Abstract:
Down
Syndrome
(DS)
is
a
common
genetic
disorder
characterized
by
an
extra
copy
of
chromosome
21,
leading
to
dysregulation
various
metabolic
pathways.
Oxidative
stress
in
DS
associated
with
neurodevelopmental
defects,
neuronal
dysfunction,
and
the
onset
dementia
re-sembling
Alzheimer's
disease.
Additionally,
chronic
oxidative
contributes
cardiovascular
diseases
certain
cancers
prevalent
individuals.
This
study
investigates
impact
ageing
on
liver
fibrosis
using
murine
model
(Ts2Cje
mice).
The
mice
shows
increased
impaired
antioxidant
defenses,
as
evidenced
reduced
glutathione
levels
lipid
peroxidation.
Furthermore,
exhibits
altered
in-flammatory
response
measured
expression
cytokines
heat
shock
proteins.
also
displays
dysregulated
metabolism,
indicated
peroxisome
prolif-erator-activated
receptors
fatty
acid
transport
Consistently,
these
changes
might
contribute
non-alcoholic
disease
development,
condition
fat
accumulation.
Finally,
histological
analysis
reveals
steatosis,
in-dicative
potential
progression
cirrhosis.
finding
highlights
risk
pathologies
individuals,
particularly
when
combined
higher
prevalence
obesity
dysfunctions
patients.
These
results
shed
light
liver's
role
DS-associated
suggest
therapeutic
strategies
targeting
metabolism
prevent
or
mitigate
liver-related
complications
Foods,
Journal Year:
2025,
Volume and Issue:
14(3), P. 347 - 347
Published: Jan. 21, 2025
Bee
pollen
is
characterized
by
an
exceptional
diversity
and
abundance
of
micronutrients
bioactive
phytochemicals.
This
richness
remains
very
sparsely
investigated,
but
accumulating
evidence
strongly
supports
a
promising
future
for
bee
in
human
nutrition
medicine.
Epigenetic
regulation
among
the
most
compelling
biomedical
topics
that
remain
completely
untapped
derivative
research.
In
our
current
research,
we
identified
numerous
ubiquitous
compounds
are
consistently
present
this
matrix,
regardless
its
botanical
geographical
origins,
have
been
well
studied
documented
as
epigenetic
regulators
recent
years.
Given
relative
newness
both
research
studies
within
nutritional,
pharmaceutical,
medical
sciences,
review
aims
to
bridge
these
valuable
fields
advance
related
experimental
investigations.
To
best
knowledge,
first
work
has
aimed
comprehensively
investigate
modulatory
potential
compounds.
Our
findings
also
unveiled
several
intriguing
phenomena,
such
dual
effect
same
compound
depending
on
cellular
context
or
some
cross-generational
heritability
traits.
Although
whole
extract
still
lacking,
study
clearly
indicates
avenue
worth
further
We
hope
constitutes
foundational
cornerstone
investigations
Frontiers in Immunology,
Journal Year:
2024,
Volume and Issue:
15
Published: May 16, 2024
Importance
Research
is
beginning
to
elucidate
the
sophisticated
mechanisms
underlying
microbiota-gut-brain-immune
interface,
moving
from
primarily
animal
models
human
studies.
Findings
support
dynamic
relationships
between
gut
microbiota
as
an
ecosystem
(microbiome)
within
(host)
and
its
intersection
with
host
immune
nervous
systems.
Adding
this
effects
on
epigenetic
regulation
of
gene
expression
further
complicates
strengthens
response.
At
heart
inflammation,
which
manifests
in
a
variety
pathologies
including
neurodegenerative
diseases
such
Alzheimer’s
disease,
Parkinson’s
Multiple
Sclerosis
(MS).
Observations
Generally,
research
date
limited
has
focused
bacteria,
likely
due
simplicity
cost-effectiveness
16s
rRNA
sequencing,
despite
lower
resolution
inability
determine
functional
ability/alterations.
However,
omits
all
other
fungi,
viruses,
phages,
are
emerging
key
members
microbiome.
Much
been
done
pre-clinical
and/or
small
studies
more
developed
parts
world.
The
observed
promising
but
cannot
be
considered
reliable
or
generalizable
at
time.
Specifically,
causal
determined
currently.
More
followed
by
then
little
MS.
data
for
MS
encouraging
this.
Conclusions
relevance
While
still
nascent,
interface
may
missing
link,
hampered
our
progress
understanding,
let
alone
preventing,
managing,
putting
into
remission
diseases.
Relationships
must
first
established
humans,
have
shown
poorly
translate
complex
physiology
environments,
especially
when
investigating
microbiome
where
often
overly
simplistic.
