Brain Sciences,
Journal Year:
2023,
Volume and Issue:
13(11), P. 1551 - 1551
Published: Nov. 5, 2023
Mitochondrial
dysfunction
is
well-established
in
Parkinson’s
disease
(PD);
however,
its
dysfunctions
associating
with
cell
organelle
connectivity
remain
unknown.
We
aimed
to
establish
the
crucial
cytosolic
protein
involved
between
mitochondria
and
endopalmic
reticulum
(ER)
through
a
computational
approach
by
constructing
an
network
extract
functional
clusters
presenting
PD
connecting
organelles.
Then,
we
assessed
influence
of
anti-parkinsonism
drugs
(n
=
35)
on
molecular
docking
dynamic
simulation
further
validated
gene
expression
participants
under,
istradefylline
25)
amantadine
treatment.
Based
our
investigation,
D-aspartate
oxidase
(DDO
)protein
was
found
be
critical
that
connects
both
ER.
Further,
showed
has
high
affinity
(−9.073
kcal/mol)
against
DDO
protein,
which
may
disrupt
mitochondrial-ER
connectivity.
While
(−4.53
shows
negligible
effects
contribute
conformational
changes
drug
binding,
Successively,
downregulated
istradefylline-treated
participants,
elucidated
likelihood
off-target
mechanism.
Overall,
findings
illuminate
medications
enabling
recommendation
off-target-free
treatments.
Molecular Pharmaceutics,
Journal Year:
2024,
Volume and Issue:
21(5), P. 2097 - 2117
Published: March 5, 2024
Currently,
one
of
the
most
significant
and
rapidly
growing
unmet
medical
challenges
is
treatment
neurodegenerative
diseases
such
as
Alzheimer's
disease
(AD)
Parkinson's
(PD).
This
challenge
encompasses
imperative
development
efficacious
therapeutic
agents
overcoming
intricacies
blood–brain
barrier
for
successful
drug
delivery.
Here
we
focus
on
delivery
aspect
with
particular
emphasis
cell-penetrating
peptides
(CPPs),
widely
used
in
basic
translational
research
they
enhance
to
challenging
targets
tissue
cellular
compartments
thus
increase
efficacy.
The
combination
CPPs
nanomaterials
nanoparticles
(NPs)
improves
performance,
accuracy,
stability
enables
higher
loads.
Our
review
presents
discusses
that
utilizes
CPPs,
either
alone
or
conjugation
NPs,
mitigate
pathogenic
effects
reference
AD
PD.
Frontiers in Cell and Developmental Biology,
Journal Year:
2023,
Volume and Issue:
11
Published: June 7, 2023
Parkinson’s
disease
(PD)
is
a
common
neurodegenerative
disorder
caused
by
genetic,
epigenetic,
and
environmental
factors.
Recent
advance
in
genomics
epigenetics
have
revealed
epigenetic
mechanisms
PD.
These
modifications
include
DNA
methylation,
post-translational
histone
modifications,
chromatin
remodeling,
RNA-based
mechanisms,
which
regulate
cellular
functions
almost
all
cells.
Epigenetic
alterations
are
involved
multiple
aspects
of
neuronal
development
neurodegeneration
In
this
review,
we
discuss
current
understanding
the
that
gene
expression
neural
degeneration
then
highlight
emerging
targets
diagnostic
therapeutic
biomarkers
for
treating
or
preventing
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(8), P. 4187 - 4187
Published: April 10, 2024
The
etiology
underlying
most
sporadic
Parkinson's'
disease
(PD)
cases
is
unknown.
Environmental
exposures
have
been
suggested
as
putative
causes
of
the
disease.
In
cell
models
and
in
animal
studies,
certain
chemicals
can
destroy
dopaminergic
neurons.
However,
mechanisms
how
these
cause
death
neurons
not
understood.
Several
agents
are
mitochondrial
toxins
that
inhibit
complex
I
electron
transport
chain.
Familial
PD
genes
also
encode
proteins
with
important
functions
mitochondria.
Mitochondrial
dysfunction
respiratory
chain,
combination
presence
redox
active
dopamine
molecules
cells,
will
lead
to
accumulation
reactive
oxygen
species
(ROS)
Here,
propose
a
mechanism
regarding
ROS
may
killing
specificity
for
One
rarely
considered
hypothesis
produced
by
defective
mitochondria
formation
oxidative
DNA
damage
nuclear
DNA.
Many
neuron-specific
extraordinary
long,
ranging
size
from
several
hundred
kilobases
well
over
megabase.
It
predictable
such
long
contain
large
numbers
damaged
bases,
example
form
8-oxoguanine
(8-oxoG),
which
major
type
ROS.
