Medical academic journal,
Journal Year:
2024,
Volume and Issue:
23(3), P. 41 - 53
Published: March 29, 2024
BACKGROUND:
Multiple
sclerosis
is
a
chronic
neurodegenerative
autoimmune
disease
characterized
by
the
presence
of
foci
inflammation
and
demyelination
in
central
nervous
system.
The
initiation
pathological
processes
multiple
caused
complex
interaction
genetic
factors,
unfavorable
environmental
factors
epigenetic
influences.
Progressive
neurological
symptoms
axonal
conduction
disorders,
death
neurodestruction
lead
to
significant
decreased
patients’
quality
life
disability.
search
for
new
markers
improve
diagnostic
therapeutic
methods,
including
taking
into
account
background
interactions,
an
urgent
task.
AIM:
work
was
aimed
study
changes
DNMT1
mRNA
expression
patients
with
different
duration,
analyze
methylation
promoter,
compare
level
homocysteine
content
blood,
polymorphic
variants
genes
coding
key
folate
cycle
enzymes.
MATERIALS
AND
METHODS:
peripheral
mononuclear
blood
cells
assessed
reversed
transcription
followed
polymerase
chain
reaction.
Fluorescent
reaction
methyl-sensitive
analysis
high-resolution
melting
curves
used
promoter.
determined
chemiluminescence
immunoassay.
real-time
genotyping
polymorphism
genes;
fluorescent
probes
LNA
modifications
were
discriminate
alleles.
RESULTS:
It
has
been
shown
that
patients,
those
at
onset
disease,
significantly
lower
than
control
group.
No
relationship
found
between
decrease
promoter
methylation.
Strong
positive
combined
effects
genotypes
MTR
A2756G
MTHFR
C677T
on
have
shown.
These
findings
suggest
genetically
features
metabolism
may
contribute
disruption
regulation
sclerosis.
CONCLUSIONS:
obtained
results
indicate
promise
research
identifying
causing
Studying
mechanisms
contribution
pathogenesis
could
be
one
possible
ways
approaches.
Frontiers in Neurology,
Journal Year:
2022,
Volume and Issue:
12
Published: Feb. 25, 2022
Aging
is
characterized,
amongst
other
features,
by
a
complex
process
of
cellular
senescence
involving
both
innate
and
adaptive
immunity,
called
immunosenescence
associated
to
inflammaging,
low-grade
chronic
inflammation.
Both
processes
fuel
each
partially
explain
increasing
incidence
cancers,
infections,
age-related
autoimmunity,
vascular
disease
as
well
reduced
response
vaccination.
Multiple
sclerosis
(MS)
lifelong
disease,
for
which
considerable
progress
in
disease-modifying
therapies
(DMTs)
management
has
improved
long-term
survival.
However,
disability
progression,
with
age
duration,
remains.
Neurologists
are
now
involved
caring
elderly
MS
patients,
comorbidities.
the
immune
system
therefore
relevant
implications
pathogenesis,
DMTs
risks
mediated
these
treatments.
We
propose
review
current
evidence
regarding
markers
molecular
mechanisms
their
relevance
understanding
pathogenesis.
will
focus
on
changes
auto-immune
diseases,
such
systemic
lupus
erythematosus
rheumatoid
arthritis.
The
consequences
pathology,
interaction
intrinsic
aging
central
nervous
resident
cells
be
discussed.
Finally,
impact
evolution
safety
efficacy
presented.
Trends in Genetics,
Journal Year:
2025,
Volume and Issue:
unknown
Published: Feb. 1, 2025
HighlightsHuman
handedness
is
a
moderately
heritable
trait.Large-scale
genome-wide
association
and
exome
sequencing
studies
have
identified
multiple
genes
associated
with
highlighted
role
of
tubulin
genes.Axon
guidance,
axon
growth,
forming
the
inner
structure
motile
cilia
are
key
processes
regulated
by
that
may
also
be
relevant
for
handedness,Tubulin
several
psychiatric
disorders
which
offer
insights
into
biological
pathways
mediating
link
between
handedness,
brain
asymmetries,
disorders.AbstractHandedness
(i.e.,
preference
to
use
either
left
or
right
hand
fine
motor
tasks)
widely
investigated
trait.
Handedness
heritability
consistently
estimated
25%.
After
decades
research,
recent
large-scale
genes.
Tubulin
play
in
during
development
ontogenesis,
including
cilia.
Moreover,
disorders.
This
finding
therefore
traits.
Complex Psychiatry,
Journal Year:
2025,
Volume and Issue:
11(1), P. 12 - 36
Published: March 3, 2025
Background:
Substance
use
disorder
(SUD)
is
closely
associated
with
epigenetic
modifications
that
significantly
impact
mental
health
outcomes.
Alcohol
and
drug
misuse
induce
widespread
changes
in
the
epigenome
transcriptome
of
central
nervous
system,
disrupting
critical
processes
such
as
reward
signaling
emotional
regulation.
These
alterations
regulation
gene
expression
often
persist
even
after
substance
cessation,
potentially
contributing
to
onset
or
worsening
psychiatric
conditions,
including
schizophrenia,
depression,
stress,
anxiety.