Only
can
robust
conducted
humans
using
mechanistic
model
Frontiers in Cellular Neuroscience,
Journal Year:
2025,
Volume and Issue:
19
Published: Feb. 11, 2025
Neurodegenerative
diseases,
such
as
Alzheimer’s
disease
(AD),
Parkinson’s
(PD),
Multiple
Sclerosis
(MS),
and
Huntington’s
(HD),
although
distinct
in
their
clinical
manifestations,
share
a
common
hallmark:
disrupted
neuroinflammatory
environment
orchestrated
by
dysregulation
of
neuroglial
intercellular
communication.
Neuroglial
crosstalk
is
physiologically
ensured
extracellular
mediators
the
activity
connexins
(Cxs),
forming
proteins
gap
junctions
(Gjs)
hemichannels
(HCs),
which
maintain
intracellular
homeostasis.
However,
accumulating
evidence
suggests
that
Cxs
can
also
act
pathological
pore
conditions,
thereby
contributing
to
neurodegenerative
phenomena
synaptic
dysfunction,
oxidative
stress,
ultimately
cell
death.
This
review
explores
mechanistic
insights
Cxs-mediated
communication
progression
diseases
discusses
therapeutic
potential
targeting
restore
cellular
Cells,
Journal Year:
2023,
Volume and Issue:
12(11), P. 1464 - 1464
Published: May 24, 2023
The
polygenic
nature
of
neurological
and
psychiatric
syndromes
the
significant
impact
environmental
factors
on
underlying
developmental,
homeostatic,
neuroplastic
mechanisms
suggest
that
an
efficient
therapy
for
these
disorders
should
be
a
complex
one.
Pharmacological
interventions
with
drugs
selectively
influencing
epigenetic
landscape
(epidrugs)
allow
one
to
hit
multiple
targets,
therefore,
assumably
addressing
wide
spectrum
genetic
central
nervous
system
(CNS)
disorders.
aim
this
review
is
understand
what
fundamental
pathological
would
optimal
target
epidrugs
in
treatment
or
complications.
To
date,
use
histone
deacetylases
DNA
methyltransferase
inhibitors
(HDACis
DNMTis)
clinic
focused
neoplasms
(mainly
glial
origin)
based
cytostatic
cytotoxic
actions
compounds.
Preclinical
data
show
besides
activity,
deacetylases,
methyltransferases,
bromodomains,
ten-eleven
translocation
(TET)
proteins
expression
neuroimmune
inflammation
mediators
(cytokines
pro-apoptotic
factors),
neurotrophins
(brain-derived
neurotropic
factor
(BDNF)
nerve
growth
(NGF)),
ion
channels,
ionotropic
receptors,
as
well
pathoproteins
(β-amyloid,
tau
protein,
α-synuclein).
Based
profile
activities,
may
favorable
neurodegenerative
diseases.
For
neurodevelopmental
disorders,
drug
addiction,
anxiety
depression,
schizophrenia,
epilepsy,
contemporary
still
require
further
development
concerning
tuning
pharmacological
effects,
reduction
toxicity,
protocols.
A
promising
strategy
clarify
potential
targets
therapeutic
means
cure
profiling
mechanisms,
which
have
evolved
upon
physiological
lifestyle
factors,
such
diet
physical
exercise,
are
effective
management
diseases
dementia.
Frontiers in Immunology,
Journal Year:
2024,
Volume and Issue:
15
Published: Sept. 23, 2024
Methylation,
a
key
epigenetic
modification,
is
essential
for
regulating
gene
expression
and
protein
function
without
altering
the
DNA
sequence,
contributing
to
various
biological
processes,
including
transcription,
embryonic
development,
cellular
functions.
Methylation
encompasses
methylation,
RNA
methylation
histone
modification.
Recent
research
indicates
that
vital
establishing
maintaining
normal
brain
functions
by
modulating
high-order
structure
of
DNA.
Alterations
in
patterns
can
exert
significant
impacts
on
both
function,
playing
role
development
numerous
diseases,
such
as
neurological
disorders,
cardiovascular
diseases
well
cancer.
Our
current
understanding
etiology
emphasizes
multifaceted
process
includes
neurodegenerative,
neuroinflammatory,
neurovascular
events.
Epigenetic
modifications,
especially
are
fundamental
control
critical
onset
progression
disorders.
Furthermore,
we
comprehensively
overview
mechanism
processes
regulation
diseases.
Understanding
mechanisms
dynamics
neural
provide
valuable
insights
into
human
biology
potentially
lead
novel
therapies
Ecotoxicology and Environmental Safety,
Journal Year:
2024,
Volume and Issue:
273, P. 116155 - 116155
Published: Feb. 27, 2024
Excessive
exposure
to
manganese
in
the
environment
or
workplace
is
strongly
linked
neurodegeneration
and
cognitive
impairment,
but
precise
pathogenic
mechanism
preventive
measures
are
still
not
fully
understood.
