The FASEB Journal,
Journal Year:
2024,
Volume and Issue:
38(17)
Published: Sept. 1, 2024
Citicoline,
a
compound
produced
naturally
in
small
amounts
the
human
body,
assumes
pivotal
role
phosphatidylcholine
synthesis,
dynamic
constituent
of
membranes
neurons.
Across
diverse
models
brain
injury
and
neurodegeneration,
citicoline
has
demonstrated
its
potential
through
neuroprotective
anti-inflammatory
effects.
This
review
aims
to
elucidate
citicoline's
mechanism
clinical
implications
conditions
such
as
ischemic
stroke,
head
trauma,
glaucoma,
age-associated
memory
impairment.
Citicoline's
prowess
is
rooted
ability
stabilize
cellular
membranes,
thereby
curbing
excessive
release
glutamate-a
pro-inflammatory
neurotransmitter.
Moreover,
it
actively
diminishes
free
radicals
inflammatory
cytokines
productions,
which
could
otherwise
harm
neurons
incite
neuroinflammation.
It
also
exhibits
modulate
microglia
activity,
brain's
resident
immune
cells,
hinder
activation
NF-κB,
transcription
factor
governing
genes.
Clinical
trials
have
subjected
rigorous
scrutiny
patients
grappling
with
acute
age-related
While
findings
from
these
are
mixed,
numerous
studies
suggest
that
confer
improvements
neurological
function,
disability
reduction,
expedited
recovery,
cognitive
decline
prevention
within
cohorts.
Additionally,
boasts
favorable
safety
profile
high
tolerability.
In
summary,
stands
promising
agent,
wielding
both
across
spectrum
conditions.
However,
further
research
imperative
delineate
optimal
dosage,
treatment
duration,
underlying
mechanisms.
identifying
specific
patient
subgroups
most
likely
reap
benefits
new
therapy
remains
critical
avenue
for
exploration.
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.
Neuropsychopharmacology Reports,
Journal Year:
2025,
Volume and Issue:
45(1)
Published: Jan. 5, 2025
Alzheimer's
disease
(AD)
is
the
most
common
neurodegenerative
associated
with
development
of
dementia.
The
hallmarks
AD
neuropathology
are
accumulations
amyloid
peptide
(Aβ)
and
neurofibrillary
tangles
(NFTs).
Aβ
derived
from
processing
APP
(amyloid
beta
precursor
protein)
by
BACE1
(beta-secretase
1)
γ-secretase
through
an
amyloidogenic
pathway.
However,
ADAM10/α-secretase
(ADAM
metallopeptidase
domain
10)
enzymes
a
non-amyloidogenic
pathway
produces
soluble
alpha
(sAPPα),
which
has
neuroprotective
effect.
It
been
shown
that
activated
platelets
implicated
in
pathogenesis
AD,
also
increases
platelet
activation.
Under
physiological
conditions,
regulate
synaptic
plasticity
increase
neuronal
differentiation
regulation
inflammatory
response.
overactivated
contribute
to
AD.
Activated
represent
main
source
circulating
may
be
involved
neuropathology.
Therefore,
there
close
relationship
between
platelets.
This
review
discusses
potential
role
how
targeting
reduce
Autophagy,
Journal Year:
2023,
Volume and Issue:
20(2), P. 259 - 274
Published: Sept. 15, 2023
Multiple
sclerosis
(MS)
is
a
chronic
progressive
demyelinating
disease
of
the
central
nervous
system
(CNS)
due
to
an
increase
abnormal
peripherally
auto-reactive
T
lymphocytes
which
elicit
autoimmunity.
The
main
pathophysiology
MS
myelin
sheath
damage
by
immune
cells
and
defect
in
generation
oligodendrocytes.
Macroautophagy/autophagy
critical
degradation
process
that
eliminates
dysfunctional
or
superfluous
cellular
components.
Autophagy
has
property
double-edged
sword
it
may
have
both
beneficial
detrimental
effects
on
neuropathology.
Therefore,
this
review
illustrates
protective
harmful
autophagy
with
regard
disease.
prevents
progression
reducing
oxidative
stress
inflammatory
disorders.
In
contrast,
over-activated
associated
neuropathology
case
use
inhibitors
alleviate
pathogenesis
MS.
Furthermore,
provokes
activation
different
supporting
play
intricate
role
functions
modulation
regulating
cell
proliferation
related
demyelination
remyelination.
enhances
remyelination
increasing
activity
oligodendrocytes,
astrocytes.
However,
induces
activating
microglia
cells.
conclusion,
specific
autophagic
activators
astrocytes,
dendritic
(DCs),
induce
against
Pharmacology Research & Perspectives,
Journal Year:
2023,
Volume and Issue:
11(2)
Published: Feb. 22, 2023
Parkinson's
disease
(PD)
is
the
second
most
frequent
neurodegenerative
brain
(NBD)
after
Alzheimer's
(AD).
Statins
are
common
lipid-lowering
agents
used
in
management
of
dyslipidemia
and
prevention
primary
secondary
cardiovascular
diseases
(CVD)
events.
In
addition,
there
a
controversial
point
regarding
role
serum
lipids
pathogenesis
PD.
this
bargain,
as
statins
reduce
cholesterol
so
they
affect
PD
neuropathology
bidirectional
ways
either
protective
or
harmful.
not
PD,
but
frequently
disorders
commonly
associated
with
elderly
population.
Therefore,
use
that
population
may
outcomes.
Concerning
potential
on
neuropathology,
conflicts
controversies
against
development
harmful
by
increasing
risk
for
review
aimed
to
clarify
precise
pros
cons
from
published
studies.
Many
studies
suggest
through
modulation
inflammatory
lysosomal
signaling
pathways.
Nevertheless,
other
observations
statin
therapy
increase
diverse
mechanisms
including
reduction
CoQ10.
conclusion,
strong
neuropathology.
retrospective
prospective
necessary
regard.
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.
