RSC Advances,
Journal Year:
2025,
Volume and Issue:
15(7), P. 5220 - 5231
Published: Jan. 1, 2025
The
optical
and
biological
properties
of
BODIPY
their
interactions
with
diverse
DNA
forms
were
studied.
dyes
1
3
interact
more
preferably
tetraplexes
than
other
forms,
the
tendency
to
destabilize
parallel
c-
MYC
G-quadruplex.
Biomolecules,
Journal Year:
2024,
Volume and Issue:
14(4), P. 402 - 402
Published: March 26, 2024
The
changes
in
the
properties
of
three
biological
events
that
occur
with
cerebral
aging
are
discussed.
These
adverse
already
begin
to
develop
early
mid-life
and
gradually
become
more
pronounced
senescence.
Essentially,
they
reflections
progressive
decline
effectiveness
key
processes,
resulting
deviation
essential
biochemical
trajectories
ineffective
ultimately
harmful
variants
these
programs.
emphasis
this
review
is
major
role
played
by
mitochondria
transition
important
processes
toward
deleterious
as
brain
proceeds.
immune
system:
shift
away
from
an
efficient
response
a
unfocused,
continuing
inflammatory
condition.
Such
state
both
harmful.
Reactive
oxygen
species
intracellular
signaling
systems.
Additionally,
microglial
phagocytic
activity
utilizing
short
lived
reactive
contribute
removal
aberrant
or
dead
cells
bacteria.
transformed
into
excessive,
untargeted,
persistent
generation
pro-oxidant
free
radicals
(oxidative
stress).
normal
neural
transmission
modified
undirected,
chronic
low-level
excitatory
activity.
Each
characterized
occurrence
continuous
inefficient
diffused.
signal/noise
ratio
several
critical
thus
reduced
beneficial
responses
replaced
their
impaired
variants.
Antioxidants,
Journal Year:
2024,
Volume and Issue:
13(12), P. 1462 - 1462
Published: Nov. 28, 2024
Upregulation
of
reactive
oxygen
species
(ROS)
levels
is
a
principal
feature
observed
in
the
brains
neurodegenerative
diseases
such
as
Parkinson’s
disease
(PD)
and
Alzheimer’s
(AD).
In
these
diseases,
oxidative
stress
can
disrupt
blood–brain
barrier
(BBB).
This
disruption
allows
neurotoxic
plasma
components,
blood
cells,
pathogens
to
enter
brain,
leading
increased
ROS
production,
mitochondrial
dysfunction,
inflammation.
Collectively,
factors
result
protein
modification,
lipid
peroxidation,
DNA
damage,
and,
ultimately,
neural
cell
damage.
this
review
article,
we
present
mechanisms
by
which
damage
leads
BBB
breakdown
brain
diseases.
Additionally,
summarize
potential
therapeutic
approaches
aimed
at
reducing
that
contributes
Brain Sciences,
Journal Year:
2023,
Volume and Issue:
14(1), P. 19 - 19
Published: Dec. 23, 2023
The
term
“neuroinflammation”
defines
the
typical
inflammatory
response
of
brain
closely
related
to
onset
many
neurodegenerative
diseases
(NDs).
Neuroinflammation
is
well
known,
but
its
mechanisms
and
pathways
are
not
entirely
comprehended.
Some
progresses
have
been
achieved
through
efforts
research.
Consequently,
new
cellular
molecular
mechanisms,
diverse
conventional,
emerging.
In
listing
some
those
that
will
be
subject
our
description
discussion,
essential
important
roles
peripheral
infiltrated
monocytes
clonotypic
cells,
alterations
in
gut–brain
axis,
dysregulation
apelinergic
system,
endothelial
glycocalyx
component
neuronal
vascular
units,
variations
expression
genes
levels
encoding
molecules
by
action
microRNAs
(miRNAs),
or
other
epigenetic
factors
distinctive
transcriptional
factors,
as
role
autophagy,
ferroptosis,
sex
differences,
modifications
circadian
cycle.
Such
can
add
significantly
understanding
complex
etiological
puzzle
neuroinflammation
ND.
addition,
they
could
represent
biomarkers
targets
ND,
which
increasing
elderly.
Redox Biology,
Journal Year:
2023,
Volume and Issue:
69, P. 102972 - 102972
Published: Nov. 24, 2023
Oxidative
stress
(OS)
is
regarded
as
the
dominant
theory
for
aging.
While
compelling
correlative
data
have
been
generated
to
support
OS
theory,
a
direct
cause-and-effect
relationship
between
accumulation
of
oxidation-mediated
damage
and
aging
has
not
firmly
established.
Superoxide
dismutase
1
(SOD1)
primary
antioxidant
in
all
cells.
It
is,
however,
susceptible
oxidation
due
gains
toxic
properties
This
study
investigates
role
oxidized
SOD1
derived
from
amyotrophic
lateral
sclerosis
(ALS)
linked
mutations
cell
senescence
Herein,
we
shown
that
line
NSC34
expressing
G93A
mutation
human
(hSOD1G93A)
entered
premature
evidenced
by
decreased
number
5-ethynyl-2′-deoxyuridine
(EdU)-positive
There
was
an
upregulation
cellular
markers
compared
cells
wild-type
(hSOD1WT).