The
study
aimed
investigate
-induced
oxidative
damage
nervous
system
from
an
epigenetic
perspective,
focusing
on
H3K36ac-dependent
antioxidant
pathway.
Additionally,
it
sought
examine
potential
of
curcumin
preventing
manganese-induced
damage.
Histopathology
transmission
electron
microscopy
revealed
that
apoptosis
necrosis
neurons
mitochondrial
ultrastructure
were
observed
striatum
manganese-exposed
rats.
suppressed
expression
genes,
leading
rats'
SH-SY5Y
cells.
With
higher
doses
manganese,
levels
histone
acetyltransferase
lysine
2
A
(KAT2A)
H3K36ac
level
decreased.
ChIP-qPCR
confirmed
enrichment
promoter
regions
genes
SOD2,
PRDX3,
TXN2
was
reduced
cells
after
exposure,
decreased
these
genes.
Overexpression
KAT2A
confirms
attenuates
by
regulating
levels,
which
turn
controls
cell
model.
Furthermore,
might
control
influencing
expression,
boosting
reducing
In
conclusion,
regulation
stress
acetylation
may
be
important
neurotoxicity.
This
could
achieved
near
region
mitochondrial-associated
via
KAT2A.
Curcumin
mitigates
mitochondria
plays
a
crucial
protective
role
injury
system.
Cells,
Journal Year:
2023,
Volume and Issue:
12(23), P. 2669 - 2669
Published: Nov. 21, 2023
Alzheimer’s
disease
(AD)
is
a
well-known
chronic
neurodegenerative
disorder
that
leads
to
the
progressive
death
of
brain
cells,
resulting
in
memory
loss
and
other
critical
body
functions.
In
March
2019,
one
major
pharmaceutical
companies
its
partners
announced
currently,
there
no
drug
cure
AD,
all
clinical
trials
new
ones
have
been
cancelled,
leaving
many
people
without
hope.
However,
despite
clear
message
startling
reality,
research
continued.
Finally,
last
two
years,
Food
Drug
Administration
(FDA)
approved
first-ever
medications
treat
Alzheimer’s,
aducanumab
lecanemab.
Despite
researchers’
support
this
decision,
are
serious
concerns
about
their
effectiveness
safety.
The
validation
by
Centers
for
Medicare
Medicaid
Services
still
pending,
lecanemab
was
authorized
considering
data
from
phase
III
trials.
Furthermore,
numerous
reports
suggest
patients
died
when
undergoing
extended
treatment.
While
evidence
may
provide
some
relief
those
suffering
impact
remains
topic
ongoing
debate
within
medical
community.
fact
even
though
considerable
efforts
regarding
pharmacological
treatment,
definitive
AD
has
found
yet.
Nevertheless,
it
strongly
believed
modern
nanotechnology
holds
promising
solutions
effective
strategies
development
diagnostic
tools
treatments
AD.
This
review
summarizes
hallmarks
etiological
mechanisms,
challenges.
It
explores
existing
therapeutic
methods
potential
nanotechnology-based
approaches
recognizing
monitoring
at
risk
irreversible
neuronal
degeneration.
Overall,
provides
broad
overview
interested
evolving
areas
neuroscience,
related
nanotechnology.
With
further
development,
offer
hope
millions
affected
devastating
disease.
Brain Sciences,
Journal Year:
2024,
Volume and Issue:
14(6), P. 553 - 553
Published: May 29, 2024
Parkinson’s
disease
(PD),
multiple
sclerosis
(MS),
and
amyotrophic
lateral
(ALS)
are
examples
of
neurodegenerative
movement
disorders
(NMDs),
which
defined
by
a
gradual
loss
motor
function
that
is
frequently
accompanied
cognitive
decline.
Although
genetic
abnormalities
have
long
been
acknowledged
as
significant
factors,
new
research
indicates
epigenetic
alterations
crucial
for
the
initiation
development
disease.
This
review
delves
into
complex
interactions
exist
between
pathophysiology
NMDs
mechanisms
such
DNA
methylation,
histone
modifications,
non-coding
RNAs.
Here,
we
examine
how
these
changes
could
affect
protein
aggregation,
neuroinflammation,
gene
expression
patterns,
thereby
influencing
viability
functionality
neurons.
Through
clarification
terrain
underpinning
disorders,
this
seeks
to
enhance
comprehension
underlying
illness
augment
creation
innovative
therapeutic
strategies.