Summary:
This
review
delves
into
key
mechanisms
underlying
SUD
its
comorbid
disorders,
a
focus
on
DNA
methylation,
histone
modifications,
noncoding
RNA
Additionally,
it
examines
influence
environmental
biological
factors
evaluates
emerging
epigenetic-based
therapeutic
strategies
aimed
at
treating
related
conditions.
Key
Messages:
Gaining
deeper
understanding
driving
disorders
crucial
for
development
effective
interventions.
highlights
potential
pharmacological
mitigate
societal
personal
burdens
linked
complications.
Metabolism Open,
Journal Year:
2024,
Volume and Issue:
22, P. 100287 - 100287
Published: May 19, 2024
The
complex
and
multidimensional
landscape
of
type
2
diabetes
mellitus
(T2D)
is
a
major
global
concern.
Despite
several
years
extensive
research,
the
precise
underlying
causes
T2D
remain
elusive,
but
evidence
suggests
that
it
influenced
by
myriad
interconnected
risk
factors
such
as
epigenetics,
genetics,
gut
microbiome,
environmental
factors,
organelle
stress,
dietary
habits.
number
influencing
pathogenesis
increasing
day
which
worsens
scenario;
meanwhile,
interconnections
shoot
up
frame.
By
gaining
deeper
insights
into
contributing
we
may
pave
way
for
development
personalized
medicine,
could
unlock
more
impactful
treatment
pathways
individuals
with
T2D.
This
review
summarizes
state
knowledge
about
pathogenesis,
focusing
on
interplay
between
various
their
implications
future
therapeutic
strategies.
Understanding
these
lead
to
tailored
treatments
targeting
specific
inform
prevention
efforts
population
level,
ultimately
improving
outcomes
reducing
its
burden
globally.
Cell Death Discovery,
Journal Year:
2024,
Volume and Issue:
10(1)
Published: June 22, 2024
The
physiological
quantum
of
stress-inducible
transcriptional
protein,
Lens
Epithelium-Derived
Growth
Factor
(LEDGF),
is
vital
for
the
maintenance
cellular
physiology.
Erratic
epigenetic
reprogramming
in
response
to
oxidative
stress
or
with
advancing
age
found
be
a
major
cause
gene
silencing,
leading
pathobiologies.
Using
aging
human
(h)
eye
lens/lens
epithelial
cells
(LECs)
coupled
redox-active
Peroxiredoxin
6
(Prdx6)-deficient
(Prdx6
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(21), P. 11602 - 11602
Published: Oct. 29, 2024
This
narrative
review
examines
the
relationship
between
dopamine-related
genetic
polymorphisms,
personality
traits,
and
athletic
success.
Advances
in
sports
genetics
have
identified
specific
single
nucleotide
polymorphisms
(SNPs)
genes
linked
to
traits
crucial
for
performance,
such
as
motivation,
cognitive
function,
emotional
resilience.
clarifies
how
variations
can
influence
predisposition
through
dopaminergic
pathways
environmental
interactions.
Key
findings
reveal
associations
SNPs
enhanced
performance
various
sports.
For
example,
COMT
Val158Met
rs4680
BDNF
Val66Met
rs6265
are
associated
with
that
could
benefit
increased
focus,
stress
resilience
conscientiousness,
especially
martial
arts.
DRD3
rs167771
is
higher
agreeableness,
benefiting
teamwork
like
football.
synthesis
underscores
multidimensional
role
of
shaping
ability
advocates
integrating
profiling
into
personalized
training
optimize
well-being.
However,
research
gaps
remain,
including
need
standardized
protocols
exploring
gene–environment
interactions
diverse
populations.
Future
studies
should
focus
on
epigenetic
factors
inform
tailored
interventions
enhance
both
physical
psychological
aspects
performance.
By
bridging
genetics,
psychology,
exercise
science,
this
paves
way
innovative
optimization
strategies.
Frontiers in Aging,
Journal Year:
2025,
Volume and Issue:
6
Published: March 31, 2025
Driven
by
genetic
and
environmental
factors,
aging
is
a
physiological
process
responsible
for
age-related
degenerative
changes
in
the
body,
cognitive
decline,
impaired
overall
wellbeing.
Notably,
premature
as
well
emergence
of
progeroid
syndromes
have
posed
concerns
regarding
chronic
health
conditions
comorbidities
population.
Accelerated
telomere
attrition
also
implicated
metabolic
dysfunction
development
disorders.
Impaired
homeostasis
arises
secondary
to
increases
synthesis
free
radicals,
decreased
oxidative
capacity,
antioxidant
defense,
disrupted
energy
metabolism.
In
particular,
several
cellular
molecular
mechanisms
been
identified
decipher
influence
on
diseases.
These
include
defective
DNA
repair,
attrition,
epigenetic
alterations,
dysregulation
nutrient-sensing
pathways.
The
role
pathogenesis
diseases
has
largely
attributed
pro-inflammatory
states
that
promote
shortening,
mutations
telomerase
reverse
transcriptase,
alteration,
stress,
mitochondrial
dysfunctions.
Nonetheless,
therapeutic
interventions
focus
restoring
length
telomeres
may
treatment
approaches
restore
enzyme
activity,
alternative
lengthening
telomeres,
counter
decrease
concentration
cytokines.
Given
significance
robust
potential
delaying
diseases,
this
review
aimed
explore
underlying
assimilating
evidence
from
both
human
animal
studies.