Transgenic
mice
carrying
hSOD1G93A
gene
showed
phenotypes
at
early
age
(135
days)
with
high
levels
P53
P16
but
low
SIRT1
SIRT6
age-matched
hSOD1WT
transgenic
mice.
Notably,
were
significantly
elevated
both
senescent
135-day
Selective
removal
our
CT4-directed
autophagy
decelerated
aging,
indicating
causal
factor
Intriguingly,
mitochondria
malfunctioned
middle-aged
hSODG93A
They
exhibited
increased
production
mitochondrial-derived
vesicles
(MDVs)
response
mild
mutant
hSOD1
younger
age;
mitochondrial
gradually
declined
In
conclusion,
show
ALS-linked
mutants
Compromised
responsiveness
may
serve
indicator
Symmetry,
Journal Year:
2024,
Volume and Issue:
16(3), P. 355 - 355
Published: March 15, 2024
The
mechanism
of
brain
information
processing
unfolds
within
spatial
and
temporal
domains
inherently
linked
to
the
concept
space–time
symmetry.
Biological
evolution,
beginning
with
prevalent
molecular
chirality,
results
in
handedness
human
cognitive
psychological
functions
(the
phenomena
known
as
biochirality).
key
element
chain
chirality
transfer
from
downstream
upstream
processes
is
pyramidal
neuron
(PyrN)
morphology–function
paradigm
(archetype).
most
apparent
landmark
PyrNs
geometry
cell
soma.
However,
“why/how
PyrN’s
soma
gains
shape
quasi-tetrahedral
symmetry”
has
never
been
explicitly
articulated.
Resolving
above
inquiry
only
possible
based
on
broad-view
assumption
that
encoding
3D
space
requires
specific
neuronal
detector
corresponding
network.
Accordingly,
our
hypothesis
states
if
primary
function
PyrNs,
at
organism
level,
sensory
symmetry
perception,
then
best
evolutionary-selected
support
sensory-motor
coupling.
biological
system’s
non-equilibrium
(NE)
state
fundamentally
an
asymmetric,
non-racemic,
steady
constituents.
chiral
theory
conceptually
agrees
living
systems
have
evolved
exchange
energy
environment.
involved
developing
studied
detail.
crucial
missing
element—the
reference
fundamental
link
between
navigation—is
main
obstacle
resolving
question
demand:
why
did
PyrNs’
gain
symmetry?
With
the
term
neuroinflammation
has
defined
typical
inflammatory
response
of
brain
closely
related
to
onset
many
neurological
diseases.
Neuroinflammation
is
well
known,
but
its
mechanisms
and
pathways
are
not
entirely
comprehended.
Currently,
some
progress
been
achieved
through
efforts
research.
Consequently,
new
cellular
molecular
mecha-nisms,
diverse
from
conventional
ones,
emerging.
In
listing
those
that
will
be
sub-ject
our
description
discussion,
essential
important
role
peripheral
infiltrated
monocytes
clonotypic
cells,
alterations
in
gut/brain
axis,
dysregulation
apelinergic
sys-tem,
as
changes
endothelial
glycocalyx
blood-brain
barrier,
variation
expres-sion
genes
levels
encoding
molecules
by
microRNAs
(miRNAs),
or
other
epige-netic
factors
distinctive
transcriptional
factors,
autophagy,
ferroptosis,
sex
differences
modifications
circadian
cycle.
Such
mentioned
can
add
significant
pieces
understanding
complex
etiological
puzzle
neuroinflammation.
addi-tion,
they
could
represent
biomarkers
targets
neurodegenerative
diseases,
increase
old
populations.
Scientific Reports,
Journal Year:
2025,
Volume and Issue:
15(1)
Published: Jan. 13, 2025
NMDAR
antagonists,
such
as
memantine
and
ketamine,
have
shown
efficacy
in
treating
neurodegenerative
diseases
major
depression.
The
mechanism
by
which
these
drugs
correct
the
aforementioned
is
still
unknown.
Our
study
reveals
that
antagonists
significantly
enhance
20S
proteasome
activity,
crucial
for
degrading
intrinsically
disordered,
oxidatively
damaged,
or
misfolded
proteins,
factors
pivotal
like
Alzheimer's
Parkinson's.
In
our
mouse
model
experiment,
ketamine
administration
notably
altered
brain
synaptic
protein
profiles
within
two
hours,
downregulating
proteins
strongly
associated
with
Parkinson's
diseases.
Furthermore,
exhibited
enrichment
terms
related
to
plasticity
potentiation,
including
retrograde
endocannabinoid
signaling—a
pathway
both
short-
long-term
may
elucidate
long-lasting
effects
of
Via
ubiquitin-independent
(UIPS),
maintain
cellular
homeostasis,
activity
declines
age,
leading
aggregation
disease
symptoms.
Therefore,
findings
hold
promise
new
treatment
options
not
only
but
also
other
systemic
conditions
unfolded
proteins.
