Journal of Cellular and Molecular Medicine,
Journal Year:
2024,
Volume and Issue:
28(12)
Published: June 1, 2024
Abstract
Parkinson
disease
(PD)
is
one
of
the
most
common
neurodegenerative
diseases
brain.
Of
note,
brain
renin‐angiotensin
system
(RAS)
intricate
in
PD
neuropathology
through
modulation
oxidative
stress,
mitochondrial
dysfunction
and
neuroinflammation.
Therefore,
RAS
by
angiotensin
receptor
blockers
(ARBs)
angiotensin‐converting
enzyme
inhibitors
(ACEIs)
may
be
effective
reducing
risk
neuropathology.
It
has
been
shown
that
all
components
including
peptides
enzymes
are
present
different
areas.
Brain
plays
a
critical
role
regulation
memory
cognitive
function,
controlling
central
blood
pressure.
However,
exaggerated
implicated
pathogenesis
PD.
Two
well‐known
pathways
recognized
including;
classical
pathway
which
mainly
mediated
AngII/AT1R
detrimental
effects.
Conversely,
non‐classical
mostly
ACE2/Ang1‐7/MASR
AngII/AT2R
beneficial
effects
against
Exaggerated
affects
viability
dopaminergic
neurons.
fundamental
mechanism
was
not
fully
elucidated.
Consequently,
purpose
this
review
to
disclose
mechanistic
In
addition,
we
try
revise
how
ACEIs
ARBs
can
developed
for
therapeutics
Journal of Cellular and Molecular Medicine,
Journal Year:
2024,
Volume and Issue:
28(10)
Published: May 1, 2024
Parkinson's
disease
(PD)
is
a
neurodegenerative
disorder
of
the
brain
and
manifested
by
motor
non-motor
symptoms
because
degenerative
changes
in
dopaminergic
neurons
substantia
nigra.
PD
neuropathology
associated
with
mitochondrial
dysfunction,
oxidative
damage
apoptosis.
Thus,
modulation
apoptosis
growth
factors
could
be
novel
boulevard
management
PD.
Brain-derived
neurotrophic
factor
(BDNF)
its
receptor
tropomyosin
kinase
type
B
(TrkB)
are
chiefly
involved
neuropathology.
BDNF
promotes
survival
nigra
enhances
functional
activity
striatal
neurons.
Deficiency
TrkB
triggers
degeneration
accumulation
α-Syn
As
well,
BDNF/TrkB
signalling
reduced
early
phase
Targeting
specific
activators
may
attenuate
this
review
aimed
to
discuss
potential
role
against
In
conclusion,
decreased
linked
severity
long-term
complications.
Activation
Parkinson's
disease
(PD)
is
a
progressive
neurodegenerative
brain
due
to
degeneration
of
dopaminergic
neurons
(DNs)
presented
with
motor
and
non-motor
symptoms.
PD
symptoms
are
developed
in
response
the
disturbance
diverse
neurotransmitters
including
γ-aminobutyric
acid
(GABA).
GABA
has
neuroprotective
effect
against
neuropathology
by
protecting
DNs
substantia
nigra
pars
compacta
(SNpc).
It
been
shown
that
GABAergic
linked
progression
neurotransmission
necessary
pathway
for
normal
sleep
patterns,
thus
deregulation
could
be
potential
cause
disorders
PD.
Cellular and Molecular Neurobiology,
Journal Year:
2023,
Volume and Issue:
43(6), P. 2743 - 2759
Published: April 19, 2023
Abstract
Parkinson’s
disease
(PD)
is
one
of
the
most
common
degenerative
brain
disorders
caused
by
loss
dopaminergic
neurons
in
substantia
nigra
(SN).
Lewy
bodies
and
-synuclein
accumulation
SN
are
hallmarks
neuropathology
PD.
Due
to
lifestyle
changes
prolonged
L-dopa
administration,
patients
with
PD
frequently
have
vitamin
deficiencies,
especially
folate,
B6,
B12.
These
augment
circulating
levels
Homocysteine
development
hyperhomocysteinemia,
which
may
contribute
pathogenesis
Therefore,
this
review
aimed
ascertain
if
hyperhomocysteinemia
play
a
part
oxidative
inflammatory
signaling
pathways
that
development.
Hyperhomocysteinemia
implicated
neurodegenerative
disorders,
including
triggers
progression
different
mechanisms,
stress,
mitochondrial
dysfunction,
apoptosis,
endothelial
dysfunction.
Particularly,
linked
high
systemic
disorders.
induces
immune
activation
stress.
In
turn,
activated
response
promotes
hyperhomocysteinemia.
hyperhomocysteinemia-induced
immunoinflammatory
abnormal
aggravate
PD,
leading
more
severity.
Also,
like
nuclear
factor
kappa
B
(NF-κB)
nod-like
receptor
pyrin
3
(NLRP3)
inflammasome
other
intricate
conclusion,
involved
either
directly
via
induction
degeneration
or
indirectly
pathways.
Molecular Medicine,
Journal Year:
2023,
Volume and Issue:
29(1)
Published: Oct. 25, 2023
Abstract
Autophagy
is
an
explicit
cellular
process
to
deliver
dissimilar
cytoplasmic
misfolded
proteins,
lipids
and
damaged
organelles
the
lysosomes
for
degradation
elimination.
The
mechanistic
target
of
rapamycin
(mTOR)
main
negative
regulator
autophagy.
mTOR
pathway
involved
in
regulating
neurogenesis,
synaptic
plasticity,
neuronal
development
excitability.
Exaggerated
activity
associated
with
temporal
lobe
epilepsy,
genetic
acquired
experimental
epilepsy.
In
particular,
complex
1
(mTORC1)
mainly
epileptogenesis.
investigation
autophagy’s
involvement
epilepsy
has
recently
been
conducted,
focusing
on
critical
role
rapamycin,
autophagy
inducer,
reducing
severity
induced
seizures
animal
model
studies.
induction
could
be
innovative
therapeutic
strategy
managing
Despite
protective
against
epileptogenesis
its
status
epilepticus
(SE)
perplexing
might
beneficial
or
detrimental.
Therefore,
present
review
aims
revise
possible
Molecular Neurobiology,
Journal Year:
2023,
Volume and Issue:
61(1), P. 341 - 357
Published: Aug. 22, 2023
Abstract
Parkinson’s
disease
(PD)
is
a
neurodegenerative
due
to
the
degeneration
of
dopaminergic
neurons
(DNs)
in
substantia
nigra
(SN).
The
liver
X
receptor
(LXR)
involved
different
diseases.
Therefore,
objective
present
review
was
clarify
possible
role
LXR
PD
neuropathology.
LXRs
are
most
common
nuclear
receptors
transcription
factors
that
regulate
cholesterol
metabolism
and
have
pleiotropic
effects,
including
anti-inflammatory
effects
reducing
intracellular
accumulation.
highly
expressed
adult
brain
act
as
endogenous
sensors
for
cholesterol.
neuroprotective
against
development
neuroinflammation
diseases
by
inhibiting
expression
pro-inflammatory
cytokines.
play
an
essential
mitigating
neuropathology
inflammatory
signaling
pathways,
neuroinflammation,
oxidative
stress,
mitochondrial
dysfunction,
enhancement
BDNF
signaling.
In
conclusion,
LXRs,
through
regulating
homeostasis,
may
be
effectual
PD.
Also,
inhibition
node-like
pyrin
3
(NLRP3)
inflammasome
factor
kappa
B
(NF-κB)
could
effectively
prevent
Taken
together,
crucial
associated
DNs.