These
lesions
slow
down
or
stall
progression
RNA
polymerase
II,
term
referred
transcription
stress.
Furthermore,
ROS-induced
mutations,
even
postmitotic
cells
impaired
mutagenesis
loss
neuronal
integrity,
eventually
leading
during
human
lifetime.
Medicina,
Journal Year:
2023,
Volume and Issue:
59(3), P. 504 - 504
Published: March 4, 2023
Helicobacter
pylori
infection
consists
a
high
global
burden
affecting
more
than
50%
of
the
world's
population.
It
is
implicated,
beyond
substantiated
local
gastric
pathologies,
i.e.,
peptic
ulcers
and
cancer,
in
pathophysiology
several
neurodegenerative
disorders,
mainly
by
inducing
hyperhomocysteinemia-related
brain
cortical
thinning
(BCT).
BCT
has
been
advocated
as
possible
biomarker
associated
with
central
nervous
system
disorders
such
Alzheimer's
disease,
Parkinson's
multiple
sclerosis,
and/or
glaucoma,
termed
"ocular
disease".
According
to
hypothesis
relation
neurodegeneration,
non-commensal
gut
microbiome
trigger
mediator
diseases,
development
disease.
Among
others,
pylori-related
inflammatory
mediators,
defensins,
autophagy,
vitamin
D,
dietary
factors,
role
probiotics,
some
pathogenetic
considerations
including
relevant
involved
genes
are
discussed
within
this
opinion
article.
In
conclusion,
controlling
impact
hyperhomocysteinemia
on
might
offer
benefits,
additional
research
warranted
clarify
crucial
topic
currently
representing
major
worldwide
burden.
Nutrients,
Journal Year:
2024,
Volume and Issue:
16(13), P. 2041 - 2041
Published: June 27, 2024
With
the
recognition
of
importance
gut-brain
axis
in
Parkinson's
disease
(PD)
etiology,
there
is
increased
interest
developing
therapeutic
strategies
that
target
α-synuclein,
hallmark
abhorrent
protein
PD
pathogenesis,
which
may
originate
gut.
Research
has
demonstrated
inhibiting
aggregation,
oligomerization,
and
fibrillation
α-synuclein
are
key
for
modification.
Polyphenols,
rich
fruits
vegetables,
drawing
attention
their
potential
role
this
context.
In
paper,
we
reviewed
how
polyphenols
influence
composition
functional
capabilities
gut
microbiota
resulting
microbial
metabolites
potentially
enhance
modulation
aggregation.
Understanding
interaction
between
identifying
specific
microbes
efficacy
crucial
precision
nutrition
based
on
microbiome.
International Journal of Molecular Sciences,
Journal Year:
2024,
Volume and Issue:
25(23), P. 12613 - 12613
Published: Nov. 24, 2024
Neurodegenerative
diseases,
such
as
Alzheimer's,
Parkinson's,
ALS,
and
Huntington's,
remain
formidable
challenges
in
medicine,
with
their
relentless
progression
limited
therapeutic
options.
These
diseases
arise
from
a
web
of
molecular
disturbances-misfolded
proteins,
chronic
neuroinflammation,
mitochondrial
dysfunction,
genetic
mutations-that
slowly
dismantle
neuronal
integrity.
Yet,
recent
scientific
breakthroughs
are
opening
new
paths
to
intervene
these
once-intractable
conditions.
This
review
synthesizes
the
latest
insights
into
underlying
dynamics
neurodegeneration,
revealing
how
intertwined
pathways
drive
course
diseases.
With
an
eye
on
most
promising
advances,
we
explore
innovative
therapies
emerging
cutting-edge
research:
nanotechnology-based
drug
delivery
systems
capable
navigating
blood-brain
barrier,
gene-editing
tools
like
CRISPR
designed
correct
harmful
variants,
stem
cell
strategies
that
not
only
replace
lost
neurons
but
foster
neuroprotective
environments.
Pharmacogenomics
is
reshaping
treatment
personalization,
enabling
tailored
align
individual
profiles,
while
diagnostics
biomarkers
ushering
era
early,
precise
disease
detection.
Furthermore,
novel
perspectives
gut-brain
axis
sparking
interest
mounting
evidence
suggests
microbiome
modulation
may
play
role
reducing
neuroinflammatory
responses
linked
neurodegenerative
progression.
Taken
together,
advances
signal
shift
toward
comprehensive,
personalized
approach
could
transform
care.
By
integrating
techniques,
this
offers
forward-looking
perspective
future
where
treatments
aim
just
manage
symptoms
fundamentally
alter
progression,
presenting
renewed
hope
for
improved
patient
outcomes.
