognized
as
one
significant
etiology
of
cognitive
loss
dementia.
Presently,
modifying
therapies
can
limit
rate
relapse
potentially
reduce
brain
volume
patients
MS,
but
unfortunately
cannot
prevent
progression
or
onset
disability.
Innovative
strategies
are
therefore
required
to
address
areas
inflammation,
immune
cell
activation,
survival
that
involve
novel
pathways
programmed
death,
mammalian
forkhead
transcription
factors
(FoxOs),
mechanistic
target
rapamycin
(mTOR),
AMP
activated
protein
kinase
(AMPK),
silent
mating
type
information
regulation
2
homolog
1
(Saccharomyces
cerevisiae)
(SIRT1),
associated
apolipoprotein
E
(APOE-ε4)
gene
severe
acute
respiratory
syndrome
coronavirus
(SARS-CoV-2).
These
intertwined
at
levels
metabolic
oversight
cellular
metabolism
dependent
upon
nicotinamide
adenine
dinucleotide
(NAD+).
Insight
into
mechanisms
these
provide
new
avenues
discovery
for
therapeutic
treatment
dementia
cognition
occurs
during
MS.
Cells,
Journal Year:
2023,
Volume and Issue:
12(22), P. 2595 - 2595
Published: Nov. 9, 2023
Metabolic
disorders
and
diabetes
(DM)
impact
more
than
five
hundred
million
individuals
throughout
the
world
are
insidious
in
onset,
chronic
nature,
yield
significant
disability
death.
Current
therapies
that
address
nutritional
status,
weight
management,
pharmacological
options
may
delay
but
cannot
alter
disease
course
or
functional
organ
loss,
such
as
dementia
degeneration
of
systemic
bodily
functions.
Underlying
these
challenges
onset
aging
associated
with
increased
lifespan,
telomere
dysfunction,
oxidative
stress
generation
lead
to
multi-system
dysfunction.
These
hurdles
point
urgent
need
underlying
mechanisms
innovative
applications.
New
treatment
strategies
involve
non-coding
RNA
pathways
microRNAs
(miRNAs)
circular
ribonucleic
acids
(circRNAs),
Wnt
signaling,
Wnt1
inducible
signaling
pathway
protein
1
(WISP1)
dependent
upon
programmed
cell
death
pathways,
cellular
metabolic
AMP-activated
kinase
(AMPK)
nicotinamide,
growth
factor
Non-coding
RNAs,
AMPK
cornerstone
for
overseeing
complex
offer
avenues
DM
will
necessitate
continued
appreciation
ability
each
independently
unison
influence
clinical
outcome.
Cellular and Molecular Neurobiology,
Journal Year:
2025,
Volume and Issue:
45(1)
Published: May 19, 2025
Abstract
As
ageing
is
linked
to
the
development
of
neurodegenerative
diseases
(NDs),
such
as
Alzheimer’s
Disease
and
Parkinson’s
Disease,
it
important
disentangle
independent
effect
age-related
changes
from
those
due
disease
processes.
To
do
so,
central
nervous
system
(CNS)
cells
a
function
advanced
age
need
better
characterisation.
Microglia
are
particular
interest
their
proposed
links
with
progression
NDs
through
control
CNS
immune
response.
Therefore,
understanding
extent
which
microglial
dysfunction
related
phyisological
ageing,
rather
than
process,
critical.
microglia
age,
they
believed
take
on
pro-inflammatory
phenotype
distinct
dystrophic
morphology.
Nevertheless,
while
established
hallmarks
have
been
investigated
across
range
other
cell
types,
macrophages,
detailed
consideration
functional
that
occur
in
aged
remains
elusive.
Here,
we
describe
dynamic
phenotypes
evaluate
current
state
focusing
recently
updated
twelve
ageing.
Understanding
how
these
present
represents
step
towards
characterisation
essential
more
representative
models
NDs.
Graphical
Microglial
different
stages
life.
diverse
functions
throughout
life;
however,
has
inconsistent
Journal of Cancer Research and Clinical Oncology,
Journal Year:
2024,
Volume and Issue:
150(7)
Published: July 16, 2024
Abstract
This
article
presents
an
in-depth
exploration
of
the
roles
Telomere
Repeat-binding
Factors
1
and
2
(TRF1
TRF2),
shelterin
complex,
in
context
cancer
biology.
It
emphasizes
their
emerging
significance
as
potential
biomarkers
targets
for
therapeutic
intervention.
Central
to
TRF1
TRF2
are
crucial
maintaining
telomere
integrity
genomic
stability,
dysregulation
often
being
a
hallmark
cancerous
cells.
The
delves
into
diagnostic
prognostic
capabilities
across
various
types,
highlighting
sensitivity
specificity.
Furthermore,
it
reviews
current
strides
drug
discovery
targeting
detailing
specific
compounds
modes
action.
review
candidly
addresses
challenges
developing
therapies
aimed
at
including
resistance,
off-target
effects,
issues
delivery.
By
synthesizing
recent
research
findings,
sheds
light
on
intricate
relationship
between
biology
development.
underscores
urgency
continued
navigate
existing
fully
leverage
TRF1,
TRF2,
complex
realm
treatment.